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At least 667 records · Page 37Linked to original sources
PubMed1995

Cerebrospinal fluid gamma-aminobutyric acid in patients with panic disorder.

Cerebrospinal fluid (CSF) gamma-aminobutyric acid (GABA) levels were measured in 11 patients with panic disorder (PD) prior to and following 7 months of treatment with alprazolam or imipramine and in six neurological control patients. Although a clear treatment response was observed in patients with PD, neither alprazolam nor imipramine significantly changed CSF GABA during the treatment period. A negative correlation was demonstrated between baseline CSF GABA and posttreatment overt psychopathology. Low pretreatment level of CSF GABA correlated significantly with poor therapeutic outcome, judged by the amount of anxiety and depression as well as by the frequency of panic attacks at the end of follow-up.

Adult↗
PubMed1986

Brain glutamate decarboxylase cloned in lambda gt-11: fusion protein produces gamma-aminobutyric acid.

Glutamate decarboxylase (GAD; E.C. 4.1.1.15) converts glutamate to gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the vertebrate central nervous system. This report describes the isolation of a GAD complementary DNA clone by immunological screening of a lambda gt-11 brain complementary DNA expression library. The fusion protein produced by this clone catalyzes the conversion of glutamate to GABA and carbon dioxide, confirming its identity as GAD. Antibodies to beta-galactosidase remove GAD enzymatic activity from solution, showing that this activity is associated with the fusion protein. In immunoblotting experiments all three available antisera to GAD reacted with the fusion polypeptide and with two major polypeptides (molecular size, 60,000 and 66,000 daltons) in brain extracts.

Animals↗
PubMed2001

Wortmannin inhibits platelet aggregation produced by interaction of gamma-aminobutyric acid and the calcium tonophore, A23187.

Platelet aggregation by gamma-aminobutyric acid (GABA) agonists combined with a calcium ionophore was studied. GABA, baclofen and mucimol markedly amplified aggregatory responses to a subthreshold concentration of the ionophore, A23187. This effect was inhibited by wortmannin, a blocker of phosphoinositide 3-kinase. However, several antagonists of GABA receptors had no effect on the response, and benzodiazepines inhibited aggregation. These results suggest that the GABA effect is not mediated by traditional neuronal GABA receptors. We propose that wortmannin inhibits aggregation at a nexus downstream from membrane mechanisms triggered by the GABA-A23187 interaction.

Androstadienes↗
PubMed1984

Regulation of neurohormone release in the fiddler crab, Uca pugilator: effects of gamma-aminobutyric acid, octopamine, Met-enkephalin, and beta-endorphin.

Gamma-aminobutyric acid (GABA) blocked concentration of the pigments in melanophores and erythrophores of intact crabs. GABA blocked the release of pigment concentrating hormones from the isolated eyestalk. Octopamine (OA) blocked black pigment dispersion in intact crabs, but did not affect red pigment dispersion or concentration. OA blocked the release of black pigment dispersing hormone from isolated eyestalks. Met-enkephalin, but not Leu-enkephalin, stimulated black and red pigment concentration in intact crabs. Met-enkephalin, but not Leu-enkephalin, stimulated the release of pigment concentrating hormones from isolated eyestalks. Naloxone blocked the effects of Met-enkephalin in intact crabs and on isolated eyestalks. Beta-endorphin induced black pigment dispersion in intact crabs and in isolated legs.

Animals↗
PubMed1991

Possible involvement of endogenous opioid peptides in the inhibition of arginine vasopressin release by gamma-aminobutyric acid in conscious rats.

We examined the effects of gamma-aminobutyric acid (GABA) and naloxone, a potent opioid antagonist, on arginine vasopressin (AVP) secretion in conscious rats in order to study the relationship of GABA and endogenous opioid peptides in the regulation of AVP secretion. Intracerebroventricular administration of GABA caused a time- and dose-dependent decrease in the plasma concentration of AVP that was elevated by hypertonic saline injection, whereas it did not affect the basal AVP. Pretreatment with naloxone (10 mg/kg) significantly attenuated the inhibitory effect of GABA (100 micrograms) on AVP release. These results suggest that GABA produces an inhibition of AVP release stimulated by hypertonic saline, and that this inhibitory effect may be mediated at least in part by the endogenous opioid systems.

