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PubMed1984

Chronic haloperidol administration enhances the gamma-aminobutyric acid level in the rat striatum without altering the glutamate level.

A dose-dependent elevation of striatal gamma-aminobutyric acid (GABA) level was found under chronic treatment with haloperidol, a classical neuroleptic drug. The unaltered GABA level in the substantia nigra is compatible with the existence of GABAergic interneurons in the striatum, which are inhibited by the afferent dopaminergic innervation to the striatum. The glutamate levels of the cerebrospinal fluid (CSF) and different brain regions investigated were not significantly changed by haloperidol. By contrast, we found in an earlier investigation with sulpiride, an atypical neuroleptic drug, a changed glutamate level in the striatum and the CSF and an unaltered GABA level. These findings may correspond to the different clinical effects of classical and atypical neuroleptics.

Animals↗
PubMed1985

Pharmacological properties of gamma-aminobutyric acid-, glutamate-, and aspartate-induced depolarizations in cultured astrocytes.

Differentiated glial fibrillary acidic protein-positive astrocytes in homogeneous cultures of early postnatal rat cerebral hemispheres respond by membrane depolarization to gamma-aminobutyric acid (GABA), glutamate, and aspartate with a threshold concentration of approximately 10(-5) M. The GABA-induced depolarization is antagonized by two blockers of the neuronal GABAA receptor, picrotoxin and bicuculline, but is not affected by the uptake blockers beta-alanine or nipecotic acid. An agonist of the GABAA receptor, muscimol, produces a dose-response curve similar to that of GABA, whereas the agonist of the GABAB receptor, baclofen, did not alter the membrane potential. When repetitive pulses of GABA are given to one cell, its responsiveness depends on the time interval between pulses. Within 30 sec after termination of the first pulse the cell remains unresponsive to the second pulse. With increased time intervals between the pulses, reactivity toward GABA recovers. Five minutes after the first pulse the cell regains 75% of its initial depolarization peak. Aspartate results in a depolarization similar in size and time course to that induced by glutamate. The glutamate agonists, quisqualate and ibotenate, and kainate are less potent than glutamate. N-Methyl-D-aspartate has no effect on the membrane potential of astrocytes. The pharmacological features of the glutamate response are therefore similar to those of the receptor mediating neuronal glutamate transport.

Animals↗
PubMed1989

Double labeling of cytochrome oxidase and gamma-aminobutyric acid in central nervous system neurons of adult cats.

The relationship between the levels of cytochrome oxidase and gamma-aminobutyric acid (GABA) was investigated within single neurons by double labeling the 2 markers in the same section. Double staining was equally effective when immunogold-silver staining of GABA was followed by indirect immunoperoxidase labeling of cytochrome oxidase, or when cytochrome oxidase histochemistry was followed by immunogold-silver staining of GABA. Neurons in the perigeniculate nucleus (PGN) and basket cell terminals in the cerebellum were GABA positive and rich in cytochrome oxidase. Interneurons of the lateral geniculate nucleus (LGN) as well as stellate and Golgi cells of the cerebellum were GABA-rich but poor in cytochrome oxidase. These results demonstrate that there is no consistent relationship between the levels of cytochrome oxidase and GABA in neurons.

Animals↗
PubMed1992

Changes in the effect of gamma-aminobutyric acid on prolactin secretion during sexual maturation in female rats.

To evaluate the effects of the gamma-aminobutyric acid (GABA)ergic system on PRL secretion during sexual development in female rats, aminooxyacetic acid (an inhibitor of GABA-transaminase which increases the hypothalamic GABA concentration) was administered to 12- to 16- and 30-day-old female rats. The increased GABA level in the hypothalamus was accompanied by a significant increase in the serum PRL concentration in rats 16 days of age and a decrease in the serum concentration of the hormone in 30-day-old rats. No changes in PRL levels were observed at 12 days of age. Muscimol, a GABA-A receptor agonist, increased serum PRL concentrations in 16-day-old rats. By contrast, in rats 30 days of age, muscimol induced a significant decrease in PRL levels. On the other hand, the administration of baclofen, a GABA-B receptor agonist, induced a pattern of PRL modification similar to that observed with muscimol, i.e. stimulation in rats 16 days of age and inhibition in 30-day-old rats. These findings indicate that both the stimulatory and inhibitory effects of the GABAergic system on PRL secretion during sexual maturation are mediated by GABA-A and GABA-B receptors. The present results show that during sexual maturation there is a qualitative modification of the effect of the GABAergic system on PRL secretion. These findings could be related to the complex neuroendocrine mechanisms involved in the onset of puberty in the female rat.

