scholarly journals Increase in the Bmax of gamma-aminobutyric acid-A recognition sites in brain regions of mice receiving diazepam.

1984 ◽  
Vol 81 (7) ◽  
pp. 2247-2251 ◽  
Author(s):  
P. Ferrero ◽  
A. Guidotti ◽  
E. Costa
Keyword(s):  
Brain Regions ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Recognition Sites

scholarly journals Heterogeneity in expression of functional ionotropic glutamate and GABA receptors in astrocytes across brain regions: insights from the thalamus

2014 ◽  
Vol 369 (1654) ◽  
pp. 20130602 ◽  
Author(s):  
Simon Höft ◽  
Stephanie Griemsmann ◽  
Gerald Seifert ◽  
Christian Steinhäuser
Keyword(s):  
Ampa Receptors ◽  
Indirect Effects ◽  
Gaba Receptors ◽  
Brain Regions ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Functional Heterogeneity ◽  
Rt Pcr ◽  
Ventrobasal Thalamus ◽  
The Impact

Astrocytes may express ionotropic glutamate and gamma-aminobutyric acid (GABA) receptors, which allow them to sense and to respond to neuronal activity. However, so far the properties of astrocytes have been studied only in a few brain regions. Here, we provide the first detailed receptor analysis of astrocytes in the murine ventrobasal thalamus and compare the properties with those in other regions. To improve voltage-clamp control and avoid indirect effects during drug applications, freshly isolated astrocytes were employed. Two sub-populations of astrocytes were found, expressing or lacking α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. AMPA receptor-bearing astrocytes displayed a lower Kir current density than cells lacking the receptors. In contrast, all cells expressed GABA A receptors. Single-cell RT-PCR was employed to identify the receptor subunits in thalamic astrocytes. Our findings add to the emerging evidence of functional heterogeneity of astrocytes, the impact of which still remains to be defined.

Basal and glucoprivic-induced changes in extracellular GABA in the ventral hypothalamus of Zucker rats

1996 ◽  
Vol 271 (2) ◽  
pp. R388-R392 ◽  
Author(s):  
S. E. Specter ◽  
B. A. Horwitz ◽  
J. L. Beverly
Keyword(s):  
Food Intake ◽  
Brain Regions ◽  
Gabaergic System ◽  
Aminobutyric Acid ◽  
Zucker Rats ◽  
Gamma Aminobutyric Acid ◽  
Zucker Rat ◽  
Obese Rats ◽  
Before And After ◽  
Induced Changes

The diminished sensitivity of genetically obese (fa/ fa) Zucker rats to the glucoprivic agent 2-deoxy-D-glucose (2-DG) may involve impaired release of the neurotransmitter gamma-aminobutyric acid (GABA) in discrete regions of the hypothalamus. Extracellular GABA concentrations in the medial (MH) and lateral (LH) hypothalamus of lean (Fa/Fa) and age-matched obese (fa/fa) male Zucker rats before and after 2-DG (1.2 mmol/kg i.v.). Basal GABA concentrations were higher (P < 0.05) in the MH of obese vs. lean rats. No differences were noted in LH GABA levels between lean and obese rats or in baseline extracellular GABA levels between brain regions in lean rats. In lean rats, a characteristic bimodal increase in GABA concentrations was apparent in the MH, whereas GABA concentrations decreased in the LH during the 60 min after 2-DG. No changes in GABA concentrations in dialysate from the MH or LH of obese rats were observed after 2-DG. The alterations in basal activity and responsiveness to glucoprivic stimuli by GABAergic system in the MH of obese rats may reflect a defect in central glucostatic control of food intake and, ultimately, in the hypothesized autonomic imbalance in fa/fa Zucker rat.

scholarly journals Dementia-related psychosis and the potential role for pimavanserin

CNS Spectrums ◽  
2020 ◽  
pp. 1-9
Author(s):  
Jeffery L. Cummings ◽  
D. P. Devanand ◽  
Stephen M. Stahl
Keyword(s):  
Visual Cortex ◽  
Motor Function ◽  
Potential Role ◽  
Pyramidal Neurons ◽  
Brain Regions ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Visual Hallucinations ◽  
Mesolimbic Pathway ◽  
Multiple Signaling

Abstract Dementia-related psychosis (DRP) is prevalent across dementias and typically manifests as delusions and/or hallucinations. The mechanisms underlying psychosis in dementia are unknown; however, neurobiological and pharmacological evidence has implicated multiple signaling pathways and brain regions. Despite differences in dementia pathology, the neurobiology underlying psychosis appears to involve dysregulation of a cortical and limbic pathway involving serotonergic, gamma-aminobutyric acid ergic, glutamatergic, and dopaminergic signaling. Thus, an imbalance in cortical and mesolimbic excitatory tone may drive symptoms of psychosis. Delusions and hallucinations may result from (1) hyperactivation of pyramidal neurons within the visual cortex, causing visual hallucinations and (2) hyperactivation of the mesolimbic pathway, causing both delusions and hallucinations. Modulation of the 5-HT2A receptor may mitigate hyperactivity at both psychosis-associated pathways. Pimavanserin, an atypical antipsychotic, is a selective serotonin inverse agonist/antagonist at 5-HT2A receptors. Pimavanserin may prove beneficial in treating the hallucinations and delusions of DRP without worsening cognitive or motor function.

