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Ghrelin receptor, also known as growth hormone secretagogue receptor (GHS-R1a), is coexpressed with its truncated isoform GHS-R1b, which does not bind ghrelin or signal, but oligomerizes with GHS-R1a, exerting a complex modulatory role that depends on its relative expression. D1dopamine receptor (D1R) and D5R constitute the two D1-like receptor subtypes. Previous studies showed that GHS-R1b also facilitates oligomerization of GHS-R1a with D1R, conferring GHS-R1a distinctive pharmacological properties. Those include a switch in the preferred coupling of GHS-R1a from Gq to Gs and the ability of D1R/D5R agonists and antagonists to counteract GHS-R1a signaling. Activation of ghrelin receptors localized in the ventral tegmental area (VTA) seems to play a significant role in the contribution of ghrelin to motivated behavior. In view of the evidence indicating that dopaminergic cells of the VTA express ghrelin receptors and D5R, but not D1R, we investigated the possible existence of functional GHS-R1a:GHS-R1b:D5R oligomeric complexes in the VTA. GHS-R1a:GHS-R1b:D5R oligomers were first demonstrated in mammalian transfected cells, and their pharmacological properties were found to be different from those of GHS-R1a:GHS-R1b:D1R oligomers, including weak Gs coupling and the ability of D1R/D5R antagonists, but not agonists, to counteract the effects of ghrelin. However, analyzing the effect of ghrelin in the rodent VTA on MAPK activation withex vivoexperiments, on somatodendritic dopamine release within vivomicrodialysis and on the activation of dopaminergic cells with patch-clamp electrophysiology, provided evidence for a predominant role of GHS-R1a:GHS-R1b:D1R oligomers in the rodent VTA as main mediators of the dopaminergic effects of ghrelin.SIGNIFICANCE STATEMENTThe activation of ghrelin receptors localized in the ventral tegmental area (VTA) plays a significant role in the contribution of ghrelin to motivated behavior. We present evidence that indicates these receptors form part of oligomeric complexes that include the functional ghrelin receptor GHS-R1a, its truncated nonsignaling isoform GHS-R1b, and the dopamine D1receptor (D1R). The binding of ghrelin to these complexes promotes activation of the dopaminergic neurons of the VTA by activation of adenylyl cyclase–protein kinase A signaling, which can be counteracted by both GHS-R1a and D1R antagonists. Our study provides evidence for a predominant role of GHS-R1a:GHS-R1b:D1R oligomers in rodent VTA as main mediators of the dopaminergic effects of ghrelin.

Akathisia is an urgent need to move that is associated with treatment with dopamine receptor blocking agents (DRBAs) and with restless legs syndrome (RLS). The pathogenetic mechanism of akathisia has not been resolved. This article proposes that it involves an increased presynaptic dopaminergic transmission in the ventral striatum and concomitant strong activation of postsynaptic dopamine D1 receptors, which form complexes (heteromers) with dopamine D3 and adenosine A1 receptors. It also proposes that in DRBA-induced akathisia, increased dopamine release depends on inactivation of autoreceptors, whereas in RLS it depends on a brain iron deficiency-induced down-regulation of striatal presynaptic A1 receptors.

Adenosine plays a very significant role in modulating striatal glutamatergic and dopaminergic neurotransmission. In the present essay we first review the extensive evidence that indicates this modulation is mediated by adenosine A1 and A2A receptors (A1Rs and A2ARs) differentially expressed by the components of the striatal microcircuit that include cortico-striatal glutamatergic and mesencephalic dopaminergic terminals, and the cholinergic interneuron. This microcircuit mediates the ability of striatal glutamate release to locally promote dopamine release through the intermediate activation of cholinergic interneurons. A1Rs and A2ARs are colocalized in the cortico-striatal glutamatergic terminals, where they form A1R-A2AR and A2AR-cannabinoid CB1 receptor (CB1R) heteromers. We then evaluate recent findings on the unique properties of A1R-A2AR and A2AR-CB1R heteromers, which depend on their different quaternary tetrameric structure. These properties involve different allosteric mechanisms in the two receptor heteromers that provide fine-tune modulation of adenosine and endocannabinoid-mediated striatal glutamate release. Finally, we evaluate the evidence supporting the use of different heteromers containing striatal adenosine receptors as targets for drug development for neuropsychiatric disorders, such as Parkinson's disease and restless legs syndrome, based on the ability or inability of the A2AR to demonstrate constitutive activity in the different heteromers, and the ability of some A2AR ligands to act preferentially as neutral antagonists or inverse agonists, or to have preferential affinity for a specific A2AR heteromer.

Akathisia is an urgent need to move that is associated with treatment with dopamine receptor blocking agents (DRBAs) and with restless legs syndrome (RLS). The pathogenetic mechanism of akathisia has not been resolved. This article proposes that it involves an increased presynaptic dopaminergic transmission in the ventral striatum and concomitant strong activation of postsynaptic dopamine D

Dopamine (DA) signals in the striatum are critical for a variety of vital processes, including motivation, motor learning, and reinforcement learning. Striatal DA signals can be evoked by direct activation of inputs from midbrain DA neurons (DANs) as well as cortical and thalamic inputs to the striatum. In this study, we show that in vivo optogenetic stimulation of prelimbic (PrL) and infralimbic (IL) cortical afferents to the striatum triggers an increase in extracellular DA concentration, which coincides with elevation of striatal acetylcholine (ACh) levels. This increase is blocked by a nicotinic ACh receptor (nAChR) antagonist. Using single or dual optogenetic stimulation in brain slices from male and female mice, we compared the properties of these PrL/IL-evoked DA signals with those evoked by stimulation from midbrain DAN axonal projections. PrL/IL-evoked DA signals are undistinguishable from DAN evoked DA signals in their amplitudes and electrochemical properties. However, PrL/IL-evoked DA signals are spatially restricted and preferentially recorded in the dorsomedial striatum. PrL/IL-evoked DA signals also differ in their pharmacological properties, requiring activation of glutamate and nicotinic ACh receptors. Thus, both in vivo and in vitro results indicate that cortical evoked DA signals rely on recruitment of cholinergic interneurons, which renders DA signals less able to summate during trains of stimulation and more sensitive to both cholinergic drugs and temperature. In conclusion, cortical and midbrain inputs to the striatum evoke DA signals with unique spatial and pharmacological properties that likely shape their functional roles and behavioral relevance. SIGNIFICANCE STATEMENT Dopamine signals in the striatum play a critical role in basal ganglia function, such as reinforcement and motor learning. Different afferents to the striatum can trigger dopamine signals, but their release properties are not well understood. Further, these input-specific dopamine signals have only been studied in separate animals. Here we show that optogenetic stimulation of cortical glutamatergic afferents to the striatum triggers dopamine signals both in vivo and in vitro. These afferents engage cholinergic interneurons, which drive dopamine release from dopamine neuron axons by activation of nicotinic acetylcholine receptors. We also show that cortically evoked dopamine signals have other unique properties, including spatial restriction and sensitivity to temperature changes than dopamine signals evoked by stimulation of midbrain dopamine neuron axons.

