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PubMed1997

Elevated plasma gamma-aminobutyric acid (GABA) levels in individuals with either Prader-Willi syndrome or Angelman syndrome.

Plasma gamma-aminobutyric acid (GABA) levels were measured in 14 subjects with Prader-Willi syndrome, 9 subjects with Angelman syndrome, and matched control subjects. Mean levels in both patient groups were 2 to 3 times higher than in nonretarded moderately obese or retarded nonobese control subjects. Levels in each patient group differed significantly from both control groups. Neither the two patient groups nor the two control groups differed. GABA levels seemed unrelated to genetic status (chromosome 15 deletion or disomy). These preliminary findings of elevated plasma GABA levels possibly represent a compensatory increase in presynaptic GABA release in response to hyposensitivity of a subset of GABA receptors and could produce increased postsynaptic activation of other normal GABA receptor subtypes, resulting in complex alterations of GABAergic function throughout the brain.

Adolescent↗

PubMed1988

Physiological correlates of responses to gamma-aminobutyric acid (GABA) recorded from rat visual cortical neurons in vitro.

Responses to focal application of gamma-aminobutyric acid (GABA) were compared to synaptic potentials elicited by afferent stimulation of rat visual cortical neurons, using a slice preparation and conventional intracellular recording techniques. GABA produced three types of responses: a brief hyperpolarization (mean reversal potential, -72 mV), brief depolarization (mean reversal potential, -50 mV), or a prolonged hyperpolarization (mean reversal potential, -80 mV). Synaptic potentials included simple or complex EPSPs and EPSPs followed by mono- or biphasic IPSPs. A comparison of the characteristics of the GABA responses and synaptic potentials indicated that GABA may mediate both phases of the IPSP in these cells. Our results suggest that despite differences in the circuitry of the visual cortex as opposed to other neocortical and allocortical (hippocampal) areas (Mountcastle and Poggio, 1968; Colonnier and Rossignol, 1969; Creutzfeldt, 1978; Kuhlenbeck, 1978), the inhibitory control of cortical pyramidal and nonpyramidal neurons by GABA is quite similar.

Action Potentials↗

PubMed1987

Effect of repeated treatment with a gamma-aminobutyric acid receptor agonist on postnatal neural development in rats.

The effect of treatment with the gamma-aminobutyric acid (GABA) agonist tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) on neural development was monitored in rats by following the expression of the neuron-specific proteins neural cell adhesion molecule (NCAM), D1, and D3 as well as the enzymes glutamate decarboxylase (GAD) and glutamate dehydrogenase (GLDH). As judged from the effect of the treatment on the expression of NCAM and GAD, GABA agonists have the capacity to accelerate and enhance neuronal development during the early postnatal period. However, as judged from the expression of D1- and D3-protein some adverse late effects may result from prolonged treatment with high doses of GABA agonists. The decrease in GLDH specific activity observed in THIP-treated rats during their late postnatal development possibly indicates a repression of glutamatergic neurons.

Animals↗

PubMed1986

Cortical acetylcholine release is increased and gamma-aminobutyric acid outflow is reduced during morphine withdrawal.

The effects of naloxone on acetylcholine (ACh) and gamma-aminobutyric acid (GABA) outflow from the cerebral cortex of freely moving, morphine-dependent guinea-pigs was studied. The cortical efflux of ACh in chronically-treated guinea-pigs was about half of that of normal animals. GABA efflux was unaffected. During opioid withdrawal precipitated by naloxone (0.1-10 mg kg-1, i.p.) the guinea-pigs showed jumping, hyperactivity and wet dog shakes, the intensity of which was directly related to the dose of naloxone. The withdrawal syndrome was accompanied by a dose-dependent increase in ACh release and reduction in GABA outflow; ACh release was increased by naloxone at doses lower (0.1-3 mg kg-1) than those acting on GABA efflux (1-10 mg kg-1). Atropine (10 mg kg-1) and diazepam (5 mg kg-1) did not prevent GABA and ACh changes.

Acetylcholine↗

PubMed1998

Small-volume on-line sensor for continuous measurement of gamma-aminobutyric acid.