Animals↗
PubMed1982

CSF levels of gamma-aminobutyric acid in schizophrenia. Low values in recently ill patients.

gamma-Aminobutyric acid (GABA) levels in CSF were not significantly different in 30 drug-free schizophrenic patients and in 39 normal control subjects, because the control subjects were significantly older. Schizophrenic women had significantly lower levels than age-matched normal control women (less than 30 years). The GABA levels increased with duration of illness, number of hospitalizations, and months of hospitalizations, as well as with age. They correlated nonsignificantly with psychosis levels. After short-term pimozide treatment, GABA levels in all patients were raised, albeit nonsignificantly. The date suggest that low GABA levels may be observed only in the early years of the illness, particularly in female schizophrenic patients, and that these levels increase with time and with long-term neuroleptic treatment.

Adult↗
PubMed1996

Multiple gamma-Aminobutyric acid plasma membrane transporters (GAT-1, GAT-2, GAT-3) in the rat retina.

gamma-Aminobutyric acid (GABA) plasma membrane transporters (GATs) influence synaptic neurotransmission by high-affinity uptake and release of GABA. The distribution and cellular localization of GAT-1, GAT-2, and GAT-3 in the rat retina have been evaluated by using affinity-purified polyclonal antibodies directed to the C terminus of each of these GAT subtypes. Small GAT-1-immunoreactive cell bodies were located in the proximal inner nuclear layer (INL) and ganglion cell layer (GCL), and processes were distributed to all laminae of the interplexiform layer (IPL). Varicose processes were in the optic fiber layer (OFL) and the outer plexiform layer (OPL). Weak GAT-1 immunostaining surrounded cells in the INL and GCL, and it was found in the OFL and OPL and in numerous processes in the outer nuclear layer (ONL) that ended at the outer limiting membrane. GAT-1 is therefore strongly expressed by amacrine, displaced amacrine, and interplexiform cells and weakly expressed by Müller cells. GAT-2 immunostaining was observed in the retina pigment epithelium and the nonpigmented ciliary epithelium. GAT-3 immunoreactivity was distributed to the OFL, to all laminae of the IPL, GCL and INL, and to processes in the ONL that ended at the outer limiting membrane. Small GAT-3-immunoreactive cell bodies were in the proximal INL and GCL. GAT-3 is therefore strongly expressed by Müller cells, and by some amacrine and displaced amacrine cells. Together, these observations demonstrate a heterologous distribution of GATs in the retina. These transporters are likely to take up GABA from, and perhaps release GABA into, the synaptic cleft and extracellular space. This suggests that GATs regulate GABA levels in these areas and thus influence synaptic neurotransmission.

Amino Acid Sequence↗
PubMed1982

Identification of gamma-aminobutyric acid and its binding sites in the rat ovary.

Gamma-aminobutyric acid (GABA), GABA synthesizing enzyme and GABA binding sites were measured in rat ovaries. The concentration of GABA in the ovary (0.56 microgram/mg protein) was less than that in the brain (1.2-3.4 microgram/mg protein), but was six-fold higher than any other non-neuronal tissue examined. Glutamate decarboxylase, the GABA synthesizing enzyme was also found in high concentrations in whole ovarian homogenate but not in enriched ovarian granulosa cells, testis, anterior pituitary or muscles. Furthermore, high affinity (Kd = 15-21 nM), specific GABA binding sites were identified in the ovaries by specific [3H]muscimol binding and the majority of GABA binding sites were associated with the granulosa cells. These data suggest a possible role of GABA in the regulation of ovarian functions.