scholarly journals Redistribution of Neuroactive Amino Acids in Hippocampus and Striatum during Hypoglycemia: A Quantitative Immunogold Study

2001 ◽  
Vol 21 (1) ◽  
pp. 41-51 ◽  
Author(s):  
Vidar Gundersen ◽  
Frode Fonnum ◽  
Ole Petter Ottersen ◽  
Jon Storm-Mathisen
Keyword(s):  
Amino Acids ◽  
Glial Cells ◽  
Pyramidal Cell ◽  
Neuronal Death ◽  
Synaptic Vesicles ◽  
Brain Regions ◽  
Aminobutyric Acid ◽  
Nerve Terminals ◽  
Gamma Aminobutyric Acid ◽  
Energy Substrates

Postembedding immunocytochemistry was used to localize aspartate, glutamate, gamma-aminobutyric acid (GABA), and glutamine in hippocampus and striatum during normo- and hypoglycemia in rat. In both brain regions, hypoglycemia caused aspartatelike immunoreactivity to increase. In hippocampus, this increase was evident particularly in the terminals of known excitatory afferents—in GABA-ergic neurons and myelinated axons. Aspartate was enriched along with glutamate in nerve terminals forming asymmetric synapses on spines and with GABA in terminals forming symmetric synapses on granule and pyramidal cell bodies. In both types of terminal, aspartate was associated with clusters of synaptic vesicles. Glutamate and glutamine immunolabeling were markedly reduced in all tissue elements in both brain regions, but less in the terminals than in the dendrosomatic compartments of excitatory neurons. In glial cells, glutamine labeling showed only slight attenuation. The level of GABA immunolabeling did not change significantly during hypoglycemia. The results support the view that glutamate and glutamine are used as energy substrates in hypoglycemia. Under these conditions both excitatory and inhibitory terminals are enriched with aspartate, which may be released from these nerve endings and thus contribute to the pattern of neuronal death characteristic of hypoglycemia.

scholarly journals Alterations in Rat Accumbens Dopamine, Endocannabinoids and GABA Content During WIN55,212-2 Treatment: The Role of Ghrelin

2020 ◽  
Vol 22 (1) ◽  
pp. 210
Author(s):  
Chrysostomos Charalambous ◽  
Marek Lapka ◽  
Tereza Havlickova ◽  
Kamila Syslova ◽  
Magdalena Sustkova-Fiserova
Keyword(s):  
Nucleus Accumbens ◽  
Food Intake ◽  
Dopamine Release ◽  
Brain Regions ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Nucleus Accumbens Shell ◽  
Gaba Content ◽  
Dopamine Efflux

The endocannabinoid/CB1R system as well as the central ghrelin signalling with its growth hormone secretagogoue receptors (GHS-R1A) are importantly involved in food intake and reward/reinforcement processing and show distinct overlaps in distribution within the relevant brain regions including the hypothalamus (food intake), the ventral tegmental area (VTA) and the nucleus accumbens (NAC) (reward/reinforcement). The significant mutual interaction between these systems in food intake has been documented; however, the possible role of ghrelin/GHS-R1A in the cannabinoid reinforcement effects and addiction remain unclear. Therefore, the principal aim of the present study was to investigate whether pretreatment with GHS-R1A antagonist/JMV2959 could reduce the CB1R agonist/WIN55,212-2–induced dopamine efflux in the nucleus accumbens shell (NACSh), which is considered a crucial trigger impulse of the addiction process. The synthetic aminoalklylindol cannabinoid WIN55,212-2 administration into the posterior VTA induced significant accumbens dopamine release, which was significantly reduced by the 3 mg/kg i.p. JMV2959 pretreatment. Simultaneously, the cannabinoid-increased accumbens dopamine metabolic turnover was significantly augmented by the JMV2959 pretreament. The intracerebral WIN55,212-2 administration also increased the endocannabinoid arachidonoylethanolamide/anandamide and the 2-arachidonoylglycerol/2-AG extracellular levels in the NACSh, which was moderately but significantly attenuated by the JMV2959 pretreatment. Moreover, the cannabinoid-induced decrease in accumbens γ-aminobutyric acid/gamma-aminobutyric acid levels was reversed by the JMV2959 pretreatment. The behavioural study in the LABORAS cage showed that 3 mg/kg JMV2959 pretreatment also significantly reduced the systemic WIN55,212-2-induced behavioural stimulation. Our results demonstrate that the ghrelin/GHS-R1A system significantly participates in the rewarding/reinforcing effects of the cannabinoid/CB1 agonist that are involved in cannabinoid addiction processing.

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