We report the first on-line electrochemical sensor for the continuous measurement of gamma-aminobutyric acid (GABA), which is a well-known inhibitory neurotransmitter in the nervous system. The sensor is composed of a glutamate oxidase (GluOx) and catalase immobilized small-volume enzymatic reactor and a glassy carbon (GC) electrode modified with a top layer film consisting of gabase and GluOx coimmobilized bovine serum albumin and an Ospoly(vinylpyrridine) bottom layer film containing horseradish peroxidase. The response of the sensor depends on the alpha-ketoglutarate concentration and is almost saturated when its concentration is 100 times higher than GABA. The sensor exhibits a sensitivity of 1.56 nA/microM for GABA under optimized conditions and shows almost no response when 10 microM glutamate is continuously injected. A detection limit of 0.1 microM is obtained with a linear range of 0.1-10 microM. GABA can be measured in the absence of alpha-ketoglutarate when there is L-glutamate in the sample solution, which is a typical condition for the extracellular measurement of cultured nerve cells.

Animals↗

PubMed1984

Site of gamma-aminobutyric acid (GABA)-mediated inhibition of growth hormone secretion in the rat.

The effect of altering gamma-aminobutyric acid (GABA) activity on growth hormone (GH) secretion of freely moving chronically cannulated male rats was studied. Systemic injection of the GABA agonist muscimol (2 mg/kg i.v.) inhibited the anticipated secretory episode. Increasing brain GABA levels by gamma-acetylenic-GABA (50 mg/kg i.v.) also inhibited the expected GH rise. When injected before the expected secretory episode, the GABA receptor antagonist bicuculline methiodide (2 mg/kg i.v.) triggered an early secretory peak. GABA and muscimol failed to change GH secretion by cultured anterior pituitary cells. When the somatostatin input to the stalk-median eminence region was interrupted by an anterolateral cut around the medial basal hypothalamus, the GH level was steadily increased and muscimol injections caused a prompt decrease of plasma GH levels. These results are consistent with the hypothesis that GABAergic tonic inhibition participates in the control of GH secretion and that GABA inhibits spontaneous GH release by inhibiting the secretion of a GH-releasing factor.

Afferent Pathways↗

PubMed1992

Gamma-aminobutyric acid immunoreactivity in the enterochromaffin cells of the rat stomach.

The present immunocytochemical study revealed gamma-aminobutyric acid (GABA) immunoreactivity in the oxyntic and pyloric mucosa of the rat stomach at light- and electron-microscopic levels. GABA-immunoreactive endocrine cells were numerously seen in the lower half portion of the pyloric mucosa but rarely in the oxyntic mucosa. These cells were round or oval in shape and sometimes had a short cytoplasmic process. Serotonin-immunoreactive enterochromaffin (EC) cells were also observed in the oxyntic and pyloric mucosa of the stomach. The distribution and shapes of the immunoreactive cells were similar to those of the GABA-immunoreactive cells. With a double immunolabeling technique using anti-GABA and antiserotonin serum, GABA-immunoreactive endocrine cells showed serotonin immunoreactivity and were identified as EC cells. At the electron-microscopic level the GABA-immunoreactive cells contained round or oval, spindle-like, pear-shaped granules in EC cells. The immunoreaction product in the EC cells was generally confined to the granular cores. These findings suggest that GABA may be synthesized in the EC cells and be released from the granules of the cells after adequate stimuli.

Animals↗

PubMed1983

Prolonged treatment with gamma-aminobutyric acid (GABA)-mimetic substances in prepubertal male rats.

The effect of chronic treatment with a gamma-aminobutyric acid (GABA)-mimetic compound, progabide, and an inhibitor of GABA-transaminase, gamma-acetylenic GABA (GAG), was tested in prepubertal male rats. The effect of gamma-butyrolactone (GBL), given orally, was also tested. The rats treated with progabide did not show any difference in body, testicular, or seminal vesicle weights or serum prolactin levels, as compared with control rats. Treatment with GAG, at both dose levels used, did not significantly affect body weight. Testicular weight was significantly lower in the group of rats treated with the low dosage of GAG (5 mg/kg), and serum prolactin was significantly lower in the rats treated with the high dosage of GAG (20 mg/kg) as compared with control rats. In the first experiment performed with GBL, the rats given this compound had significantly lower body and testicular weights as compared with control rats. In the second experiment, GBL-treated rats had body weights similar to those of control rats, but testicular weights were significantly decreased. Prolonged treatment with GABA mimetics may affect the hypothalamic-pituitary-testicular axis.

4-Butyrolactone↗

PubMed1986

Maitotoxin-induced release of gamma-[3H]aminobutyric acid from cultures of striatal neurons.

