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Transcranial photobiomodulation improves cerebral cortex metabolism. We hypothesized that chronic laser treatment may stimulate neuronal growth. To test this hypothesis, we investigated the morphology of neurons in the cerebral cortex of rats submitted to brief (2.5 min) daily sham or transcranial laser treatment (810 nm wavelength at 100 mW) for 58 consecutive days. Laser treatment increased the number of dendritic nodes and ends, and reduced the total dendritic length in neurons of the cerebral cortex. Taken together, our data indicate that chronic transcranial photobiomodulation induces morphological neuroplasticity in the cerebral cortex of rats., (Copyright © 2022 Elsevier B.V. All rights reserved.)

The rostroventromedial medulla (RVM), together with the periaqueductal gray matter (PAG), constitutes the descendent antinociceptive system. Additionally, these structures mutually regulate defensive behaviors, including tonic immobility (TI) in guinea pigs. The current study was undertaken to evaluate the connections of the RVM with the PAG and the spinal cord in guinea pigs in order to provide an anatomical basis for the role played by RVM in the modulation of TI. To address this goal, five guinea pigs were treated with non-fluorescent biotinylated dextran amine (BDA) neurotracer by injection into the RVM. After four days of survival, the encephalon and spinal cord were removed from each rodent, and BDA labeling was visualized with a standard avidin-biotinylated horseradish peroxidase method through reaction with nickel-intensified peroxidase 3,3'-diaminobenzidine dihydrochloride. The microinjection of BDA into the RVM stained fibers in the ventral horn, dorsal horn and intermediate gray matter of the spinal cord. BDA-labeled fibers, terminal buttons suggesting synaptic contacts, and perikarya were found in the dorsomedial, dorsolateral, lateral and ventrolateral PAG, and neuronal somata were identified in the cuneiform nucleus. Together, the current data demonstrate neuroanatomical evidence that supports the role of the RVM in the modulation of TI defensive behavior., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

This study examined the effects of motor stimulation via treadmill on the behavior of male gerbils after external carotid ischemic brain lesion. The animals were assigned to five groups; ischemic with no stimulation (SIG), ischemic with stimulation (SIG 12/24/48/72h after surgery), non-ischemic with no stimulation (CC), non-ischemic with stimulation (CE) and sham, surgery without occlusion with no stimulation (SH). All the animals were tested in the open-field (OF) and rotarod (RR), 4 days after surgery in order to evaluate exploratory behaviors and motor performance. Data were submitted to one-way variance (ANOVA) and Dunnett's post hoc comparisons. SIG and SIG 12 groups showed a significant decrease in motor response (crossing) when compared to the control group (CC) (F=20.65, P<0.05) in the OF. SIG 12 group showed an increase in grooming behavior (F=23.136, P<0.05) and all ischemia groups (SIG, SIG12/24/48/72) spent less time on the RR (F=10.40, P<0.05), when compared to the control group (CC). Histological analyses show extensive lesions in the hippocampus and neostriatum for all groups with ischemia (SIG, SIG12/24/48/72), which are structures involved in the organization of motor behavior. Interestingly, the most pronounced damage was found in animals submitted to motor stimulation 12h after ischemia which can be correlated to the increased number of grooming behavior showed by them in the OF. These findings suggest that motor stimulation through treadmill training improve motor behavior after ischemia, except when it starts 12h after surgery.

In order to investigate the effects of monoaminergic neurons of the dorsal raphe nucleus (DRN) and locus coeruleus (LC) on the elaboration and control of sweet-substance-induced antinociception, male albino Wistar rats weighing 180-200 g received sucrose solution (250 g/L) for 7-14 days as their only source of liquid. After the chronic consumption of sucrose solution, each animal was pretreated with unilateral microinjection of ibotenic acid (1.0 microg/0.2 microL) in the DRN or in the LC. The tail withdrawal latencies of the rats in the tail-flick test were measured immediately before and 7 days after this treatment. The neurochemical lesion of locus coeruleus, but not of DRN neural networks with ibotenic acid, after the chronic intake of sweetened solution, decreased the sweet-substance-induced antinociception. These results indicate the involvement of noradrenaline-containing neurons of the LC in the sucrose-induced antinociception. We also consider the possibility of DRN serotonergic neurons exerting some inhibitory effect on the LC neural networks involved with the elaboration of the sweet-substance-induced antinociception.