Surveillance of overhead power line installations can be conveniently addressed using unmanned aerial vehicles (UAV). UAV are robotic platforms able to perform sophisticated tasks such as autonomous flight based on visual information. In this paper, we propose a novel solution to the problem of following a power line autonomously based on monocular vision. The method uses Deep Neural Networks (DNN) and the Hough transform to successfully discern power line images from environmental information, which is an essential result to accomplish fully autonomous vision-based navigation. A simulated navigation test demonstrates the efficiency of the proposed method, in the special condition of following right-angled changes of direction, which is a known restriction in many navigation methods reported in literature. The design of the proposed method is modular and can be incorporated in navigation strategies for automatic surveillance applications.

Our working hypothesis is that a hypoadenosinergic state is a main pathogenetic factor that determines the sensory-motor symptoms and hyperarousal of restless legs syndrome (RLS). We have recently demonstrated that brain iron deficiency (BID) in rodents, a well-accepted animal model of RLS, is associated with a generalized downregulation of adenosine A1 receptors (A1R) in the brain and with hypersensitivity of corticostriatal glutamatergic terminals. Here, we first review the experimental evidence for a pivotal role of adenosine and A1R in the control of striatal glutamatergic transmission and the rationale for targeting putative downregulated striatal A1R in RLS patients, which is supported by recent clinical results obtained with dipyridamole, an inhibitor of the nucleoside transporters ENT1 and ENT2. Second, we perform optogenetic-microdialysis experiments in rats to demonstrate that A1R determine the sensitivity of corticostriatal glutamatergic terminals and the ability of dipyridamole to counteract optogenetically-induced corticostriatal glutamate release in both animals with BID and controls. Thus, a frequency of optogenetic stimulation that was ineffective at inducing cortico-striatal glutamate release in control rats became effective with the local perfusion of a selective A1R antagonist. Furthermore, in animals with and without BID, the striatal application of dipyridamole blocked the optogenetic-induced glutamate release and decreased basal levels of glutamate, which was counteracted by the A1R antagonist. The results support the clinical application of ENT1 inhibitors in RLS.

Several studies found in vitro evidence for heteromerization of dopamine D(1) receptors (D1R) and D(3) receptors (D3R), and it has been postulated that functional D1R-D3R heteromers that are normally present in the ventral striatum mediate synergistic locomotor-activating effects of D1R and D3R agonists in rodents. Based also on results obtained in vitro, with mammalian transfected cells, it has been hypothesized that those behavioral effects depend on a D1R-D3R heteromer-mediated G protein-independent signaling. Here, we demonstrate the presence on D1R-D3R heteromers in the mouse ventral striatum by using a synthetic peptide that selectively destabilizes D1R-D3R heteromers. Parallel locomotor activity and ex vivo experiments in reserpinized mice and in vitro experiments in D1R-D3R mammalian transfected cells were performed to dissect the signaling mechanisms of D1R-D3R heteromers. Co-administration of D1R and D3R agonists in reserpinized mice produced synergistic locomotor activation and a selective synergistic AKT phosphorylation in the most ventromedial region of the striatum, in the shell of the nucleus accumbens. Application of the destabilizing peptide in transfected cells and in the shell of the nucleus accumbens allowed demonstrating that, both in vitro and in vivo, co-activation of D3R induces a switch from G protein-dependent to G protein-independent D1R-mediated signaling determined by D1R-D3R heteromerization. The results therefore demonstrate that a biased G protein-independent signaling of D1R-D3R heteromers localized in the shell of the nucleus accumbens mediate the locomotor synergistic effects of D1R and D3R agonists in reserpinized mice.

O presente trabalho teve como objetivo desenvolver o protótipo de um robô móvel seguidor de linha para circuitos com obstáculos. Os estudos iniciais foram divididos em módulos de eletricidade, eletrônica analógica e digital, lógica de programação e microcontroladores. A partir disso, com os conceitos aprendidos, realizou-se a integração com um robô móvel para seguir uma linha preta em uma pista com dimensão de 295mm x 420 mm. A programação foi feita na plataforma Arduino UNO baseada em C/C++, no qual foram conectados seis sensores IR, dois sensores ultrassônicos e dois atuadores. O projeto foi implementado e teve seu funcionamento como esperado. Ainda durante a finalização do robô, foi implementado um controle Proporcional/Derivativo pelos monitores para obter um controle de movimento mais suave em curvas no percurso elaborado.

This paper applies to an adaptation of a Visual Odometry (VO) technique, originally created for outdoor real datasets, to an indoor virtual environment, and the integration of this environment with a dynamic model of a wheelchair. Thus, it were used three software; Matlab® running the dynamic model of the wheelchair, generating the pose vector for each step of the trajectory, and sending these values; Blender receiving the chair's position (x,y) and orientation (β), moving the robot to the specified position, rendering the images and saving them in a directory; and an OpenCV/C++ application using these images to estimate the traveled trajectory. The objective is to show a methodology to combine a model in Matlab® with a computer graphics platform, and a very powerful monocular visual odometry technique for outdoor environments, adapted to indoor, comparing with the ground truth values provided by this simulator. In addition, to the best of our knowledge, no adaption of this monocular method for indoor environments are available yet.