The potent marine toxin, maitotoxin, induced the release of gamma-[3H]aminobutyric acid (GABA) from reaggregate cultures of striatal neurons in a dose-dependent manner. Maitotoxin-induced release occurred following a lag period of several minutes and was persistent. Release induced by 70 mM K+ on the other hand was immediate and transient in nature. Co2+ (3 mM) and Cd2+ (1 mM) inhibited maitotoxin-induced release of GABA as did removal of extracellular Ca2+. However, the organic calcium antagonists nisoldipine, nitrendipine, and D-600 at concentrations of 10(-6) M did not block maitotoxin-induced or 70 mM K+-induced release. High concentrations of D-600 (10(-4) M) partially blocked both maitotoxin- and 70 mM K+-induced release. The dihydropyridine calcium agonist BAY K8644 (10(-6) M) did not enhance maitotoxin-induced or 70 mM K+-induced release. Replacement of Na+ in the incubation medium with choline led to an increased basal output of GABA and an apparent inhibition of the effect of maitotoxin. These data are discussed with reference to the hypothesis that maitotoxin can directly activate voltage-sensitive calcium channels.

Animals↗

PubMed1996

Low plasma gamma-aminobutyric acid levels during the late luteal phase of women with premenstrual dysphoric disorder.

OBJECTIVE: Plasma gamma-aminobutyric acid (GABA) levels have been reported to be low in some patients with major depressive disorder. Premenstrual dysphoric disorder is often associated with major depressive disorder. Therefore, the authors sought to determine whether women with premenstrual dysphoric disorder with or without prior major depressive disorder also had low plasma GABA levels. METHOD: Plasma GABA levels were measured in 27 women with premenstrual dysphoric disorder and 21 comparison women during the the mid-follicular and late luteal phases of the menstrual cycle. RESULTS: In comparison women, plasma GABA levels increased from the mid-follicular to the late luteal phase. Women with premenstrual dysphoric disorder and a past history of major depressive disorder had low plasma GABA levels during both phases. In women with premenstrual dysphoric disorder but no past major depressive disorder, plasma GABA levels decreased from the nonsymptomatic, mid-follicular phase to the symptomatic, late luteal phase. CONCLUSIONS: Decreased GABA function may represent a common biological link between subtypes of depressive and premenstrual dysphoric disorders. A trait in major depressive disorder and a state-dependent decrease in premenstrual dysphoric disorder might imply a possible continuum between the two disorders.

Adult↗

PubMed1985

gamma-Aminobutyric acid plasma levels and brain binding in Eck fistula dogs.

It has been hypothesized that gamma-aminobutyric acid (GABA), the principle inhibitory neurotransmitter of the mammalian brain, contributes to the neural inhibition of hepatic encephalopathy. Eck fistulae were created in seven dogs and celiotomy alone performed in five dogs to determine plasma GABA levels, brain GABA binding, and synaptic membrane changes in dogs after creation of Eck fistulae. Eck fistula dogs lost 19 +/- 9% body weight, lost hair, ate poorly, and developed atrophic livers with classic hepatic histological changes. Control dogs maintained body weight, normal behavior, and normal liver histology. Plasma GABA levels were elevated significantly in the Eck fistula dogs (312 +/- 105.9 nM) both as compared to controls (154.4 +/- 69.8) and to preoperative levels (161.6 +/- 56.7, P less than 0.05). Brain GABA binding for animals sacrificed at 6-9 weeks was not statistically different from sham-operated dogs sacrificed at 6 weeks (1.87 +/- .54 pmole/mg protein vs 1.186 +/- 24, P less than 0.2). Synaptic membrane fluidity and cholesterol were likewise unchanged. Plasma GABA levels are increased significantly following complete portal diversion but do not correlate with the degree of encephalopathy. GABA binding to neural membranes are not significantly increased in Eck fistula dogs. These findings do not support a direct relationship between plasma GABA levels and neurologic impairment in Eck fistula dogs.

Animals↗

PubMed1985

Evidence for gamma-aminobutyric acid mediation of the sympathetic nerve inhibitory response to vagal afferent stimulation.

The involvement of gamma-aminobutyric acid (GABA) in the vagal-stimulated reflex inhibition of sympathetic nerve discharge (SND) was investigated in the cat. Computer summation was used to assess the sympathoinhibitory response to vagal afferent stimulation and the resultant changes seen with agents known to effect GABAergic neurotransmission. The GABA antagonists picrotoxin and bicuculline at 0.25 to 1.0 mg/kg i.v. attenuated the vagal sympathetic inhibitory response, but increased the 1:1 locking of SND to the arterial pulse. Conversely, the GABA agonist diazepam at 0.3 mg/kg i.v. potentiated the vagal sympathoinhibition, reduced total SND and diminished SND locking to the arterial pulse. Picrotoxin also blocked the vagal sympathoinhibitory response in midcollicular transected cats and when applied topically to the dorsal brain stem. Midcollicular transection forestalled the irregular SND spiking normally seen with picrotoxin in the intact cat, thus resulting in improved 3 cycle/sec SND periodicity. None of these drug-induced changes effected the SND shutoff response to vasopressor tests, however. These results suggest that GABA plays a role in the SND inhibitory response to vagal afferent stimulation in the brain stem, independent of the sinoarterial baroreceptors, and may also be involved in the entrainment of SND to the arterial pulse.