4-Aminobutyrate Transaminase↗
PubMed1986

Gamma-aminobutyric acid affects the developmental expression of neuron-associated proteins in cerebellar granule cell cultures.

The effect of gamma-aminobutyric acid (GABA) on the expression of the neuron-associated D2 and neuron-specific enolase (NSE) was studied during development in culture of cerebellar granule cells. It was found that the presence of GABA during culture development increased the overall protein content. D2 content was also increased but not above the general increase in protein whereas NSE increased above the general level of protein. The presence of GABA in the growth medium also appeared to accelerate the changes in molecular forms of D2 and NSE seen during neuronal development. This suggests that GABA promotes or accelerates the general maturation of neurons, as these two neuron-associated proteins otherwise differ from each other with respect to their subcellular localization and their physiological and biochemical properties.

Animals↗
PubMed2005

Synthesis and characterization of an electroactive surface that releases gamma-aminobutyric acid (GABA).

We report the synthesis and characterization of a new electroactive surface capable of releasing the neurotransmitter gamma-aminobutyric acid (GABA) upon reduction. The GABA was anchored to an alkanethiol via electrochemically active quinone (abbreviation, TM-GABA). The quinone unit, upon reduction to the hydroquinone, cyclizes to release GABA into solution. The half-life is 99 s. The self-assembled monolayer (SAM) of TM-GABA on gold was prepared and characterized with several surface sensitive techniques. X-ray photoelectron spectroscopy (XPS) explored the SAM formation of TM-GABA on Au surfaces. Cyclic voltammograms showed the ability to electrochemically control the quinone unit at the distal end of the chain. GABA was selectively released upon electrochemical reduction at a potential of -700 mV. The functional GABA terminal group was detected by surface plasmon resonance measurements of anti-GABA antibody binding.

Biocompatible Materials↗
PubMed1993

gamma-Aminobutyric acid (GABA) autoreceptors in rat cerebral cortex and spinal cord represent pharmacologically distinct subtypes of the GABAB receptor.

gamma-Aminobutyric acid (GABA) autoreceptors regulating release of [3H]GABA have been characterized pharmacologically by using rat cerebral cortex and spinal cord synaptosomes exposed in superfusion to mild depolarization (9 mM KCl). In both regions GABA inhibited the K(+)-evoked overflow of [3H]GABA. The EC50 values amounted to 1.23 microM (cortex) and to 1.01 microM (spinal cord). Also the GABAB receptor agonist 3-aminopropylphosphonous acid (3-APPA) decreased the [3H]GABA overflow: EC50 values = 0.095 microM (cortex) and 0.078 microM (spinal cord). The classical GABAB receptor agonist (-)-baclofen was equipotent to GABA at the cortical autoreceptor (EC50 = 1.37 microM), whereas it was almost ineffective in the spinal cord (EC50 = 425 microM). (+)-Baclofen was extremely weak in both brain areas. Two GABAB receptor antagonists, phaclofen and (CGP 35348) [3-aminopropyl(diethoxymethyl)phosphinic acid] provided opposite results at the two autoreceptors examined. The IC50 values for phaclofen amounted to 47.9 microM (cortex) and to > 1000 microM (spinal cord), respectively. In contrast, CGP 35348 was almost ineffective at the cortex autoreceptors (IC50 > 300 microM), but was rather potent in the spinal cord (IC50 = 1.07 microM). To conclude, GABA autoreceptors in the cerebral cortex are classically sensitive to (-)-baclofen and to 3-APPA; they are also sensitive to phaclofen, but resistant to CGP 35348. Surprisingly, GABA autoreceptors in the spinal cord are poorly sensitive to (-)-baclofen, although they are as sensitive as the cortical autoreceptors to 3-APPA; moreover they are resistant to phaclofen, but highly sensitive to CGP 35348. The data show that pharmacologically distinct release-regulating GABAB autoreceptors exist in the central nervous system of a same animal species.