The symptomatology of Restless Legs Syndrome (RLS) includes periodic leg movements during sleep (PLMS), dysesthesias, and hyperarousal. Alterations in the dopaminergic system, a presynaptic hyperdopaminergic state, seem to be involved in PLMS, while alterations in glutamatergic neurotransmission, a presynaptic hyperglutamatergic state, seem to be involved in hyperarousal and also PLMS. Brain iron deficiency (BID) is well-recognized as a main initial pathophysiological mechanism of RLS. BID in rodents have provided a pathogenetic model of RLS that recapitulates the biochemical alterations of the dopaminergic system of RLS, although without PLMS-like motor abnormalities. On the other hand, BID in rodents reproduces the circadian sleep architecture of RLS, indicating the model could provide clues for the hyperglutamatergic state in RLS. We recently showed that BID in rodents is associated with changes in adenosinergic transmission, with downregulation of adenosine A1 receptors (A1R) as the most sensitive biochemical finding. It was hypothesized that A1R downregulation leads to hypersensitive striatal glutamatergic terminals and facilitation of striatal dopamine release. Hypersensitivity of striatal glutamatergic terminals was demonstrated by an optogenetic-microdialysis approach in the rodent with BID, indicating that it could represent a main pathogenetic factor that leads to PLMS in RLS. In fact, the dopaminergic agonists pramipexole and ropinirole and the α2δ ligand gabapentin, used in the initial symptomatic treatment of RLS, completely counteracted optogenetically-induced glutamate release from both normal and BID-induced hypersensitive corticostriatal glutamatergic terminals. It is a main tenet of this essay that, in RLS, a single alteration in the adenosinergic system, downregulation of A1R, disrupts the adenosine-dopamine-glutamate balance uniquely controlled by adenosine and dopamine receptor heteromers in the striatum and also the A1R-mediated inhibitory control of glutamatergic neurotransmission in the cortex and other non-striatal brain areas, which altogether determine both PLMS and hyperarousal. Since A1R agonists would be associated with severe cardiovascular effects, it was hypothesized that inhibitors of nucleoside equilibrative transporters, such as dipyridamole, by increasing the tonic A1R activation mediated by endogenous adenosine, could represent a new alternative therapeutic strategy for RLS. In fact, preliminary clinical data indicate that dipyridamole can significantly improve the symptomatology of RLS.

A cephalometric analysis of the upper airway in patients with cleft lip and palate sequelae who underwent orthognathic surgery was performed. The study aims to determine if changes in upper airway morphology occur. Study design: A retrospective, descriptive, open, comparative, and cross-sectional study with a sample of 28 patients with unilateral cleft lip and palate sequelae (UCLPS) was performed. The study sample consisted of 50% male and 50% female patients whose ages ranged between 16 and 29 years of age and averaged 19.32 years. Measurements were made on pre- and post-surgical lateral headfi lms. A total of 672 cephalometric measurements were made. The study’s fi ndings indicate that changes in the upper airway after bone mobilization techniques in orthognathic surgery do exist. Statistical signifi cance was set at p < 0.05 and was met on three of the assessed variables: upper pharynx (p = 0.001), bony pharynx dimension (p = .000), and nasopharyngeal depth (p = .000). Key words: Cephalometric analysis, upper airway, unilateral cleft lip and palate sequelae, orthognathic surgery, upper pharynx, bony pharynx dimension, nasopharyngeal depth.

RESUMENSe realizó un estudio cefalométrico de la vía aérea superior en pacientes con secuela de labio y paladar hendido unilateral (SLPHU) sometidos a procedimientos de cirugía ortognática, con la finalidad de conocer si existen cambios en la morfología de la vía aérea pre- y postquirúrgicos. El diseño del estudio fue observacional descriptivo, abierto, comparativo, retrospectivo y transversal en una muestra de 28 pacientes con SLPHU, correspondiendo el 50% al género masculino y 50% al femenino. El rango de edad fue de 16 a 29 años con un promedio de 19.32 años. Las mediciones fueron realizadas en radiografías laterales de cráneo pre- y postquirúrgicas, con un total de 672 trazos cefalométricos. Los hallazgos encontrados en el presente estudio muestran que sí existen cambios en la vía aérea superior después de los procedimientos de movilización ósea con cirugía ortognática. Se observó una diferencia estadísticamente significativa (p

Release of the neuropeptides corticotropin-releasing factor (CRF) and orexin-A in the ventral tegmental area (VTA) play an important role in stress-induced cocaine-seeking behavior. We provide evidence for pharmacologically significant interactions between CRF and orexin-A that depend on oligomerization of CRF1receptor (CRF1R) and orexin OX1receptors (OX1R). CRF1R–OX1R heteromers are the conduits of a negative crosstalk between orexin-A and CRF as demonstrated in transfected cells and rat VTA, in which they significantly modulate dendritic dopamine release. The cocaine target σ1receptor (σ1R) also associates with the CRF1R–OX1R heteromer. Cocaine binding to the σ1R–CRF1R–OX1R complex promotes a long-term disruption of the orexin-A–CRF negative crosstalk. Through this mechanism, cocaine sensitizes VTA cells to the excitatory effects of both CRF and orexin-A, thus providing a mechanism by which stress induces cocaine seeking.

The central adenosine system and adenosine receptors play a fundamental role in the modulation of dopaminergic neurotransmission. This is mostly achieved by the strategic co-localization of different adenosine and dopamine receptor subtypes in the two populations of striatal efferent neurons, striatonigral and striatopallidal, that give rise to the direct and indirect striatal efferent pathways, respectively. With optogenetic techniques it has been possible to dissect a differential role of the direct and indirect pathways in mediating “Go” responses upon exposure to reward-related stimuli and “NoGo” responses upon exposure to non-rewarded or aversive-related stimuli, respectively, which depends on their different connecting output structures and their differential expression of dopamine and adenosine receptor subtypes. The striatopallidal neuron selectively expresses dopamine D2 receptors (D2R) and adenosine A2A receptors (A2AR), and numerous experiments using multiple genetic and pharmacological in vitro, in situ and in vivo approaches, demonstrate they can form A2AR-D2R heteromers. It was initially assumed that different pharmacological interactions between dopamine and adenosine receptor ligands indicated the existence of different subpopulations of A2AR and D2R in the striatopallidal neuron. However, as elaborated in the present essay, most evidence now indicates that all interactions can be explained with a predominant population of striatal A2AR-D2R heteromers forming complexes with adenylyl cyclase subtype 5 (AC5). The A2AR-D2R heteromer has a tetrameric structure, with two homodimers, which allows not only multiple allosteric interactions between different orthosteric ligands, agonists, and antagonists, but also the canonical Gs-Gi antagonistic interaction at the level of AC5. We present a model of the function of the A2AR-D2R heterotetramer-AC5 complex, which acts as an integrative device of adenosine and dopamine signals that determine the excitability and gene expression of the striatopallidal neurons. The model can explain most behavioral effects of A2AR and D2R ligands, including the psychostimulant effects of caffeine. The model is also discussed in the context of different functional striatal compartments, mainly the dorsal and the ventral striatum. The current accumulated knowledge of the biochemical properties of the A2AR-D2R heterotetramer-AC5 complex offers new therapeutic possibilities for Parkinson’s disease, schizophrenia, SUD and other neuropsychiatric disorders with dysfunction of dorsal or ventral striatopallidal neurons.

