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At least 1,387 records · Page 77Linked to original sources
PubMed1996

The effect of gabapentin on brain gamma-aminobutyric acid in patients with epilepsy.

Gabapentin has come into clinical use as adjunctive therapy in the treatment of epilepsy. Designed to mimic gamma-aminobutyric acid (GABA), its mechanism of action remains elusive. In vivo measurements of GABA in human brain were made using 1H magnetic resonance spectroscopy. We used a 2.1-T magnetic resonance imager-spectrometer and an 8-cm surface coil to measure a 13.5-cm3 volume in the occipital cortex. GABA levels were measured in 14 patients enrolled in an open-lbel trial of gabapentin. GABA was elevated in patients taking gabapentin compared with 14 complex partial epilepsy patients, matched for antiepileptic drug treatment. Brain GABA levels appeared to be higher in patients taking high-dose gabapentin (3,300-3,600 mg/day) than in those taking standard doses (1,200-2,400 mg/day). Gabapentin appears to increase human brain GABA levels.

Acetates↗
PubMed1983

Reductions of gamma-aminobutyric acid and glutamate uptake and (Na+ + K+)-ATPase activity in brain slices and synaptosomes by arachidonic acid.

Arachidonic acid, a major polyunsaturated fatty acid of membrane phospholipids in the CNS, reduced the high-affinity uptake of glutamate and gamma-aminobutyric acid (GABA) in both rat brain cortical slices and synaptosomes. alpha-Aminoisobutyric acid uptake was not affected. Intrasynaptosomal sodium was increased concomitant with decreased (Na+ + K+)-ATPase activity in synaptosomal membranes. The reduction of GABA uptake in synaptosomes could be partially reversed by alpha-tocopherol. The inhibition of membrane-bound (Na+ + K+)-ATPase by arachidonic acid was not due to a simple detergent-like action on membranes, since sodium dodecyl sulfate stimulated the sodium pump activity in synaptosomes. These data indicate that arachidonic acid selectively modifies membrane stability and integrity associated with reductions of GABA and glutamate uptake and of (Na+ + K+)-ATPase activity.

Aminoisobutyric Acids↗
PubMed2000

[Changes of glutamate and gamma-aminobutyric acid contents in brain tissue of brain edema and effects of baicalin on them in rats].

OBJECTIVE: To observe the changes of glutamates (Glu) and gamma-aminobutyric acid (GABA) contents in brain tissue of infectious brain edema, and effects of baicalin on them in rats. METHODS: The high performance liquid chromatography (HPLC) was used to determine the Glu and GABA contents in homogenized brain tissue after baicalin was injected intraperitoneally on infectious brain edema induced by pertussis bacilli in rats. RESULTS: Glu contents of homogenized brain tissue in blank control group (C), normal saline group (NS), pertussis bacilli group (PB) and baicalin group (BC) had no significant difference (P > 0.05). The concentration of GABA was more significantly increased in the BC group (4.06 +/- 0.52) than that in the PB group (2.71 +/- 0.29) (P < 0.05). Water content of brain was reduced in the BC group (79.8 +/- 0.4) as compared with the PB group (82.2 +/- 0.3)(P < 0.01). CONCLUSION: Baicalin has a protective effect against the pertussis bacilli-induced brain edema in rats, and protective effect was correlated to the increased content of GABA in the brain tissue in rats.

Animals↗
PubMed1990

Kainate receptors coupled to the evoked release of [3H]-gamma-aminobutyric acid from striatal neurons in primary culture: potentiation by lithium ions.

