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3 results on '"glutamatergic terminals"'

1. Up-regulation of CB1 cannabinoid receptors located at glutamatergic terminals in the medial prefrontal cortex of the obese Zucker rat

Author

Leyre Echeazarra, Sergio Barrondo, Gontzal García del Caño, Itziar Bonilla-Del Río, Jon Egaña-Huguet, Nagore Puente, Xabier Aretxabala, Mario Montaña, Maider López de Jesús, Imanol González-Burguera, Miquel Saumell-Esnaola, María Aránzazu Goicolea, Pedro Grandes, and Joan Sallés

Subjects
obese Zucker rat, CB1 receptor, Gi/o proteins, 2-AG levels, medial prefrontal cortex, glutamatergic terminals, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571, Human anatomy, QM1-695
Abstract

The present study describes a detailed neuroanatomical distribution map of the cannabinoid type 1 (CB1) receptor, along with the biochemical characterization of the expression and functional coupling to their cognate Gi/o proteins in the medial prefrontal cortex (mPCx) of the obese Zucker rats. The CB1 receptor density was higher in the prelimbic (PL) and infralimbic (IL) subregions of the mPCx of obese Zucker rats relative to their lean littermates which was associated with a higher percentage of CB1 receptor immunopositive excitatory presynaptic terminals in PL and IL. Also, a higher expression of CB1 receptors and WIN55,212-2-stimulated [35S]GTPγS binding was observed in the mPCx but not in the neocortex (NCx) and hippocampus of obese rats. Low-frequency stimulation in layers II/III of the mPCx induced CB1 receptor-dependent long-term synaptic plasticity in IL of area obese Zucker but not lean rats. Overall, the elevated 2-AG levels, up-regulation of CB1 receptors, and increased agonist-stimulated [35S]GTPγS binding strongly suggest that hyperactivity of the endocannabinoid signaling takes place at the glutamatergic terminals of the mPCx in the obese Zucker rat. These findings could endorse the importance of the CB1 receptors located in the mPCx in the development of obesity in Zucker rats.

Published
2022
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2. Abnormal Tau Phosphorylation in the Thorny Excrescences of CA3 Hippocampal Neurons in Patients with Alzheimer's Disease

Author

Lidia Blazquez-Llorca, Paula Merino-Serrais, Javier DeFelipe, Virginia García-Marín, Jesús Avila, Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (España), Fundación Centro de Investigación de Enfermedades Neurológicas, Fundación 'la Caixa', and Ministerio de Ciencia e Innovación (España)

Subjects
Adult, Male, Dendritic spine, Tau protein, Phosphorilation, Polycomb-Group Proteins, Plaque, Amyloid, tau Proteins, Hippocampal formation, Biology, Thorny excrescences, Temporal lobe, Young Adult, medicine, Biological neural network, Humans, Phosphorylation, Mossy Fibers, Aged, Aged, 80 and over, Neurons, Amyloid beta-Peptides, Microscopy, Confocal, General Neuroscience, Neurofibrillary Tangles, General Medicine, Middle Aged, Glutamatergic terminals, Granule cell, medicine.disease, CA3 Region, Hippocampal, Immunohistochemistry, Axons, DNA-Binding Proteins, Psychiatry and Mental health, Clinical Psychology, medicine.anatomical_structure, biology.protein, Female, Alzheimer disease, Geriatrics and Gerontology, Alzheimer's disease, Neuroscience, Transcription Factors
Abstract

A key symptom in the early stages of Alzheimer's disease (AD) is the loss of declarative memory. The anatomical substrate that supports this kind of memory involves the neural circuits of the medial temporal lobe, and in particular, of the hippocampal formation and adjacent cortex. A main feature of AD is the abnormal phosphorylation of the tau protein and the presence of tangles. The sequence of cellular changes related to tau phosphorylation and tangle formation has been studied with an antibody that binds to diffuse phosphotau (AT8). Moreover, another tau antibody (PHF-1) has been used to follow the pathway of neurofibrillary (tau aggregation) degeneration in AD. We have used a variety of quantitative immunocytochemical techniques and confocal microscopy to visualize and characterize neurons labeled with AT8 and PHF-1 antibodies. We present here the rather unexpected discovery that in AD, there is conspicuous abnormal phosphorylation of the tau protein in a selective subset of dendritic spines. We identified these spines as the typical thorny excrescences of hippocampal CA3 neurons in a pre-tangle state. Since thorny excrescences represent a major synaptic target of granule cell axons (mossy fibers), such aberrant phosphorylation may play an essential role in the memory impairment typical of AD patients., Thisworkwas supported by grants from the following entities: CIBERNED (CB06/05/0066), Fundación CIEN (Financiación de Proyectos de Investigación de Enfermedad de Alzheimer y enfermedades relacionadas 2008), Fundación Caixa (BM05-47-0), the Spanish Ministerio de Ciencia e Innovación (SAF2009-09394).

Published
2011
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3. Abnormal Tau Phosphorylation in the Thorny Excrescences of CA3 Hippocampal Neurons in Patients with Alzheimer's Disease

Author

Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (España), Fundación Centro de Investigación de Enfermedades Neurológicas, Fundación la Caixa, Ministerio de Ciencia e Innovación (España), Blázquez-Llorca, Lidia, García-Marín, Virginia, Merino-Serrais, Paula, Ávila, Jesús, DeFelipe, Javier, Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (España), Fundación Centro de Investigación de Enfermedades Neurológicas, Fundación la Caixa, Ministerio de Ciencia e Innovación (España), Blázquez-Llorca, Lidia, García-Marín, Virginia, Merino-Serrais, Paula, Ávila, Jesús, and DeFelipe, Javier

Abstract

A key symptom in the early stages of Alzheimer's disease (AD) is the loss of declarative memory. The anatomical substrate that supports this kind of memory involves the neural circuits of the medial temporal lobe, and in particular, of the hippocampal formation and adjacent cortex. A main feature of AD is the abnormal phosphorylation of the tau protein and the presence of tangles. The sequence of cellular changes related to tau phosphorylation and tangle formation has been studied with an antibody that binds to diffuse phosphotau (AT8). Moreover, another tau antibody (PHF-1) has been used to follow the pathway of neurofibrillary (tau aggregation) degeneration in AD. We have used a variety of quantitative immunocytochemical techniques and confocal microscopy to visualize and characterize neurons labeled with AT8 and PHF-1 antibodies. We present here the rather unexpected discovery that in AD, there is conspicuous abnormal phosphorylation of the tau protein in a selective subset of dendritic spines. We identified these spines as the typical thorny excrescences of hippocampal CA3 neurons in a pre-tangle state. Since thorny excrescences represent a major synaptic target of granule cell axons (mossy fibers), such aberrant phosphorylation may play an essential role in the memory impairment typical of AD patients.

Published
2011

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