Localization is one of the main tasks of autonomous mobile robots. There are many approaches on how to determine the robot's position with reasonable precision, as with the use of sensor fusion (IMU, GPS, Image, LiDAR). Even though it is possible to achieve high precision with these sensors combined, a solution that requires less resources in terms of processing, energy consumption and yet provide a good enough estimation for position control is sought. This paper presents the application of an artificial neural network to improve position estimates from inertial measurement in a mobile robot navigating in an indoor environment.

Objective The first aim was to demonstrate a previously hypothesized increased sensitivity of corticostriatal glutamatergic terminals in the rodent with brain iron deficiency (BID), a pathogenetic model of restless legs syndrome (RLS). The second aim was to determine whether these putative hypersensitive terminals could constitute a significant target for drugs effective in RLS, including dopamine agonists (pramipexole and ropinirole) and α2 δ ligands (gabapentin). Methods A recently introduced in vivo optogenetic-microdialysis approach was used, which allows the measurement of the extracellular concentration of glutamate upon local light-induced stimulation of corticostriatal glutamatergic terminals. The method also allows analysis of the effect of local perfusion of compounds within the same area being sampled for glutamate. Results BID rats showed hypersensitivity of corticostriatal glutamatergic terminals (lower frequency of optogenetic stimulation to induce glutamate release). Both hypersensitive and control glutamatergic terminals were significant targets for locally perfused pramipexole, ropinirole, and gabapentin, which significantly counteracted optogenetically induced glutamate release. The use of selective antagonists demonstrated the involvement of dopamine D4 and D2 receptor subtypes in the effects of pramipexole. Interpretation Hypersensitivity of corticostriatal glutamatergic terminals can constitute a main pathogenetic mechanism of RLS symptoms. Selective D4 receptor agonists, by specifically targeting these terminals, should provide a new efficient treatment with fewer secondary effects. Ann Neurol 2017;82:951-960.

The function of the dopamine D4 receptor and the product of a clinically significant gene polymorphic variant is revealed., Polymorphic variants of the dopamine D4 receptor gene (DRD4) have been repeatedly associated with numerous neuropsychiatric disorders. Yet, the functional role of the D4 receptor and the functional differences of the products of DRD4 polymorphic variants remained enigmatic. Immunohistochemical and optogenetic-microdialysis experiments were performed in knock-in mice expressing a D4 receptor with the long intracellular domain of a human DRD4 polymorphic variant associated with attention deficit hyperactivity disorder (ADHD). When compared with the wild-type mouse D4 receptor, the expanded intracellular domain of the humanized D4 receptor conferred a gain of function, blunting methamphetamine-induced cortical activation and optogenetic and methamphetamine-induced corticostriatal glutamate release. The results demonstrate a key role of the D4 receptor in the modulation of corticostriatal glutamatergic neurotransmission. Furthermore, these data imply that enhanced D4 receptor–mediated dopaminergic control of corticostriatal transmission constitutes a vulnerability factor of ADHD and other neuropsychiatric disorders.

ResumenEl labio y paladar hendidos es una malformación congénita que puede afectar los mecanismos respiratorios, deglutorios, articulatorios, del lenguaje, la audición y la voz. A los pacientes que les falta un crecimiento maxilar adecuado presentan una relación esquelética maxilomandibular clase III por retrusión maxilar. El tratamiento ortopédico con máscara facial en estos pacientes con secuela de labio y paladar hendidos unilaterales durante un periodo adecuado puede estimular y redirigir el crecimiento del maxilar. En este trabajo se estudiaron 90 expedientes (antes y después del tratamiento) de pacientes con secuela de labio y paladar hendidos unilaterales completos (fisura labio-alveolo-palatino) que fueron atendidos en la División de Estomatología-Ortodoncia del Hospital General «Dr. Manuel Gea González» durante los años de 1996 a 2007, y que fueron tratados con máscara de protracción facial con apoyo frontomentoniano y un aparato intraoral con un tornillo de expansión rápida palatina con caras oclusales de acrílico. Para evaluar los cambios maxilares en sentido anteroposterior y vertical. Se utilizó la prueba t, de Wilcoxon y χ2 (SPSS v.10). Se concluyó que el uso de la máscara facial en estos pacientes aumenta la dimensión vertical y reduce la discrepancia maxilomandibular por una estimulación del crecimiento maxilar hacia abajo y adelante.AbstractCleft lip and palate is a congenital malformation which can affect breathing, swallowing, language articulation, audition and voice. These patients show an insufficient maxillary growth and a class III skeletal malocclusion due to maxillary retrusion. Orthopedic treatment of the unilateral cleft lip and cleft palate patient by means of a facemask during the right time can stimulate maxillary growth. This study reviewed 90 clinical charts (pre and post treatment) of patients with complete unilateral cleft lip and cleft palate, treated from 1996 to 2007 with rapid palatal expansion through an occlusal acrylic plate and facemask at the Orthodontic Department, General Hospital «Dr. Manuel Gea Gonzalez» in Mexico City. To evaluate the sagittal and vertical maxillomandibular change the Student’s T test, Wilcoxon test and χ2 test (SPSS v.10) were used. Our results show that the use of this appliance increases vertical dimension and reduces maxillomandibular discrepancy due to downward and forward growth of the maxilla.

The aim of this study was to compare cephalometric results of three and two dimensional surgical predictions in patients that underwent orthognatic surgery. The study involved two groups of 15 to 30 years old patients with craniofacial anomalies. The fi rst group of patients had orthognatic surgery from April 2004 to January 2005. Pre and post-surgical lateral cephalometric measurements were done using Simplant program, (version CMF 8.2 of Materialise, NV, Belgium). The second group of patients had orthognatic surgery from January 1999 to January 2004. Pre and post-surgical lateral cephalometric measurements were done manually. The results of this study showed a more accurate surgical prediction with the Simplant program. In group I (three-dimensional cephalometric measurement) there was not a statistically significant difference between the prediction measurements done before the surgery and those compared with the post-surgically result. In group II, (two-dimensional cephalometric measurements) on the surgical predictions done previously by hand using cut and paste mobiles taken from the patient’s Hospital records, we observed that in the SNA angle and the maxillary length measurements there was a statistically difference (p < .05). Therefore we conclude that the three-dimensional method is more accurate than the twodimensional method in planning surgical orthognatic procedures. Key words: Three-dimensional cephalometry, bi-dimensional cephalometry, craniofacial anomalies, cleft lip and palate, maxillary protrusion, mandibular pragmatism, orthognatic surgery.