Animals↗
PubMed1981

The effects of 4-aminopyridine on the isolated vas deferens and its effects on the inhibitory properties of adenosine, morphine, noradrenaline and gamma-aminobutyric acid.

1 Adenosine, adenosine 5'-triphosphate (ATP), morphine, noradrenaline, gamma-aminobutyric acid (GABA) phentolamine and amyl nitrite were used to inhibit electrically-evoked contractions of the isolated superfused vas deferens of the mouse. 2 The inhibitory effects of adenosine ATP, morphine, noradrenaline and GABA, which are thought to be due to presynaptic action, were reduced by perfusion with media containing 4-aminopyridine (4AP) or tetraethylammonium (TEA) ions. The inhibitory effects of phentolamine and amyl nitrite were unaffected by 4AP or TEA. 3 Quinidine, which like 4AP and TEA produced some increase to twitch height, did not reduce responses to the various agonists, indicating that an increased muscle contraction was not itself responsible for the reduced responses. 4 It is concluded that antagonism between 4AP and adenosine is not a specific interaction, as had been suggested, but probably reflects an interaction with Ca2+ requiring processes in the presynaptic terminal.

4-Aminopyridine↗
PubMedDate not supplied

Relationship between levels of cyclic nucleotides and gamma-aminobutyric acid during ethanol withdrawal in rats.

Cyclic nucleotide and gamma-aminobutyric acid (GABA) levels were measured in four brain areas of control rats and rats undergoing ethanol withdrawal. Cyclic adenosine 3',5' monophosphate (cyclic AMP) was increased in the cerebral cortex and pons-medulla oblongata; cyclic guanosine 3',5'-monophosphate (cyclic GMP) was increased in the cerebellum and cerebral cortex; and GABA was decreased in the cerebellum, subcortex and pons-medulla oblongata. Individual values in withdrawn animals were correlated and subjected to a factor analysis. One of the common factors identified by this analysis was important for all but one of the levels which changed during ethanol withdrawal. Significant correlations of levels correlated with this factor included a negative correlation between cyclic GMP and GABA levels in the cerebellum, a positive correlation between cyclic GMP levels in the cerebellum and cyclic AMP levels in the pons-medulla oblongata and a positive correlation between cyclic AMP levels in the pons-medulla oblongata and cerebral cortex. These results indicate that multiple brain areas and neurotransmitters are involved in ethanol withdrawal.

Alcoholism↗
PubMed1990

Activation of subconductance states by gamma-aminobutyric acid and its analogs in chick cerebral neurons.

The action of gamma-aminobutyric acid (GABA) and the GABAA-receptor agonists muscimol, isoguvacine and 4,5,6,7-tetrahydroisoxazolo [5,4-c]pyridin-3-ol (THIP) were studied at the single-channel level in outside-out membrane patches from cultured chick cerebral neurons. All agonists activated channels with multiple-conductance states. The main-state conductance activated by all agonists had a value around 26 pS in symmetrical TRIS/Cl solutions. Subconductance states of around 13 pS and 18 pS were seen with application of each agonist. Muscimol and isoguvacine tended preferentially to activate subconductance states. Gating by all agonists was complex. Open-time distributions for main-state activity gated by GABA, isoguvacine and THIP were best described by the sum of two exponential curves with similar time constants. Muscimol-gated activity was best described by the sum of three exponentials indicating the presence of an additional longer open state. These results indicate that certain GABAA-receptor agonists are capable of preferentially activating subconductance states.

Analgesics↗
PubMed2006

Protective role of gamma-aminobutyric acid against chronic renal failure in rats.