Animals↗
PubMed1985

gamma-Aminobutyric acid in CSF of children with febrile seizures.

Previous studies have suggested that levels of cerebrospinal fluid (CSF) gamma-aminobutyric acid (GABA) may be decreased in children with febrile seizures. We used gas chromatography and mass spectrometry to measure CSF GABA levels in 14 children with febrile seizures. The results were compared with the GABA levels in six children with first-time afebrile seizures, three with recurrent febrile seizures, and 13 controls (febrile children undergoing lumbar puncture to rule out meningitis). Children with central nervous system infections or known neurologic disease were excluded. The CSF GABA levels in children with febrile seizures were not significantly different from those in controls and children with afebrile or recurrent febrile seizures. In the control group, CSF GABA levels correlated with increasing age. There was no correlation with severity of febrile response in any group. The results indicated that the CSF GABA level may not be abnormal in patients with first-time febrile convulsions.

Child↗
PubMed1988

[Circadian variations in the incorporation of gamma-aminobutyric acid (GABA) and tritiated taurine into the pineal body of CD mice].

Pineal uptake of two putative neurotransmitters, gamma-aminobutyric acid (GABA) and taurine, was investigated during the 24 h-cycle in mice kept in long (14L/10D) or short (10L/14D) photoperiods. Tritiated mediators were intraperitoneally injected and their concentration both in pineal gland and cerebellum were measured at several times along the nycthemere. A circadian rhythm of exogenous GABA uptake was observed in mice kept in long photoperiods: GABA uptake was high during the night, when the gland was active and low during the day. It corresponded to the pineal cycle of indoleamine synthesis. It was particularly sensitive to sudden changes of lighting. In short photoperiods, a similar cycle was observed but the result was not significant because of individual variations. Taurine uptake did not show such a circadian rhythm either in long or in short photoperiods: it was constant and rather low with large variations from one animal to another.

Animals↗
PubMed2005

Brain gamma-aminobutyric acid changes in stiff-person syndrome.

BACKGROUND: Patients with stiff-person syndrome (SPS) have circulating antibodies against glutamic acid decarboxylase, the rate-limiting enzyme responsible for the synthesis of gamma-aminobutyric acid (GABA). Although the patients' symptoms of stiffness and unexpected spasms can be explained on the basis of reduced or impaired inhibitory neurotransmitters, such as GABA, it is unclear whether the level of GABA in the brains of these patients is reduced and, if so, whether the reduction is due to anti-glutamic acid decarboxylase antibodies. OBJECTIVE: To measure GABA levels in the brains of patients with SPS. DESIGN: Prospective case-control study. SETTING: National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md. PATIENTS: Eight patients with SPS with high titers of circulating anti-glutamic acid decarboxylase antibodies and typical clinical symptoms of SPS and 16 control subjects. MAIN OUTCOME MEASURES: Results of brain magnetic resonance imaging and magnetic resonance spectroscopy, which measures GABA levels in specific brain regions. RESULTS: No abnormalities were noted on brain magnetic resonance images. A prominent and significant decrease in GABA level was, however, observed in the sensorimotor cortex and a smaller decrease in the posterior occipital cortex but not in the cingulate cortex or pons. CONCLUSIONS: The reduction of brain GABA in patients with SPS supports the clinical symptoms and indicates that the inhibitory GABAergic pathways are involved in the disease. Regardless of the responsible autoantigens, in SPS autoantibodies block the function of GABAergic neurons and interfere with the synthesis of GABA but do not cause structural changes in the brain.

Adult↗
PubMed1985

Mechanisms of seizure control mediated by gamma-aminobutyric acid: role of the substantia nigra.

The substantia nigra has been identified as a critical site at which gamma-aminobutyric acid (GABA) agonist drugs act to reduce susceptibility to a number of types of experimentally induced generalized seizures. Moreover, the ability of systemically administered GABA-elevating agents to protect against maximal electroshock seizures is directly correlated with an increase in GABA specifically in the nerve-terminal compartment of substantia nigra. The significance of these findings is discussed in terms of the role of specific nigral synapses for the control of seizure propagation. Evidence from lesion studies, as well as studies with opiates and substance P analogs, further supports the hypothesis that Inhibition of nigral efferents reduces susceptibility to generalized seizures. Inhibition of nigral outflow causes a decreased sensitivity to chemoconvulsants without precluding the animal's ability to exhibit any or all of the motor components of a seizure. We therefore propose that nigral outputs are capable of facilitating seizure propagation and can function as a gating mechanism for the generalization of convulsive activity.