The pharmacological properties and modulation by lithium of the kainate (KA) receptor system coupled to the evoked release of [3H]-gamma-aminobutyric acid [( 3H]GABA) from purified populations of striatal neurons in primary culture were examined. KA evoked a dose-dependent (EC50, 100 microM) and saturable increase in [3H]GABA release from striatal neurons that was unaffected by the removal of extracellular calcium and resistant to the actions of tetrodotoxin. The release of [3H]GABA evoked by 100 microM KA was attenuated in a dose-dependent manner by the following excitatory amino acid antagonists (IC50):6-cyano-2, 3-dihydroxy-7-nitroquinoxaline (2 microM),2,3-dihydroxy-6,7-dinitroquinoxaline (2 microM), kynurenate (0.3 mM), and gamma-D-glutamylglycine (2 mM). The antagonist properties of 6-cyano-2,3-dihydroxy-7-nitroquinoxaline, kynurenate, and gamma-D-glutamylglycine were competitive in nature, inducing parallel rightward shifts of the KA dose-response curves. At concentrations at which it did not significantly increase basal levels of [3H]GABA release, quisqualate attenuated in a dose-dependent manner (IC50, 10 microM) the release due to 100 microM KA. The quisqualate receptor agonist alpha-amino-3-hydroxyisoxazolepropionic acid (AMPA), however, exerted a biphasic effect on 100 microM KA-evoked release of [3H]GABA. At lower concentrations of AMPA (0.1-10 microM), the release due to 100 microM KA was potentiated 25-50%; at higher concentrations (greater than 10 microM) AMPA induced a dose-dependent (IC50, 100 microM) attenuation of KA-evoked release. The release of [3H]GABA due to 100 microM KA was significantly potentiated by the replacement of sodium with lithium in the extracellular medium. A significant potentiation (20-30%) was detected with as little as 5-10 mM lithium, and maximal effects (100-110% increase) were obtained with 50-75 mM lithium. Replacement of sodium with choline or N-methyl-D-glucamine could not mimic the actions of lithium. Lithium (25 mM) also induced a 4-fold increase in the levels of endogenous GABA release due to 100 microM KA. Whole-cell voltage-clamp recordings of these striatal neurons indicated that the 100 microM KA-induced inward current was not significantly altered in the presence of 25 mM lithium. Lithium attenuated vasoactive intestinal polypeptide-stimulated cyclic AMP formation by 50%, with a dose dependence similar to that of its actions on KA-evoked release. The results of this study demonstrate a distinct pharmacological profile for the KA receptor system coupled to the evoked release of [3H]GABA from striatal neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Roles of gamma-aminobutyric acid and serotonin in the arcuate nucleus in the control of prolactin and luteinizing hormone secretion.

The effects of implantation of gamma-aminobutyric acid (GABA) and serotonin (5-HT) into the arcuate nucleus (ARC) on serum luteinizing hormone (LH) and prolactin (PRL) were examined in the conscious ovariectomized rat. Following implantation of 5-HT, but not GABA, serum PRL was significantly increased. While 5-HT did not affect pulsatile LH secretion, GABA significantly decreased the mean LH concentration and pulse frequency, but not amplitude.

Animals↗
PubMed2004

An Intrinsic gamma-aminobutyric acid (GABA)ergic system in the adrenal cortex: findings from human and rat adrenal glands and the NCI-H295R cell line.

gamma-Aminobutyric acid (GABA), a major neurotransmitter in the central nervous system, also acts as a paracrine or autocrine signaling molecule in endocrine tissues such as the pancreatic islets, adenohypophysis, and testis. In the present study, we describe local GABA production and functional GABA(B) receptors in the adrenal cortex, possibly forming an auto- or paracrine GABAergic system. Using immunohistochemistry and RT-PCR, we localized the GABA-synthesizing enzyme glutamate decarboxylase 67 and the vesicular GABA transporter in steroid-producing cells of the human and rat adrenal cortex. Immunocytochemistry, Western blots, and RT-PCR experiments demonstrated the presence of glutamate decarboxylase 67 in the human adrenocortical cell line NCI-H295R. Measurements of glutamate decarboxylase activity confirmed that, in these cells and in rat adrenals, glutamate is decarboxylated to form GABA. In addition, we found expression of the GABA(B(1a)), GABA(B(1e)), and GABA(B(2)) subunits of the heterodimeric GABA(B) receptor in NCI-H295R cells as shown by RT-PCR. GABA(B(1a)) and its truncated splice variant GABA(B(1e)) were also found in human and rat adrenal glands. Immunostaining for the GABA(B(2)) subunit revealed its presence in the human and rat adrenal cortex and in NCI-H295R cells. The GABA(B) receptors we identified were functional because the GABA(B) agonist baclofen inhibited T-type Ca(2+) currents in whole-cell patch clamp experiments on NCI-H295R cells. This effect was blocked by pertussis toxin. Furthermore, the alpha(2)-, alpha(3)-, beta(2)-, beta(3)- gamma(2)-, and epsilon-subunits of the GABA(A) receptor were detected in this cell line by RT-PCR. Hence, we conclude that GABA is synthesized and stored by steroid-producing cells of the adrenal cortex and may influence these cells in a paracrine or autocrine manner.