The protective effect of gamma-aminobutyric acid (GABA) against chronic renal failure (CRF) was investigated using a remnant kidney model with 5/6 nephrectomized rats. Nephrectomy led to renal dysfunction, which was evaluated via several parameters including serum urea nitrogen, creatinine (Cr) and Cr clearance. However, the administration of GABA ameliorated renal dysfunction, and a longer administration period of GABA increased its protective effect. In addition, nephrectomized control rats showed an elevation in the fractional excretion of sodium (FE(Na)) with an increase in urinary sodium, while GABA led to a significant decline in FE(Na). Moreover, nephrectomy resulted in a decrease of serum albumin and an increase of urinary protein with a change in the urinary protein pattern, whereas the rats administered GABA showed improvement in these changes associated with CRF caused by nephrectomy. This suggests that GABA would inhibit the disease progression and have a protective role against CRF. As one of the risk factors for CRF progression, hypertension was also regulated by GABA. The results also indicate that GABA may play a protective role against CRF through improvement of the serum lipid profile, with reductions in triglyceride and total cholesterol. Furthermore, nephrectomy led to renal oxidative stress with a decrease in the activity of antioxidative enzymes and elevation of lipid peroxidation. The administration of GABA attenuated oxidative stress induced by nephrectomy through an increase in superoxide dismutase and catalase, and decrease in lipid peroxidation. The histopathological lesions, including glomerular, tubular and interstitial lesions, under nephrectomy were also improved by GABA with the inhibition of fibronectin expression. This study demonstrated that GABA attenuated renal dysfunction via regulation of blood pressure and lipid profile, and it also ameliorated the oxidative stress induced by nephrectomy, suggesting the promising potential of GABA in protecting against renal failure progression.

Administration, Oral↗
PubMed1984

Central gamma-aminobutyric acid involvement in blood pressure control.

The role of gamma-aminobutyric acid (GABA) in central nervous system (CNS) control of arterial blood pressure has been studied by testing the effects of drugs that either counteract or enhance CNS GABAergic mechanisms while monitoring the arterial pressure of normotensive and hypertensive animals. Drugs that antagonize the effects of GABA (either directly by blocking GABA-mediated responses or indirectly by inhibiting GABA synthesis) cause an increase in arterial pressure. This effect occurs in the forebrain and leads to an increase in sympathetic outflow to the vasculature, including the coronary vessels. GABA and drugs that stimulate GABA receptors (either directly or indirectly by inhibiting GABA metabolism, competing with an endogenous inhibitor of GABA, or activating a GABA chloride ionophore) cause a decrease in arterial pressure. This effect is, in some cases, associated with respiratory depression, and it occurs in the hindbrain, especially at the intermediate area on the ventral surface of the medulla. Hypertensive animals appear to be more sensitive to the hypotensive action of these agents. These results suggest that CNS GABA may have an important role in controlling blood pressure.

Animals↗
PubMed1983

Granule cells in the rat olfactory tubercle accumulate 3H-gamma-aminobutyric acid.

The rat olfactory tubercle contains high concentrations of gamma-aminobutyric acid (GABA) and its synthetic enzyme, glutamic acid decarboxylase (GAD). We previously demonstrated that GABA and GAD are most concentrated in the polymorphic layer of the tubercle and relatively absent from the plexiform and pyramidal layers. Here we report that the granule cells (the islands of Calleja) in the polymorphic layer accumulate 3H-GABA. 3H-GABA (34.5 Ci/mmole; 1.5 microliter) was injected into the tubercle and an hour later the rat was perfused with a mixture of paraformaldehyde and glutaraldehyde. The tissue was osmicated, dehydrated, and embedded in epon. Silver grains were sparse over the pyramidal and polymorphic cell bodies but numerous over the granule cell bodies in the islands of Calleja and dendrites in the surrounding neuropil. Grain densities for the granule cells were 41/100 micrometer3 compared to 4.2 for the pyramidal and polymorphic cells. Within the island, all the granule cells appeared to be labeled. These results, combined with previous demonstrations of the presence in this region of endogenous GABA and GAD, suggest that the granule neurons of the rat olfactory tubercle are GABA-ergic. These neurons also appear to receive dopamine input and therefore form part of a circuit that includes targets for both major and minor tranquilizers.

Animals↗
PubMed1992

Platelet gamma-aminobutyric acid levels in migraine and tension-type headache.

