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PubMed2002

Circadian rhythm in intracellular Cl(-) activity of acutely dissociated neurons of suprachiasmatic nucleus.

A link between the circadian rhythm and the function of Cl(-)-permeable gamma-aminobutyric acid (GABA) type A (GABA(A)) receptors on suprachiasmatic nucleus (SCN) neurons was studied by measuring intracellular activity of Cl(-) (aCl) at different times during a circadian cycle in SCN neurons acutely dissociated from rat brains. To measure aCl, the voltage-clamp mode of the gramicidin-perforated patch-clamp technique was used, and reversal potential of GABA-induced currents (E(GABA)) was converted to aCl. Measured aCl was significantly higher at around noon (20.1 +/- 1.4 mM) than at three other time zones of a circadian cycle (means ranging from 11.6 to 14.3 mM). Chord conductance of GABA-induced currents showed no circadian changes, indicating a lack of circadian changes in the number or single-channel conductance of GABA(A) receptors. These results suggest that aCl participates in modulating GABA(A) receptor functions on SCN neurons during the circadian rhythm.

Animals↗
PubMed1987

Immunoreactive GABA transaminase within the pancreatic islet is localized in mitochondria of the B-cell.

Subcellular localization of gamma aminobutyrate-alpha-ketoglutarate transaminase (GABA-T) in the pancreatic islets of Langerhans was determined by use of an electron microscopic, immunogold post-embedding protocol. The objective of this study was to define the islet cell distribution and subcellular localization of GABA-T. Within the islet, GABA-T was found only in the B-cells and was localized in mitochondria; 78 mitochondria contained 336 gold particles, whereas 245 secretory granules contained only 18 gold particles. Although studies utilizing either the isolated perfused pancreas or cultured islets have shown that exogenous GABA modulates D-cell secretion, in this study immunoreactive GABA-T, the catabolic enzyme for GABA, was not detectable in A- and D-cells of the islet. Control studies substituting normal rabbit serum for the GABA-T antiserum resulted in absence of labeling. These results indicate that the high concentration of GABA present in islet B-cells is catabolized by GABA-T in the mitochondrial compartment, consistent with the possibility that GABA functions as a mediator of B-cell activity.

4-Aminobutyrate Transaminase↗
PubMed2003

Gamma-aminobutyric acid as a promoting factor of cancer metastasis; induction of matrix metalloproteinase production is potentially its underlying mechanism.

We investigated expression of gamma-aminobutyric acid (GABA), glutamate decarboxylase, and matrix metalloproteinase (MMP) in the prostates of patients with cancer or benign prostatic hypertrophy by immunohistochemical study. Marked expression of GABA, glutamate decarboxylase 67, and MMPs was observed in the prostates of cancer patients with metastasis (n = 72) and lymph node metastasis, although only sparse expression was noted in those of cancer patients without metastasis (n = 76) or patients with benign prostatic hypertrophy (n = 152). We then investigated the influence of GABA stimulation on in vitro MMP production and the invasive ability of cancer cells using human prostate cancer cell line C4-2. The production of MMPs increased significantly in cancer cells after a 24-h incubation with GABA. Cell invasion assay using a BioCoat Matrigel Invasion Chamber kit revealed that GABA stimulation significantly promoted the invasive ability of cancer cells and that addition of MMP inhibitor GM6001 significantly decreased GABA-induced migration. This may indicate the involvement of MMP activity in GABA-induced cancer cell invasion. We further analyzed the transmission pathway by performing GABA receptor modulation. The GABA(B) receptor agonist baclofen significantly increased MMP production as well as invasive ability. Moreover, blockade of the GABA(B) receptor pathway using GABA(B) receptor antagonist CGP 35348 significantly inhibited GABA-induced MMP production and invasive ability in cancer cells, whereas GABA(A) receptor modulation did not influence MMP production or the invasive ability of cancer cells. Thus, increased expression of GABA may be implicated in cancer metastasis by promoting MMP production in cancer cells, and the GABA(B) receptor pathway may be involved in the process.

Aged↗
PubMedDate not supplied

[Role of GABA in the modulation of Na, K-pump activity in nerve cells after irradiation and experimental modification of membrane lipid component].