This work proposes a low cost calibration method for micro-electro-mechanical inertial (MEMS) gyroscopes, using a camera pan-tilt base. The use of MEMS gyroscopes in practical robotics measurements requires preliminary calibration. Three calibration procedures are currently found in the literature to estimate the sensor calibration parameters which are based on static, quasi-static and dynamic measurements. This paper focus in the investigation of quasi-static calibration procedure which consists in moving the sensor in a path with known kinematics. High complexity calibration mechanisms were proposed in the literature, which require user intervention. This paper proposes a simple procedure to calibrate a gyroscope using an automatic camera pan tilt base. The sensor parameters are estimated using direct pseudo inversion of a coefficients matrix. The method is validated experimentally on two different IMU platforms.

The neuropeptide galanin has been shown to interact with the opioid system. More specifically, galanin counteracts the behavioral effects of the systemic administration of μ-opioid receptor (MOR) agonists. Yet the mechanism responsible for this galanin–opioid interaction has remained elusive. Using biophysical techniques in mammalian transfected cells, we found evidence for selective heteromerization of MOR and the galanin receptor subtype Gal1 (Gal1R). Also in transfected cells, a synthetic peptide selectively disrupted MOR–Gal1R heteromerization as well as specific interactions between MOR and Gal1R ligands: a negative cross talk, by which galanin counteracted MAPK activation induced by the endogenous MOR agonist endomorphin-1, and a cross-antagonism, by which a MOR antagonist counteracted MAPK activation induced by galanin. These specific interactions, which represented biochemical properties of the MOR-Gal1R heteromer, could then be identifiedin situin slices of rat ventral tegmental area (VTA) with MAPK activation and two additional cell signaling pathways, AKT and CREB phosphorylation. Furthermore,in vivomicrodialysis experiments showed that the disruptive peptide selectively counteracted the ability of galanin to block the dendritic dopamine release in the rat VTA induced by local infusion of endomorphin-1, demonstrating a key role of MOR-Gal1R heteromers localized in the VTA in the direct control of dopamine cell function and their ability to mediate antagonistic interactions between MOR and Gal1R ligands. The results also indicate that MOR-Gal1R heteromers should be viewed as targets for the treatment of opioid use disorders.SIGNIFICANCE STATEMENTThe μ-opioid receptor (MOR) localized in the ventral tegmental area (VTA) plays a key role in the reinforcing and addictive properties of opioids. With parallelin vitroexperiments in mammalian transfected cells andin situandin vivoexperiments in rat VTA, we demonstrate that a significant population of these MORs form functional heteromers with the galanin receptor subtype Gal1 (Gal1R), which modulate the activity of the VTA dopaminergic neurons. The MOR-Gal1R heteromer can explain previous results showing antagonistic galanin–opioid interactions and offers a new therapeutic target for the treatment of opioid use disorder.

Deficits of sensorimotor integration with periodic limb movements during sleep (PLMS) and hyperarousal and sleep disturbances in Restless Legs Syndrome (RLS) constitute two pathophysiologically distinct but interrelated clinical phenomena, which seem to depend mostly on alterations in dopaminergic and glutamatergic neurotransmission, respectively. Brain iron deficiency is considered as a main pathogenetic mechanism in RLS. Rodents with brain iron deficiency represent a valuable pathophysiological model of RLS, although they do not display motor disturbances. Nevertheless, they develop the main neurochemical dopaminergic changes found in RLS, such as decrease in striatal dopamine D2 receptor density. On the other hand, brain iron deficient mice exhibit the characteristic pattern of hyperarousal in RLS, providing a tool to find the link between brain iron deficiency and sleep disturbances in RLS. The present study provides evidence for a role of the endogenous sleep-promoting factor adenosine. Three different experimental preparations, long-term (22 weeks) severe or moderate iron-deficient (ID) diets (3- or 7-ppm iron diet) in mice and short-term (3 weeks) severe ID diet (3-ppm iron diet) in rats, demonstrated a significant downregulation (Western blotting in mouse and radioligand binding saturation experiments in rat brain tissue) of adenosine A1 receptors (A1R) in the cortex and striatum, concomitant to striatal D2R downregulation. On the other hand, the previously reported upregulation of adenosine A2A receptors (A2AR) was only observed with severe ID in both mice and rats. The results suggest a key role for A1R downregulation in the PLMS and hyperarousal in RLS.

It is generally assumed that infralimbic cortex (ILC) and prelimbic cortex, two adjacent areas of the medial prefrontal cortex (mPFC) in rodents, provide selective excitatory glutamatergic inputs to the nucleus accumbens (NAc) shell and core, respectively. It is also generally believed that mPFC influences the extracellular levels of dopamine in the NAc primarily by an excitatory collateral to the ventral tegmental area (VTA). In the present study, we first established the existence of a selective functional connection between ILC and the posteromedial portions of the VTA (pmVTA) and the mNAc shell (pmNAc shell), by measuring striatal neuronal activation (immunohistochemical analysis of ERK1/2 phosphorylation) and glutamate release (in vivomicrodialysis) upon ILC electrical stimulation. A novel optogenetic-microdialysis approach allowed the measurement of extracellular concentrations of glutamate and dopamine in the pmNAc shell upon local light-induced stimulation of glutamatergic terminals from ILC. Cortical electrical and local optogenetic stimulation produced significant increases in the extracellular concentrations of glutamate and dopamine in the pmNAc shell. Local blockade of glutamate release by perfusion of an adenosine A2Areceptor antagonist in the pmNAc shell blocked the dopamine release induced by local optogenetic stimulation but only partially antagonized dopamine release induced by cortical electrical stimulation. The results demonstrate that ILC excitatory afferents directly modulate the extracellular concentration of dopamine in the pmNAc shell, but also support the involvement of an indirect mechanism of dopamine control, through a concomitant ILC-mediated activation of the pmVTA.SIGNIFICANCE STATEMENTWe established the existence of a functional connection between the infralimbic cortex (ILC) and the posteromedial portions of the ventral tegmental area (pmVTA) and the medial nucleus acumbens shell (pmNAc shell). A novel optogenetic-microdialysis approach allowed us to demonstrate that local glutamate release from glutamatergic terminals from the ILC exert a significant modulation of extracellular concentration of dopamine in the pmNAc shell. This mechanism provides the frame for a selective cortical-mediated tonic dopaminergic modulation of specific striatal compartments.