Animals↗
PubMed1991

Effects of p-chloroamphetamine on release of [3H]gamma-aminobutyric acid from slices of rat caudate-putamen.

The effect of endogenous serotonin on the release of [3H]gamma-aminobutyric acid ([3H]GABA) from slices of rat caudate-putamen was studied. p-Chloroamphetamine was used to release endogenous serotonin. p-Chloroamphetamine (100 nM) enhanced the release of [3H]GABA induced by 20 mM K+, while 1000 nM p-chloroamphetamine decreased it. The 5-HT3 receptor antagonists ICS 205-930 (50 nM) and MDL 72222 (100 nM) prevented this facilitation caused by 100 nM p-chloroamphetamine. ICS 205-903 (50 nM), when used alone, reduced the release of [3H]GABA caused by 23 mM K+. This finding confirmed the hypothesis that endogenous serotonin can enhance the release of [3H]GABA via 5-HT3 receptors. In contrast, an effect of 5-HT1 and 5-HT2 receptors could not be clearly established. It is likely that the release of endogenous GABA from striatonigral GABA neurons may also be affected by serotonin via 5-HT3 receptors.

Animals↗
PubMed1986

Elicitation of intraspecific defensive behaviors in the rat by microinjection of picrotoxin, a gamma-aminobutyric acid antagonist, into the midbrain periaqueductal gray matter.

Behavioral reactions induced in the rat by microinjections of a gamma-aminobutyric acid (GABA) antagonist (picrotoxin; 25 and 50 ng in 0.25 microliter) into the midbrain periaqueductal gray matter were measured in an open-field test and when the animal was confronted by a conspecific introduced into its cage (i.e. resident-intruder paradigm). In the open-field, microinjections of picrotoxin significantly increased backward locomotion while decreasing self-grooming. In the resident-intruder paradigm, microinjections of picrotoxin selectively increased defensive reactions (defensive uprights, defensive sideways, retreat) while offensive behaviors were rather reduced. In addition, the actual nature of the effects was found to depend upon the intruder's relative position. Defensive reactions were significantly increased when the partner was on the side contralateral to the injection site, whereas social approach behaviors (fur investigation, anogenital investigation) were decreased when the partner was located on the ipsilateral side. These data suggest the involvement of GABAergic synapses within the midbrain periaqueductal gray matter in the control of intraspecific defensive behaviors in the rat.

Aggression↗
PubMed2005

Proximity of transmembrane domains 1 and 3 of the gamma-aminobutyric acid transporter GAT-1 inferred from paired cysteine mutagenesis.

GAT-1 is a sodium- and chloride-dependent gamma-aminobutyric acid transporter and is the first identified member of a family of transporters that maintain low synaptic neurotransmitter levels and thereby enable efficient synaptic transmission. Because transmembrane domains 1 and 3 contain amino acid residues important for transport activity, we hypothesized that these domains may participate in the formation of the binding pocket of the transporter. Pairwise substitutions have been introduced in several predicted transmembrane domains and in the first extracellular loop of GAT-1. In the double mutant W68C/I143C, in which the cysteines were introduced at locations at the extracellular part of transmembrane domains 1 and 3, respectively, approximately 70% inhibition of transport was observed by cadmium with an IC50 of approximately 10 microm. This inhibition was not observed in the corresponding single mutants and also not in > 10 other double mutants, except for V67C/I143C, where the half-maximal effect was obtained at approximately 50 microm. The inhibition by cadmium was only observed when the cysteine pairs were introduced in the same polypeptide. Our results suggest that transmembrane domains 1 and 3 come in close proximity within the transporter monomer.

Biological Transport↗
PubMed1990

Influence of gamma-aminobutyric acid on the changes of blood pressure in rats.

