Distribution of Γ‐aminobutyric Acid in the Layers of the Cerebral and Cerebellar Cortex. Implications for Its Physiological Role*

Hirsch, Hilde E.; Robins, Eli

doi:10.1111/j.1471-4159.1962.tb07494.x

Cited by 113 publications

(22 citation statements)

References 13 publications

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“…GABA contents of these samples were determined with the enzymatic method described by Hirsch and Robins [9]. Figure 1 is a map of GABA distribution in the human nigra.…”

Section: Gaba Distribution In the Human Substantia Nigramentioning

confidence: 99%

Quantitative Histochemistry of <i>γ</i>-Aminobutyric Acid (GABA) in the Human Substantia nigra and Globus pallidus

Kanazawa¹,

Toyokura²

1974

Stereotact Funct Neurosurg

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“…GABA contents of these samples were determined with the enzymatic method described by Hirsch and Robins [9]. Figure 1 is a map of GABA distribution in the human nigra.…”

Section: Gaba Distribution In the Human Substantia Nigramentioning

confidence: 99%

Quantitative Histochemistry of <i>γ</i>-Aminobutyric Acid (GABA) in the Human Substantia nigra and Globus pallidus

Kanazawa¹,

Toyokura²

1974

Stereotact Funct Neurosurg

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“…Bilateral punches of substantia nigra, caudate nucleus, cingulate and cerebellar cortex were obtained from 3-mm transversal slices as described elsewhere [Periâié et al, 1977], Approximately 5 mg of brain tissue was homogenized imme diately in 300 pi of 0.1 N HC1. GABA was determined by a modifi cation [Periâié et al, 1977] of the enzymatic fluorimetric method of Hirsh and Robins [1962]. Protein was determined in 10 pi of homog enate according to Lowry et al ] 1951 ].…”

Section: Methodsmentioning

confidence: 99%

Effect of Phenoxybenzamine on the GABA System and on Convulsive Activity

Peričić¹,

Manev²

1983

Neuropsychobiology

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The effect of phenoxybenzamine on the concentration of GABA and the aminooxyacetic acid (AOAA) induced accumulation of GABA in four brain regions was compared with its effect on the occurrence and latency of picrotoxin-induced convulsions. Also the effect of phenoxybenzamine on post-decapitation convulsions was followed. Whereas 0.1 mg/kg of phenoxybenzamine decreased the levels and the AOAA-induced accumulation of GABA in the substantia nigra and cerebellar cortex, 1.0 mg/kg produced an increased GABA accumulation in the substantia nigra. Both doses of the drug decreased the AOAA-induced accumulation of GABA in the cingulate cortex. Administration of phenoxybenzamine decreased the latency and increased or decreased the occurrence of picrotoxin-induced convulsions depending on the intensity of picrotoxin effect. Phenoxybenzamine also prolonged the latency and shortened the duration of post-decapitation convulsions in rats. The results suggest that two different mechanisms mediate the effects of phenoxybenzamine on the latency and occurrence of picrotoxin-induced convulsions.

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“…GABA was determined by a modification [Periëié et al, 1977] of the enzymatic fluori metrie method of Hirsh and Robins [1962]. Protein was determined in 10 /al of homogenate according to Lowry et al [1951].…”

Section: Methodsmentioning

confidence: 99%

Dihydroergotoxine and the Seizure Threshold1

Peričić¹

1981

Int Pharmacopsychiatry

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Dihydroergotoxine administration shortened the latency of allylglycine-and picrotoxin-induced convulsions in rats and increased the incidence of convulsions elicited by picrotoxin, i.e., it lowered ED(50) for picrotoxin. The same drug (0.1-10.0 mg/kg) decreased the levels of γ-aminobutyric acid (GABA) in the caudate nucleus and cingulate cortex, but enhanced the aminooxyacetic acid induced accumulation of GABA indicating an increased synthesis of GABA in these brain regions. The concentrations of 5-hydroxytryptamine, 5-hydroxyindoleacetic acid, noradrenaline, and dopamine in the whole rate brain were not affected with doses of dihydroergotoxine up to 10.0 mg/kg, but this dose of the drug slowed down the turnover of dopamine, as evidenced by a diminished disappearance of dopamine induced by α-methyl-p-tyrosine administration. The results suggest that dihydroergotoxine decreases GABA-ergic transmission and, therefore, presumably lowers the seizure threshold.

show abstract

Distribution of Γ‐aminobutyric Acid in the Layers of the Cerebral and Cerebellar Cortex. Implications for Its Physiological Role*

Cited by 113 publications

References 13 publications

Quantitative Histochemistry of <i>γ</i>-Aminobutyric Acid (GABA) in the Human Substantia nigra and Globus pallidus

Quantitative Histochemistry of <i>γ</i>-Aminobutyric Acid (GABA) in the Human Substantia nigra and Globus pallidus

Effect of Phenoxybenzamine on the GABA System and on Convulsive Activity

Dihydroergotoxine and the Seizure Threshold1

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