Huntington disease (HD) is a neurodegenerative disorder involving preferential loss of striatal GABAergic medium spiny neurons. Adenosine A(2A) receptors (A(2A)Rs) are present in the striatum at both presynaptic and post-synaptic levels. Blocking pre-synaptic A(2A)Rs, localized in glutamatergic terminals that contact striatal GABAergic dynorphinergic neurons, reduces glutamate release, which could be beneficial in HD. On the other hand, blockade of post-synaptic A(2A)Rs, localized in striatal GABAergic enkephalinergic neurons, could exacerbate the motor dysfunction. To evaluate the function of pre- or post-synaptic A(2A)Rs in HD we used selective antagonists for these receptors in a transgenic rat model of HD. Locomotor activity after systemic administration of the postsynaptic A(2A)R antagonist KW-6002 was used to investigate the function of post-synaptic A(2A)Rs. The role of pre-synaptic A(2A)Rs was instead evaluated by measuring the reduction of the electromyographic response of mastication muscles during electrical stimulation of the orofacial motor cortex after the systemic administration of the presynaptic A(2A)R antagonist SCH-442416. The ability of KW-6002 to produce locomotor activation was lost at 6 and 12 month-old of age in heterozygous and homozygous transgenic rats, but not in wild-type littermates. Nevertheless, no significant changes were observed up to 12 months of age in the potency of SCH-442416 to decrease the electromyographic response after cortical electrical stimulation. These results agree with a selective impairment of the striatal GABAergic enkephalinergic neuronal function during pre-symptomatic stages in HD. Since presynaptic A(2A)R function is not impaired, this receptor could probably be used as a target for the symptomatic treatment of the disease.

Adenosine A(2A) receptors (A(2A)Rs) are highly concentrated in the striatum. Two pharmacological different functional populations of A(2A)Rs have been recently described based on their different affinities for the A(2A)R antagonist SCH-442416. This compound has high affinity for A(2A)Rs not forming heteromers or forming heteromers with adenosine A(1) receptors (A(1)Rs) while showing very low affinity for A(2A)Rs forming heteromers with dopamine D(2) receptors (D(2)Rs). It has been widely described that striatal A(1)R-A(2A)R heteromers are preferentially localized presynaptically in the glutamatergic terminals that contact GABAergic dynorphinergic neurons, and that A(2A)R-D(2)R heteromers are localized postsynaptically in GABAergic enkephalinergic neurons. In the present study we provide evidence suggesting that SCH-442416 also targets postsynaptic A(2A)R not forming heteromers with D(2)R, which are involved in the motor depressant effects induced by D(2)R antagonists. SCH-442416 counteracted motor depression in rats induced by the D(2)R antagonist raclopride at a dose that did not produce motor activation or that blocked motor depression induced by an A(2A)R agonist. Furthermore, we re-evaluated the recently suggested key role of cannabinoid CB(1) receptors (CB(1)Rs) in the effects of A(2A)R antagonists acting at postsynaptic A(2A)Rs. By recording locomotor activity and monitoring striatal glutamate release induced by cortical electrical stimulation in rats after administration of A(2A)R and CB(1)R antagonists, we did not find evidence for any significant role of endocannabinoids in the post- or presynaptic effects of A(2A)R antagonists. The present results further suggest the existence of at least two functionally and pharmacologically different populations of striatal postsynaptic A(2A)Rs.

Brain iron deficiency leads to altered dopaminergic function in experimental animals, which can provide a mechanistic explanation for iron deficiency-related human sensory-motor disorders, such as Restless Legs Syndrome (RLS). However, mechanisms linking both conditions have not been determined. Considering the strong modulation exerted by adenosine on dopamine signaling, one connection could involve changes in adenosine receptor expression or function. In the striatum, presynaptic A(2A) receptors are localized in glutamatergic terminals contacting GABAergic dynorphinergic neurons and their function can be analyzed by the ability of A(2A) receptor antagonists to block the motor output induced by cortical electrical stimulation. Postsynaptic A(2A) receptors are localized in the dendritic field of GABAergic enkephalinergic neurons and their function can be analyzed by studying the ability of A(2A) receptor antagonists to produce locomotor activity and to counteract striatal ERK1/2 phosphorylation induced by cortical electrical stimulation. Increased density of striatal A(2A) receptors was found in rats fed during 3 weeks with an iron-deficient diet during the post-weaning period. In iron-deficient rats, the selective A(2A) receptor antagonist MSX-3, at doses of 1 and 3 mg/kg, was more effective at blocking motor output induced by cortical electrical stimulation (presynaptic A(2A) receptor-mediated effect) and at enhancing locomotor activation and blocking striatal ERK phosphorylation induced by cortical electrical stimulation (postsynaptic A(2A) receptor-mediated effects). These results indicate that brain iron deficiency induces a functional up-regulation of both striatal pre- and postsynaptic A(2A) receptor, which could be involved in sensory-motor disorders associated with iron deficiency such as RLS.

Adenosine and endocannabinoids are very ubiquitous non-classical neurotransmitters that exert a modulatory role on the transmission of other more ‘classical’ neurotransmitters. In this review we will focus on their common role as modulators of dopamine and glutamate neurotransmission in the striatum, the main input structure of the basal ganglia. We will pay particular attention to the role of adenosine A2A receptors and cannabinoid CB1 receptors. Experimental results suggest that presynaptic CB1 receptors interacting with A2A receptors in cortico-striatal glutamatergic terminals that make synaptic contact with dynorphinergic medium-sized spiny neurons (MSNs) are involved in the motor-depressant and addictive effects of cannabinoids. On the other hand, postsynaptic CB1 receptors interacting with A2A and D2 receptors in the dendritic spines of enkephalinergic MSNs and postsynaptic CB1 receptors in the dendritic spines of dynorphinergic MSN are probably involved in the cataleptogenic effects of cannabinoids. These receptor interactions most probably depend on the existence of a variety of heteromers of A2A, CB1 and D2 receptors in different elements of striatal spine modules. Drugs selective for the different striatal A2A and CB1 receptor heteromers could be used for the treatment of neuropsychiatric disorders and drug addiction and they could provide effective drugs with fewer side effects than currently used drugs. This article is part of a themed issue on Cannabinoids. To view the editorial for this themed issue visit http://dx.doi.org/10.1111/j.1476-5381.2010.00831.x