Afferent Pathways↗

PubMed1984

Early undernutrition and [3H]gamma-aminobutyric acid binding in rat brain.

The effect of early undernutrition and dietary rehabilitation on [3H]gamma-aminobutyric acid ([3H]GABA) binding in rat brain cerebral cortex and hippocampus was examined. Undernourished animals were obtained by exposing their mothers to a protein-deficient diet during both gestation and lactation. Saturation analysis of [3H]GABA binding in the cerebral cortex and hippocampus revealed high- and low-affinity components in the undernourished group, whereas control animals possessed only a low-affinity site. The concentration of low-affinity binding sites was greater in the undernourished animals. Rehabilitation of undernourished animals completely abolished the binding site differences. Treatment of brain membranes with Triton X-100 yielded two binding components in both the undernourished and control animals, although the concentration of lower affinity sites was still greater in the undernourished group. Neither the efficacy nor the potency of GABA to activate benzodiazepine binding in cerebral cortex was modified by undernutrition. These data suggest that early undernourishment modifies the characteristics of [3H]GABA binding, perhaps by reducing the brain content of endogenous inhibitors of the higher affinity binding site. The lack of effect on GABA-activated benzodiazepine binding suggests the possibility that neither the high- nor the low-affinity GABA binding sites are coupled to this receptor component.

Aging↗

PubMed1991

Negative modulation of the gamma-aminobutyric acid response by extracellular zinc.

We have studied the effects of divalent cations on the gamma-aminobutyric acid (GABA) response of voltage-clamped spinal cord neurons, using the whole-cell recording configuration. Zn, Cd, Ni, and Mn (but not Ba, Ca, or Mg) inhibit GABA-induced whole-cell currents when applied extracellularly. Although Zn is an effective inhibitor when applied extracellularly, it is ineffective when applied intracellularly. Inhibition by these cations is mediated by a common saturable recognition site that is distinct from the recognition sites for GABA, benzodiazepines, barbiturates, picrotoxin, or steroids. The maximal inhibition, or efficacy of inhibition, of GABA-induced currents is greater for Zn than for Cd, Ni, or Mn. The order of potency is Cd greater than Zn much greater than Ni much greater than Mn. Inhibition by Zn is partially surmountable by GABA, consistent with a decrease in both the maximum response and the affinity for GABA. The dose-response curve for inhibition of the GABA response by Zn is shifted to the right at a high GABA concentration but is unaffected by the presence of chlordiazepoxide, pentobarbital, or 5 beta-pregnan-3 alpha-ol-20-one. The results are consistent with a model in which a Zn-sensitive modulatory site exerts negative allosteric control over GABA receptor function.

Allosteric Regulation↗

PubMed1991

Coexistence of gamma-aminobutyric acid type A and type B receptors in testicular interstitial cells.

The existence of specific gamma-aminobutyric acid (GABA)ergic receptors in testicular interstitial cells was investigated in the present study. Specific binding of [3H]GABA to interstitial cell membranes was found to be time- and temperature-dependent and varied according to Ca2+ concentration present in the incubation medium. We analyzed the ability of different GABAergic agonists and antagonists to displace the bound radioactivity. In the absence of Ca2+ (1 mM EDTA), GABA and the GABAergic agonist isoguvacine displaced the bound radioactivity. When the radioligand assay was performed in the presence of 2.5 mM CaCl2, the [3H]GABA specifically bound increased twofold. Under such conditions, the specific GABAergic agonist baclofen, as well as GABA and isoguvacine, displaced the [3H]GABA bound. Saturation analysis revealed the presence of a population of GABAA binding sites with a KD value of 45.2 nM and a maximal number of binding sites of 57.4 fmol/mg of protein. The maximal binding increased on addition of 2.5 mM CaCl2 to 102 fmol/mg of protein, indicating the existence of a second population of GABAergic receptors, i.e., type B, with essentially the same affinity. In addition, the incubation of testicular interstitial cells with GABA and baclofen resulted in an increase in androgen production. These results support a functional role of GABA in the neuroendocrine control of the male gonad.