After irradiation acute (12 Gy, 600 mGy/min), single prolonged (0.25 Gy, 1.75 mG/min), chronic (0.01 Gy/day, 0.25 Gy, 0.50 Gy, 1.75 mGy/min), and experimental disturbances of cell membranes with phospholipases-A2, -D, and arachidonic acid administration the considerable changes in Na,K-pump function were found in rat brain cortex slices, with their reduction almost to the control level in presence of gamma-aminobutyric acid (0.1-10.0 mcM). It had been supposed existing of the GABA-ergic "homeostasis control" mechanism, which restores the intracellular potassium homeostasis via GABA-modulation of the Na,K-pump activity by principles of receptor-mediated structural-membrane regulation under extreme factor influence.

Animals↗
PubMed2000

Positive and negative modulation of the GABA(A) receptor and outcome after traumatic brain injury in rats.

Glutamate-mediated excitotoxicity has been shown to contribute to cellular dysfunction following traumatic brain injury (TBI). Increasing inhibitory function through stimulation of gamma-aminobutyric acid (GABA(A)) receptors may attenuate excitotoxic effects and improve outcome. The present experiment examined the effects of diazepam, a positive modulator at the GABA(A) receptor, on survival and cognitive performance in traumatically brain-injured animals. In experiment 1, 15 min prior to central fluid percussion brain injury, rats (n=8 per group) were injected (i.p.) with saline or diazepam (5 mg/kg or 10 mg/kg). Additional rats (n=8) were surgically prepared but not injured (sham-injury). Rats pre-treated with the 5 mg/kg dose of diazepam had significantly lower mortality (0%) than injured, saline-treated rats (53%). Also, diazepam-treated (5 mg/kg) rats had significantly shorter latencies to reach the goal platform in the Morris water maze test performed 11-15 days post-injury. In experiment 2, at 15 min post-injury, rats were given either saline (n=5) or 5 mg/kg diazepam (n=6). Rats treated with diazepam did not differ in mortality from injured rats treated with vehicle. However, rats treated with diazepam at 15 min post-injury had significantly shorter latencies to reach the goal platform in the Morris water maze than injured, vehicle-treated rats. In experiment 3, the post-injury administration of bicuculline (1.5 mg/kg, n=8), a GABA(A) antagonist, increased Morris water maze goal latencies compared to injured animals treated with saline (n=8). These results suggest that enhancing inhibitory function during the acute post-injury period produces beneficial effects on both survival and outcome following experimental TBI.

Animals↗
PubMed2006

The pheromone androstenol (5 alpha-androst-16-en-3 alpha-ol) is a neurosteroid positive modulator of GABAA receptors.

Androstenol is a steroidal compound belonging to the group of odorous 16-androstenes, first isolated from boar testes and also found in humans. Androstenol has pheromone-like properties in both animals and humans, but the molecular targets of its pheromonal activity are unknown. Androstenol is structurally similar to endogenous A-ring reduced neurosteroids that act as positive modulators of GABA(A) receptors. Here we show that androstenol has neurosteroid-like activity as a GABA(A) receptor modulator. In whole-cell recordings from cerebellar granule cells, androstenol (but not its 3beta-epimer) caused a concentration-dependent enhancement of GABA-activated currents (EC(50), 0.4 microM in cultures; 1.4 microM in slices) and prolonged the duration of spontaneous and miniature inhibitory postsynaptic currents. Androstenol (0.1-1 microM) also potentiated the amplitude of GABA-activated currents in human embryonic kidney 293 cells transfected with recombinant alpha1beta2gamma2 and alpha2beta2gamma2 GABA(A) receptors and, at high concentrations (10-300 microM), directly activated currents in these cells. Systemic administration of androstenol (30-50 mg/kg) caused anxiolytic-like effects in mice in the open-field test and elevated zero-maze and antidepressant-like effects in the forced swim test (5-10 mg/kg). Androstenol, but not its 3beta-epimer, conferred seizure protection in the 6-Hz electroshock and pentylenetetrazol models (ED(50) values, 21.9 and 48.9 mg/kg, respectively). The various actions of androstenol in the whole-animal models are consistent with its activity as a GABA(A) receptor modulator. GABA(A) receptors could represent a target for androstenol as a pheromone, for which it is well suited because of high volatility and lipophilicity, or as a conventional hormonal neurosteroid.

Androstenols↗
PubMed2000

Effects of GABA agonists and GABA-A receptor modulators on cocaine discrimination in rhesus monkeys.