Gamma-aminobutyric acid (GABA) levels in platelets were measured in 19 patients with migraine (7 males and 12 females, average age: 36.5 years) and 27 patients with chronic tension-type headache (TH; 9 males and 18 females, average age: 48.9 years). Twenty-one normal healthy volunteers composed the control group (11 males and 10 females, average age 34.9 years). The GABA levels in platelets were determined using high performance liquid chromatography with fluorescent detection (HPLC-FC). The GABA levels in platelets were 30.8 +/- 11.7 pmol/10(9) platelets (mean +/- S.D.) in the patients with migraine, 43.1 +/- 11.8 pmol/10(9) platelets in the patients with TH and 34.7 +/- 8.1 pmol/10(9) platelets in the healthy controls. The platelet GABA levels in the patients with TH were significantly higher than in the migraine patients and the healthy controls (p less than 0.05). The possible role of GABA in headache is discussed. We consider that TH may be a state of neuronal hyperexcitability similar to migraine and that GABA in the platelets of patients during TH attacks may be elevated to counterbalance it. Alternatively, we suggest that the rise of GABA levels in platelets is related to emotional factors, such as depression, in the TH patients. Further studies must be undertaken concerning the relationship between platelet GABA levels and headache.

Adult↗
PubMed1993

Cholecystokinin-8 increases K(+)-evoked [3H] gamma-aminobutyric acid release in slices from various brain areas.

[3H] gamma-Aminobutyric acid (GABA) release was studied in rat brain slices in the absence or presence of cholecystokinin-8 (CCK-8). [3H]GABA release under the conditions used was Ca(2+)-dependent and insensitive to the presence of the glial uptake blocker beta-alanine. While the basal release of [3H]GABA was not affected by CCK-8, the K(+)-stimulated release of [3H]GABA was significantly enhanced by 300 nM of CCK-8 in the caudate putamen, the substantia nigra, the hippocampal formation and the parietofrontal cortex. In the cerebral cortex the CCK-8 enhancement of [3H]GABA release was concentration-dependent and abolished by the CCKB receptor antagonists PD135,158 (1.0 nM) and L-365,260 (100 nM). A significant counteraction of the CCK-8 action was also found with the CCKA receptor antagonist L-364,718 (100 nM) but only in concentrations at which both CCKA and CCKB receptors are blocked. No CCK-8 effects on [3H]GABA release were observed when tetrodotoxin was superfused 5 min before the K(+)-induced [3H]GABA release. It is suggested that the enhancing actions of CCK-8 on K(+)-stimulated [3H]GABA release is mainly related to an activation of CCKB receptors.

Animals↗
PubMed2002

Amiloride inhibition of gamma-aminobutyric acid(A) receptors depends upon the alpha subunit subtype.

gamma-Aminobutyric acid(A) (GABA(A)) receptors (GABARs) are responsible for most fast inhibitory neurotransmission in the mammalian brain. The GABARs contain several allosteric modulatory sites, many of which are useful clinically. The activity of most of these modulators depends upon the subunit composition of the receptor. The diuretic amiloride was previously reported to inhibit GABARs in frog sensory neurons. We measured its effects on recombinant GABARs to determine its mechanism of action at mammalian receptors and to examine the effect of subunit composition. Amiloride acted primarily as a competitive antagonist, reducing the sensitivity of the receptor to GABA without affecting the maximal current amplitude. Receptors containing an alpha6 subunit were about 10-fold more sensitive to amiloride than those containing other alpha subunits. In contrast, the identity of the beta or gamma subtype had little effect on amiloride sensitivity. Although several other modulators have specific effects at alpha6-containing receptors, amiloride is the first inhibitor to be reported with no additional dependence on the identity of the beta or gamma subunit. Therefore, it probably represents a unique modulatory site on the GABAR, which could be useful for developing drugs targeting these receptors. The selective activity of amiloride could also be helpful for isolating the contribution of receptors composed of alpha6 subtypes in heterogeneous native GABAR populations.

Amiloride↗