Adrenal Cortex↗
PubMed1978

Inhibition of gamma-aminobutyric acid release from rat cerebral cortex slices by barbiturate anesthesia.

Amobarbital and pentobarbital anesthesia inhibited the potassium-stimulated, Ca-dependent release of gamma-aminobutyric acid (GABA) from rat cerebral cortex slices during incubation in vitro. Inhibition of GABA release was not found when slices were prepared from rats shortly after they awakened from amobarbital anesthesia. Phenobarbital anesthesia did not affect the release of GABA.

Amino Acids↗
PubMed1989

Dual effects of 5-hydroxytryptamine on the release of gamma-aminobutyric acid from myenteric neurones of the guinea-pig ileum.

The effects of 5-hydroxytryptamine (5-HT) on the release of gamma-aminobutyric acid (GABA) were examined in the longitudinal muscle-myenteric plexus (LM-MP) preparation of guinea-pig ileum. 5-HT increased the spontaneous release and inhibited the electrically-evoked release of [3H]-GABA. The 5-HT-evoked release was Ca2+-dependent and tetrodotoxin-sensitive, and was antagonized by (3 alpha-tropanyl)-1H-indole-3-carboxylic acid ester (ICS 205-930), but not by methysergide and ketanserin. The inhibitory effect of 5-HT was antagonized by methysergide, but not by ketanserin and ICS 205-930. 8-Hydroxy-2-(di-n-propylamino)tetralin mimicked the inhibitory effect of 5-HT. Thus, 5-HT may exert an excitatory effect on the enteric GABAergic neurone via the 5-HT3 receptor and an inhibitory effect via the 5-HT1A receptor.

Animals↗
PubMed1988

Quantitative studies of enkephalin's coexistence with gamma-aminobutyric acid, glycine and neurotensin in amacrine cells of the chicken retina.

Previous double-label studies demonstrate that enkephalin coexists with gamma-aminobutyric acid, glycine or neurotensin in amacrine cells of the chicken retina. The present study utilizes double- and triple-label paradigms to quantitatively analyze these coexisting relationships. Twenty-eight percent of enkephalin-like immunoreactive amacrine cells were found to exhibit high-affinity uptake of [3H]GABA, while 53% of enkephalin-amacrine cells specifically accumulate [3H]glycine. Moreover, the present study predicts that at least 26% of enkephalin-amacrine cells which accumulate [3H]glycine should also be immunoreactive for neurotensin.

Animals↗
PubMed1986

Immunohistochemical evidence of plasticity of gamma-aminobutyric acid neurons in the red nucleus and adjacent reticular formation after contralateral cerebellectomy in the adult cat.

A comparative mapping of gamma-aminobutyric acid neurons identified by means of glutamic acid decarboxylase (GAD) immunohistochemistry was performed in the red nucleus (RN) in both intact and hemicerebellectomized adult cats (21 days postoperative). In the deafferented RN (contralateral to the lesion) as well as in the adjacent dorsolateral reticular formation, a marked increase in the number of GAD-positive perikarya was observed. In this mesencephalic area, some neurons may therefore increase their endogenous levels of immunodetectable GAD, as a response to cerebellar deafferentation. This can be viewed as one of the events contributing to functional recovery.

Animals↗
PubMed1981

A comparison of the effects of flurazepam on gamma-aminobutyric acid mediated depression of cerebellar and cerebral cortical neurons.

With standard extracellular recording and microiontophoretic techniques, the effects of flurazepam on gamma-aminobutyric acid (GABA) evoked depression of cerebellar and cerebral cortical neurons in rats have been studied. It was found that although flurazepam potentiated the GABA-mediated inhibition of most Purkinje cells (25 or 36), it caused only a weak potentiation of GABA action on some cerebral cortical neurons (14 of 37). The difference between the action of flurazepam in these two structures was statistically significant. The results confirm a previous report that the enhancement of GABA-evoked inhibition by benzodiazepines is more readily elicited on cerebellar cortical neurons than on cerebral cortical neurons.

Action Potentials↗