Glial cell line-derived neurotrophic factor (GDNF) affords neuroprotection in Parkinson’s disease in accordance with its ability to bolster nigrostriatal innervation. We previously found that GDNF facilitates dopamine release in a manner dependent on adenosine A2A receptor activation. As motor dysfunction also involves modifications of striatal glutamatergic innervation, we now tested if GDNF and its receptor system, Ret (rearranged during transfection) and GDNF family receptor α1 controlled the cortico-striatal glutamatergic pathway in an A2A receptor-dependent manner. GDNF (10 ng/mL) enhanced (by ≈13%) glutamate release from rat striatal nerve endings, an effect potentiated (up to ≈30%) by the A2A receptor agonist CGS 21680 (10 nM) and prevented by the A2A receptor antagonist, SCH 58261 (50 nM). Triple immunocytochemical studies revealed that Ret and GDNF family receptor α1 were located in 50% of rat striatal glutamatergic terminals (immunopositive for vesicular glutamate transporters-1/2), where they were found to be co-located with A2A receptors. Activation of the glutamatergic system upon in vivo electrical stimulation of the rat cortico-striatal input induced striatal Ret phosphorylation that was prevented by pre-treatment with the A2A receptor antagonist, MSX-3 (3 mg/kg). The results provide the first functional and morphological evidence that GDNF controls cortico-striatal glutamatergic pathways in a manner largely dependent on the co-activation of adenosine A2A receptors.

Previous studies have shown that the dopamine (DA) uptake blocker methylphenidate, a psychostimulant widely used for the treatment of attention-deficit hyperactivity disorder (ADHD), prevents the neurotoxic effects of the highly abused DA releaser methamphetamine. However, there is a lack of information about the pharmacological interactions of these two drugs at the behavioral level. When systemically administered within an interval of 2 h, previous administration of methylphenidate (10 mg/kg, intraperitoneal (i.p.)) did not modify locomotor activation induced by methamphetamine. On the other hand, previous administration of methamphetamine (1 mg/kg, i.p.) markedly potentiated methylphenidate-induced motor activation. With in vivo microdialysis experiments, methamphetamine and methylphenidate were found to increase DA extracellular levels in the nucleus accumbens (NAs). Methamphetamine, but not methylphenidate, significantly increased the extracellular levels of serotonin (5-HT) in the NAs. Methamphetamine-induced 5-HT release remained significantly elevated for more than 2 h after its administration, suggesting that the increased 5-HT could be responsible for the potentiation of methylphenidate-induced locomotor activation. In fact, previous administration of the 5-HT uptake blocker fluoxetine (10 mg/kg, i.p.) also potentiated the motor activation induced by methylphenidate. A selective 5-HT 1B receptor antagonist (GR 55562; 1 mg/kg), but not a 5-HT2 receptor antagonist (ritanserin; 2 mg/kg, i.p.), counteracted the effects of methamphetamine and fluoxetine on the motor activation induced by methylphenidate. Furthermore, a 5-HT 1B receptor agonist (CP 94253; 1-10 mg/kg, i.p.) strongly and dose-dependently potentiated methylphenidate-induced locomotor activation. The 5-HT 1B receptor-mediated modulation of methylphenidate-induced locomotor activation in rat could have implications for the treatment of ADHD.

Rats were trained on an inhibitory avoidance task to study the effects of post-training administration of tetrodotoxin (TTX, which temporarily inactivates neural activity) on memory consolidation. During training, independent groups of rats received either a mild foot shock (0.8 mA) or a stronger (1.0 mA) foot shock. TTX was administered bilaterally into the dorsal hippocampus immediately after training, and memory of the task was measured 48 h later. We corroborated the typical amnesic effect of intrahippocampal infusions of TTX in those rats trained with the mild-intensity foot shock. More importantly, with the stronger foot shock, the same treatment was ineffective in producing amnesia. These results suggest that, after an enhanced learning experience, other brain regions are also activated, which may compensate for the amnesic effect of TTX infusions into the hippocampus.

El objetivo del estudio fue evaluar la magnitud de las variaciones horizontales, verticales y transversales en la relación céntrica (RC) en pacientes con Disfunción Temporomandibular (DTM) y síntomas otológicos (SO) comparando con pacientes que no presenten DTM ni SO, mediante el uso del articulador MG2, fueron valorados en la División de Estomatología-Ortodoncia del Hospital General “Dr. Manuel Gea González” (HGMGG). En un periodo comprendido del 2005 al 2006, con rango de edad entre 20 a 60 años.Para la realización de este estudio, se incluyeron 27 pacientes con DTM y SO, y 15 pacientes sin DTM ni SO.Los resultados de este estudio mostraron que los pacientes con DTM y SO presentan una discrepancia horizontal, vertical y transversal en relación a la máxima intercuspidación (MI) y la relación céntrica (RC), significativa. Presentándose en 15 de los 27 casos estudiados variaciones anteroposteriores. Siendo menos significativa las variaciones verticales presentándose solo en 10 de los casos estudiados.

A very significant density of adenosine A2A receptors (A2AR) is present in the striatum, where they are preferentially localized postsynaptically in enkephalinergic-GABAergic-medium spiny neurons (enkephalinergic MSN). In this localization, different subpopulations of A2AR with different functions exist. Their differential function seems to depend mostly on their ability to form heteromers with other G-protein-coupled receptors, such as dopamine D2, cannabinoid CB1 and glutamate mGlu5 receptors. Furthermore, striatal A2AR are also localized presynaptically, in corticostriatal glutamatergic terminals that contact dynorphinergic-GABAergic-medium spiny neurons (dynorphinergic MSN). These presynaptic A2AR heteromerize with A1 receptors and their activation facilitates glutamate release. Pharmacological tools are becoming available that allow the functional evaluation of some of these different subpopulations of A2AR, which can therefore provide selective targets for drug development in different basal ganglia disorders. In fact, alterations in the function of different A2AR subpopulations have recently been observed in Parkinson’s disease and in animal models of Huntington disease and Restless Legs Syndrome.