This is an attempt to investigate the effect of gamma-aminobutyric acid (GABA), a well-known major inhibitory neurotransmitter in the central nervous system, on the blood pressure response in rats and to elucidate the mechanism of its action. GABA injected into a femoral vein of the rat produced a dose-related fall in blood pressure followed by a secondary pressor response. The depressor response evoked by GABA was clearly blocked by pretreatment with chlorisondamine, diazepam and picrotoxin but was unaffected by atropine, prazosin and debrisoquin. GABA-induced pressor responses were significantly attenuated by pretreatment with prazosin or picrotoxin, while not affected by atropine, diazepam, debrisoquin and chlorisondamine. These experimental data suggest that GABA causes biphasically depressor and pressor responses in rats, and that the hypotensive activity evoked by GABA may be exerted through activation of GABAergic receptors and hypertensive activity due to stimulation of the adrenergic alpha-receptors, which appears to be associated with GABAergic receptors.

Animals↗
PubMed2003

Inhibition of high K+-evoked gamma-aminobutyric acid release by sodium nitroprusside in rat hippocampus.

To clarify whether nitric oxide (NO) modifies high K(+)-evoked gamma-aminobutyric acid (GABA) release, we examined the effects of sodium nitroprusside, an NO donor; diethyldithiocarbamate, an NO trapper; dithiothreitol, a superoxide radical scavenger; and 1H-(1,2,4)oxadiazole(4,3-a)quinoxalin-1-one, a specific guanylyl cyclase inhibitor, on high (100 mM) K(+)-evoked GABA release from rat hippocampus in vivo using microdialysis. Perfusion with 0.5 or 5 mM sodium nitroprusside significantly reduced high K(+)-evoked GABA release. Co-perfusion with 0.5 mM sodium nitroprusside and 5 mM diethyldithiocarbamate or 0.5 mM 1H-(1,2,4)oxadiazole(4,3-a)quinoxalin-1-one significantly enhanced high K(+)-evoked GABA release. Co-perfusion with 0.5 mM sodium nitroprusside and 1 mM dithiothreitol tended to increase it. These results demonstrate that sodium nitroprusside reduces high K(+)-evoked GABA release both via an NO/cyclic GMP-dependent pathway and via an NO-dependent, but cyclic GMP-independent, pathway in rat hippocampus in vivo.

Animals↗
PubMed1989

Very rapid assay of gamma-aminobutyric acid in mouse brain regions within 3 minutes by high-performance liquid chromatography with electrochemical detection.

For assay of gamma-aminobutyric acid (GABA) in brain tissue, a very rapid and simple chromatographic procedure using high-performance liquid chromatography (HPLC) with electrochemical detection (ECD) in combination with precolumn o-phthalaldehyde (OPA) derivatization is described. Perchloric acid extracts of the tissue were mixed with OPA/beta-mercaptoethanol solution and the mixture was injected onto the HPLC system. The present method permits GABA assay within less than 3 min in one chromatographic run. Up to 100 samples a working day can be analyzed in the present method. The present method has been applied to the measurement of GABA levels in discrete brain regions of mice treated with aminooxyacetic acid and isoniazid.

Aminooxyacetic Acid↗
PubMed2005

[Distribution of gama-aminobutyric acid (GABA)ergic neurons in rats cochlear nuclei after unilateral cochlea ablation].

OBJECTIVE: To observe the distribution of gama-aminobutyric acid (GABA) ergic neurons in rats cochlear nuclei (CN) in pre-and post-operation of unilateral cochlea ablation. METHOD: The technique of direct anti-GABA immunocytochemistry (SP) was used in this study. RESULT: The GABAergic neurons existed extensively in cochlear nuclei(CN). The number was more, the volume was larger of GABAergic cells in CN and those cells were stained heavily before ablation. The number of GABAergic cells in lesion side was far less than that in intact side after unilateral cochlea ablation one to two weeks (P < 0.01), then the number of GABAergic cells increased after three weeks which was still less (P > 0.05) and almost reached normal after a month (P > 0.05). CONCLUSION: The changes of GABAergic neurons reflect the balance between excitatory and inhibitory of neurons. It suggests that changes in the extent of GABAergic inhibition have been shown to contribute to the reorganization of primary auditory central system after unilateral cochlea ablation in rats. The decrease and increase of the number of GABAergic-neurons are essential for this reorganization.

Animals↗