Ammonium Chloride↗

PubMed1978

Quantitative visualization of gamma-aminobutyric acid receptors in hippocampus and area dentata demonstrated by [3H]muscimol autoradiography.

Muscimol, a potent gamma-aminobutyric acid (GABA) agonist, was used in a radioactively labeled form for the quantitative localization of GABA receptors in the rat's hippocampus (CA(1) to CA(4)) and area dentata. [(3)H]Muscimol was injected directly in vivo or used in the incubation medium of tissue slices, and the tissues were then fixed and prepared for autoradiography. [(3)H]Muscimol-bound GABA receptors are weakly though evenly distributed over the fimbria of the fornix. There was a laminar distribution in CA(1) to CA(4) and the area dentata, with an increasing density of the GABA receptors in that order. The lowest density was found in the alveus of CA(1) and CA(2) and the highest in the stratum granulosum of the area dentata. The greatest density was found in the neuropil between granule cells, in which are found dendrites and the basket-like plexuses of the inhibitory GABA-containing local circuit neurons. The molecular layers of the area dentata, CA(1), and CA(2) also have a high density of GABA receptors, indicating a probable distribution over the dendrites of granule and pyramidal cells. The laminar distribution of GABA receptors in the hippocampus and area dentata is similar to the distributions of the GABA-synthesizing enzyme, glutamate decarboxylase, and of GABA previously published. Neurons with label of various density are found in the polymorphic cell layer of the area dentata, in the stratum radiatum of CA(3), and in CA(4). These are possibly the GABA-containing basket local circuit neurons.

Amanita↗

PubMed2004

Protective effect of gamma-aminobutyric acid against glycerol-induced acute renal failure in rats.

To investigate the effect of gamma-aminobutyric acid (GABA) on acute renal failure, we used a rat model of acute tubular necrosis induced by glycerol. After deprivation of water for 6h, the rats received an injection of 50% glycerol into the muscle of the rear limb at 10 ml/kg body weight. GABA was then administered orally to the rats (100 or 500 mg/kg body weight/day) once every 12h for 3 days. The rats with acute renal failure showed arrested body weight gain and an increase of kidney weight, whereas oral administration of GABA attenuated the physiological changes induced by acute renal failure. However, GABA administration had no significant effect on increased urine volume. Oral administration of GABA at a dose of 100 or 500 mg/kg body weight/day for 3 days significantly improved the markedly elevated levels of blood urea nitrogen and creatinine and the reduced creatinine clearance related to progression of renal failure. Moreover, the rats with acute renal failure exhibited high levels of fractional excretion of sodium (FE(Na)) due to alteration of tubule function following injection of glycerol. However, administration of GABA lowered the FE(Na) levels dose-dependently. Furthermore, urine osmolarity was markedly reduced in control rats with acute renal failure as compared with normal rats, whereas it was significantly increased by administration of GABA at a dose of 500 mg/kg body weight/day. These results indicate that GABA has potential as a therapeutic agent against the renal damage involved in acute renal failure.

Acute Kidney Injury↗

PubMed1983

Effect of gamma-aminobutyric acid on excitability of tubero-infundibular neurons in rat hypothalamic slices.

The effect of gamma-aminobutyric acid (GABA) on antidromically identified tubero-infundibular (TI) neurons was examined in hypothalamic slices of ovariectomized female rats. Twenty antidromically evoked spikes were obtained in the medial basal hypothalamus, including the arcuate and ventromedial nuclei, by electrical stimulation of the median eminence. Sixteen of them had a notch in the rising phase and fractionation of the initial segment (IS)- and somatodendritic (SD)-spikes was elicited by repeated stimulation at frequencies higher than 10 Hz. The application of 0.5-1.5 mM GABA to the incubation medium inhibited SD spikes in 7 of these 16 neurons. The latency, amplitude and threshold of IS spikes were not affected by GABA except for one spike whose latency fluctuated. On the remaining 9 neurons having the notch, no effect of 5-10 mM GABA was discernible. Four of 20 antidromically evoked spikes, which had a smooth rising phase and a shorter duration, were not inhibited by 5-10 mM GABA, but a fluctuation of the latency was observed in one neuron. Fifteen neurons having spontaneous unit activity were also obtained in the arcuate nucleus and its adjacent area and tested with GABA. In 10 of the 15 neurons, spontaneous unit activity disappeared following 0.1-1.5 mM GABA perfusion, while the firing rate in the remaining 5 neurons was not affected by 5-10 mM GABA. These results provide evidence for a direct inhibitory effect of GABA on TI neurons and support the involvement of GABAergic neurons in regulating neuroendocrine functions.

Animals↗