Previous studies have shown that dopamine and galanin modulate cholinergic transmission in the hippocampus, but little is known about the mechanisms involved and their possible interactions. By using resonance energy transfer techniques in transfected mammalian cells, we demonstrated the existence of heteromers between the dopamine D1-like receptors (D1and D5) and galanin Gal1, but not Gal2receptors. Within the D1–Gal1and D5–Gal1receptor heteromers, dopamine receptor activation potentiated and dopamine receptor blockade counteracted MAPK activation induced by stimulation of Gal1receptors, whereas Gal1receptor activation or blockade did not modify D1-like receptor-mediated MAPK activation. Ability of a D1-like receptor antagonist to block galanin-induced MAPK activation (cross-antagonism) was used as a “biochemical fingerprint” of D1-like–Gal1receptor heteromers, allowing their identification in the rat ventral hippocampus. The functional role of D1-like–Gal receptor heteromers was demonstrated in synaptosomes from rat ventral hippocampus, where galanin facilitated acetylcholine release, but only with costimulation of D1-like receptors. Electrophysiological experiments in rat ventral hippocampal slices showed that these receptor interactions modulate hippocampal synaptic transmission. Thus, a D1-like receptor agonist that was ineffective when administered alone turned an inhibitory effect of galanin into an excitatory effect, an interaction that required cholinergic neurotransmission. Altogether, our results strongly suggest that D1-like–Gal1receptor heteromers act as processors that integrate signals of two different neurotransmitters, dopamine and galanin, to modulate hippocampal cholinergic neurotransmission.

Se hace una descripción somera de las técnicas clásicas utilizadas en el estudio de la neurobiología de la memoria, y de los resultados experimentales que dieron base a la teoría de la consolidación de la memoria. Asimismo, se describen los experimentos que han dado lugar a una reinterpretación de dicha teoría, aplicable a la formación de la memoria de altos niveles de aprendizaje. Los datos derivados de estudios neurobiológicos en los que se han utilizado diseños que implican aprendizajes mediados por niveles relativamente bajos de reforzamiento o de número de ensayos o de sesiones de entrenamiento, así como los derivados de situaciones de aprendizaje incrementado pueden se explicados en forma sencilla por dos modelos que hemos propuesto: la del procesamiento en serie y la del procesamiento en paralelo, que se discuten en el texto.

Striatal adenosine A(2A) receptors (A(2A)Rs) are highly expressed in medium spiny neurons (MSNs) of the indirect efferent pathway, where they heteromerize with dopamine D(2) receptors (D(2)Rs). A(2A)Rs are also localized presynaptically in cortico-striatal glutamatergic terminals contacting MSNs of the direct efferent pathway, where they heteromerize with adenosine A(1) receptors (A(1)Rs). It has been hypothesized that postsynaptic A(2A)R antagonists should be useful in Parkinson's disease, while presynaptic A(2A)R antagonists could be beneficial in dyskinetic disorders, such as Huntington's disease, obsessive-compulsive disorders and drug addiction. The aim or this work was to determine whether selective A(2A)R antagonists may be subdivided according to a preferential pre- versus postsynaptic mechanism of action. The potency at blocking the motor output and striatal glutamate release induced by cortical electrical stimulation and the potency at inducing locomotor activation were used as in vivo measures of pre- and postsynaptic activities, respectively. SCH-442416 and KW-6002 showed a significant preferential pre- and postsynaptic profile, respectively, while the other tested compounds (MSX-2, SCH-420814, ZM-241385 and SCH-58261) showed no clear preference. Radioligand-binding experiments were performed in cells expressing A(2A)R-D(2)R and A(1)R-A(2A)R heteromers to determine possible differences in the affinity of these compounds for different A(2A)R heteromers. Heteromerization played a key role in the presynaptic profile of SCH-442416, since it bound with much less affinity to A(2A)R when co-expressed with D(2)R than with A(1)R. KW-6002 showed the best relative affinity for A(2A)R co-expressed with D(2)R than co-expressed with A(1)R, which can at least partially explain the postsynaptic profile of this compound. Also, the in vitro pharmacological profile of MSX-2, SCH-420814, ZM-241385 and SCH-58261 was is in accordance with their mixed pre- and postsynaptic profile. On the basis of their preferential pre- versus postsynaptic actions, SCH-442416 and KW-6002 may be used as lead compounds to obtain more effective antidyskinetic and antiparkinsonian compounds, respectively.

A very significant density of adenosine A(2A) receptors (A(2A)Rs) is present in the striatum, where they are preferentially localized postsynaptically in striatopallidal medium spiny neurons (MSNs). In this localization A(2A)Rs establish reciprocal antagonistic interactions with dopamine D(2) receptors (D(2)Rs). In one type of interaction, A(2A)R and D(2)R are forming heteromers and, by means of an allosteric interaction, A(2A)R counteracts D(2)R-mediated inhibitory modulation of the effects of NMDA receptor stimulation in the striatopallidal neuron. This interaction is probably mostly responsible for the locomotor depressant and activating effects of A(2A)R agonist and antagonists, respectively. The second type of interaction involves A(2A)R and D(2)R that do not form heteromers and takes place at the level of adenylyl cyclase (AC). Due to a strong tonic effect of endogenous dopamine on striatal D(2)R, this interaction keeps A(2A)R from signaling through AC. However, under conditions of dopamine depletion or with blockade of D(2)R, A(2A)R-mediated AC activation is unleashed with an increased gene expression and activity of the striatopallidal neuron and with a consequent motor depression. This interaction is probably the main mechanism responsible for the locomotor depression induced by D(2)R antagonists. Finally, striatal A(2A)Rs are also localized presynaptically, in cortico-striatal glutamatergic terminals that contact the striato-nigral MSN. These presynaptic A(2A)Rs heteromerize with A(1) receptors (A(1)Rs) and their activation facilitates glutamate release. These three different types of A(2A)Rs can be pharmacologically dissected by their ability to bind ligands with different affinity and can therefore provide selective targets for drug development in different basal ganglia disorders.

Introducción: El propósito del presente estudio es estimar el promedio de valores cefalométricos de niñas y niños mexicanos de 8 años de edad, residentes en la ciudad de México y comparar la información obtenida con estándares extranjeros. Métodos: Se determinaron los valores promedio de cuatro medidas mandibulares y doce del análisis de McNamara, se utilizaron 50 cefalogramas laterales de niños y 50 de niñas de 8 años de edad con oclusión clase I de Angle, sin tratamiento ortodóncico ni ortopédico. Resultados: Las muestras de los niños resentan mayor tamaño en sus estructuras óseas; el espacio faríngeo superior e inferior es mayor en las niñas. Hay diferencias estadísticamente significativas entre niños y niñas en la longitud mandibular total, la longitud del cuerpo mandibular, la altura del tercio facial inferior y la proyección anterior del mentón. Conclusiones: El presente estudio demuestra que existen diferencias cefalométricas significativas entre niños y niñas, así como entre las muestras italiana, americana y mexicana.