The role of lipid peroxidation in the possible involvement of membrane-Bound monoamine oxidases in gamma-aminobutyric acid and glucosamine deamination in rat brain

1992 ◽  
Vol 16 (1-2) ◽  
pp. 187-201 ◽  
Author(s):  
A. E. Medvedev ◽  
D. I. Rajgorodskaya ◽  
V. Z. Gorkin ◽  
I. B. Fedotova ◽  
A. F. Semiokhina
Keyword(s):  
Lipid Peroxidation ◽  
Rat Brain ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Monoamine Oxidases ◽  
Membrane Bound

Role of cholinergic system in modulating gamma-aminobutyric acid and dopamine functions in rat brain

1985 ◽  
Vol 6 (1) ◽  
pp. 47-54 ◽  
Author(s):  
S. K. Rastogi ◽  
R. B. Rastogi ◽  
R. L. Singhal ◽  
Y. D. Lapierre
Keyword(s):  
Rat Brain ◽  
Cholinergic System ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid

Changes in gamma-aminobutyric acid and somatostatin in epileptic cortex associated with low-grade gliomas

1992 ◽  
Vol 77 (2) ◽  
pp. 209-216 ◽  
Author(s):  
Michael M. Haglund ◽  
Mitchel S. Berger ◽  
Dennis D. Kunkel ◽  
JoAnn E. Franck ◽  
Saadi Ghatan ◽  
...  
Keyword(s):  
Epileptiform Activity ◽  
Aminobutyric Acid ◽  
Low Grade ◽  
Tumor Infiltration ◽  
Gamma Aminobutyric Acid ◽  
Content Type ◽  
Low Grade Gliomas ◽  
Neuronal Populations ◽  
Significant Difference

✓ The role of specific neuronal populations in epileptic foci was studied by comparing epileptic and nonepileptic cortex removed from patients with low-grade gliomas. Epileptic and nearby (within 1 to 2 cm) nonepileptic temporal lobe neocortex was identified using electrocorticography. Cortical specimens taken from four patients identified as epileptic and nonepileptic were all void of tumor infiltration. Somatostatin- and γ-aminobutyric acid (GABAergic)-immunoreactive neurons were identified and counted. Although there was no significant difference in the overall cell count, the authors found a significant decrease in both somatostatin- and GABAergic-immunoreactive neurons (74% and 51 %, respectively) in the epileptic cortex compared to that in nonepileptic cortex from the same patient. It is suggested that these findings demonstrate changes in neuronal subpopulations that may account for the onset and propagation of epileptiform activity in patients with low-grade gliomas.

Brain amino acid concentrations during diving and acid-base stress in turtles

1985 ◽  
Vol 58 (6) ◽  
pp. 1751-1754 ◽  
Author(s):  
B. M. Hitzig ◽  
M. P. Kneussl ◽  
V. Shih ◽  
R. D. Brandstetter ◽  
H. Kazemi
Keyword(s):  
Amino Acid ◽  
Aminobutyric Acid ◽  
Breath Hold ◽  
Gamma Aminobutyric Acid ◽  
Amino Acid Neurotransmitters ◽  
Acid Base ◽  
Ventilatory Drive ◽  
Amino Acid Concentrations ◽  
Brain Amino Acid

To assess the role of brain amino acid neurotransmitters in the breath hold of diving animals, concentrations of free amino acids present in the brains of turtles immediately after 2 h of apneic diving (at 20 degrees C) were measured. Additionally, the same measurements were performed on four other groups of animals subjected to 2 h of hypercapnia (8% CO2 in air), anoxia (N2 breathing), anoxia plus hypercapnia (8% CO2–92% N2), or air breathing (control). Significant changes in the concentrations of the inhibitory amino acid neurotransmitters known to affect respiration [gamma-aminobutyric acid (GABA) and taurine] were seen. GABA increased significantly in those animals subjected to anoxia, whereas taurine decreased significantly in the diving animals and increased significantly in those subjected to anoxia plus hypercapnia. These results suggest that the attenuated central ventilatory drive during diving in these animals may be related to alterations in brain concentrations of GABA and taurine.

scholarly journals NEUROTRANSMITTER AND BRAIN PARTS INVOLVED IN SCHIZOPHRENIA

2018 ◽  
Vol 11 (6) ◽  
pp. 4
Author(s):  
Ashwani Arya ◽  
Gulshan Sindhwani ◽  
Renu Kadian
Keyword(s):  
Depressive Symptoms ◽  
Effective Treatment ◽  
Aminobutyric Acid ◽  
Cognitive Symptoms ◽  
Gamma Aminobutyric Acid ◽  
Atypical Symptoms ◽  
Impaired Attention ◽  
Brain Parts ◽  
Pathogenic Process

Schizophrenia (SCZ) is a major debilitating, complex, and costly illness that strikes 1% of the world’s population. It is characterized by three general types of symptoms: Atypical symptoms (aggressiveness, agitation, delusions, hallucinations), depressive symptoms (alogia, avolition, anhedonia, apathy), and cognitive symptoms (impaired attention, learning, memory). The etiology of SCZ has still not been fully understood. Alteration in various neurochemical systems such as dopamine, serotonin, norepinephrine, gamma-aminobutyric acid, and glutamate are involved in the pathophysiology of SCZ. The lack of understanding regarding the exact pathogenic process may be the likely a reason for the non-availability of effective treatment, which can prevent onset and progression of the SCZ. The tools of modern neuroscience, drawing from neuroanatomy, neurophysiology, brain imaging, and psychopharmacology, promise to provide a host of new insights into the etiology and treatment of SCZ. In this review, we will discuss the role of the various neurotransmitter concerned and brain parts exaggerated in the SCZ.

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