In order to investigate the effects of monoaminergic mechanisms of the dorsal raphe nucleus on the elaboration and control of sweet-substance-induced antinociception, male albino Wistar rats weighing 180-200 g received sucrose solution (250 g/L) for 14 days as their only source of liquid. After the chronic consumption of sucrose solution, each animal was pretreated with unilateral microinjection of methiothepin mesylate (5.0 microg/0.2 microL), or methysergide maleate (5.0 microg/0.2 microL) in the dorsal raphe nucleus. Each rat consumed an average of 15.6g sucrose/day. Their tail withdrawal latencies in the tail-flick test were measured immediately before and after this treatment. An analgesia index was calculated from the withdrawal latencies before and after the pharmacological treatment. The blockade of serotonergic receptor in the dorsal raphe nucleus with methysergide after the chronic intake of sucrose decreased the sweet-induced antinociception. However, microinjections of methiothepin in the dorsal raphe nucleus did not cause a similar effect on the tail-flick latencies after the chronic intake of sucrose solution, increasing the sweet-substance-induced analgesia. These results indicate the involvement of serotonin as a neurotransmitter in the sucrose-produced antinociception. Considering that the blockade of pre-synaptic serotonergic receptors of the neural networks of the dorsal raphe nucleus with methiothepin did not decrease the sweet-substance-induced antinociception, and the central blockade of post-synaptic serotonergic receptors decreased the sucrose-induced analgesia, the modulation of the release of serotonin in the neural substrate of the dorsal raphe nucleus seems to be crucial for the organization of this interesting antinociceptive process.

The nucleus raphe magnus (NRM) is one of the brainstem cell groups involved in physiological responses to hypoxia. Thus, we tested the hypothesis that the NRM modulates hypoxia-induced hyperventilation and anapyrexia. To this end, we assessed the participation of NRM in the respiratory and thermoregulatory responses to hypoxia using ibotenic acid lesions produced in the NRM of rats. Our results demonstrated that, under resting breathing, NRM plays no role in ventilation or body temperature. Hypoxia caused hyperventilation and anapyrexia in all groups. NMR lesions elicited an increased ventilatory response to hypoxia due to a higher tidal volume (V(T)) but did not affect hypoxia-induced anapyrexia. Therefore, we conclude that NRM exerts an inhibitory modulation of breathing during hypoxia, acting on V(T), but plays no role in the hypoxia-induced anapyrexia.

In order to investigate the effects of sweet substance intake on pain modulation, male albino Wistar rats weighing 180-200 g received either tap water or sucrose solutions (250 g/l) for 14 days as their only source of liquid. Each rat consumed an average of 15.6 g sucrose/day. Their tail withdrawal latencies in the tail-flick test (probably a spinal reflex) were measured immediately before and after this treatment. An analgesia index was calculated from the withdrawal latencies before and after treatment. The index (mean +/- SEM, N = 8) for the groups receiving sucrose solution plus saline (NaCl; 0.9%) for 14 days was 0.70 +/- 0.01. Atropine (1 and 2 mg/kg)-treated rats (N = 8) after intake of sucrose exhibited an analgesia index of 0.39 +/- 0.09 and 0.39 +/- 0.08, respectively, while mecamylamine (1 and 2 mg/kg)-treated rats (N = 10) after intake of sucrose had an index of -0.02 +/- 0.07 and 0.03 +/- 0.07, respectively. These results indicate that the effect of sucrose intake on nociceptive thresholds is controlled by neurotransmission of acetylcholine and depends on the nicotinic cholinergic receptors for its major analgesic effect, although muscarinic receptors were also involved in this antinociceptive process.