RATIONALE: Dopaminergic systems thought to mediate the abuse-related effects of cocaine are under inhibitory control by GABAergic systems. These findings suggest that GABA agonists may attenuate some abuse-related effects of cocaine. OBJECTIVE: To assess the effects of GABA receptor agonists and GABA-A receptor modulators on cocaine discrimination in rhesus monkeys. METHODS: Rhesus monkeys were trained to discriminate 0.4 mg/kg cocaine from saline in a two-key, food-reinforced drug discrimination task. The effects of the GABA-A agonist muscimol, the GABA-B agonist baclofen, the barbiturate GABA-A receptor modulator pentobarbital, and the benzodiazepine GABA-A modulators triazolam and imidazenil were examined alone and as pretreatments to cocaine. For comparison, the effects of pentobarbital pretreatment on the cocaine-like discriminative stimulus effects of amphetamine were also examined. RESULTS: When administered alone, the GABA agonists and GABA-A receptor modulators produced primarily saline-appropriate responding. When administered as pretreatments to cocaine, pentobarbital attenuated the discriminative stimulus effects of cocaine in all monkeys tested, and the high efficacy benzodiazepine agonist triazolam attenuated cocaine's effects in three of five monkeys. Muscimol, baclofen and the low efficacy benzodiazepine agonist imidazenil did not alter cocaine's discriminative stimulus effects. Although pentobarbital blocked the effects of the monoamine reuptake blocker cocaine, it did not alter the cocaine-like effects of the monoamine releaser amphetamine. CONCLUSIONS: These results are consistent with the hypothesis that GABA-A receptor modulators attenuate the discriminative stimulus effects of cocaine in rhesus monkeys by decreasing the activity of dopaminergic systems. Direct GABA receptor agonists may be less effective in blocking the abuse-related effects of cocaine in rhesus monkeys.

Amphetamine↗
PubMed2000

Chronic modulation of the GABA(A) receptor complex regulates Y1 receptor gene expression in the medial amygdala of transgenic mice.

NPY exerts anxiolytic effects, which are mediated by activation of Y1 receptors in the amygdala. It has been shown that diazepam counteracts the anxiogenic effect of Y1 receptor antagonists, suggesting that NPYergic and GABAergic systems are coupled in the regulation of anxiety. We used a transgenic mouse model, expressing a mouse Y1 receptor-beta-galactosidase fusion gene (Y1R/LacZ), to study the effect of positive or negative modulators of GABA(A) receptors on Y1 receptor gene expression. Mice were treated for 14 days with diazepam (4 or 20 mg/kg), the anxiolytic beta-carboline-derivative abecarnil (0.3 or 6 mg/kg) and the anxiogenic beta-carboline FG7142 (20 mg/kg). Transgene expression was determined by quantitative analysis of beta-galactosidase histochemical staining in the medial amygdala and in the medial habenula as a control region. Chronic treatment with 20 mg/kg diazepam or 6 mg/kg abecarnil significantly increased, whereas FG 7142 decreased, transgene expression in the medial amygdala. A transient decrease in transgene expression was observed in the medial amygdala six hours after the acute treatment with 20 mg/kg FG 7142 but not with diazepam or abecarnil. No significant changes were observed in the medial habenula. These data suggest that modulation of GABA(A) receptor function may regulate Y1 receptor gene expression in medial amygdala.

Allosteric Regulation↗
PubMed2002

Dual effects of 5-HT4 receptor activation on GABA release from guinea pig hippocampal slices.

The effects of BIMU-8, a 5-HT4 receptor agonist, were studied on GABA release in guinea pig hippocampal slices. BIMU-8 did not modify GABA outflow at rest but did display a complex action in electrically stimulated slices: at low concentrations it increased, and at higher concentrations inhibited, GABA release. These responses were competitively counteracted by GR 125487, a selective 5-HT4 receptor antagonist. The dual effects of BIMU-8 are consistent with its indirect cholinergic action since the M1 and M3 antagonist, 4-DAMP, prevented BIMU-8-elicited GABA facilitation, whereas the M2 antagonist AFDX-116 cancelled GABA inhibition. These results provide evidence that serotonin exerts a complex modulation on the GABAergic system, via 5-HT4 receptors, and suggest that the amine releases acetylcholine which, in turn, bidirectionally modulates GABA release.

Acetylcholine↗
PubMed1986

[Electrophysiological and biochemical studies of GABA receptors in a primary cell culture of the pars intermedia of the porcine pituitary].

Using a primary culture of intermediate lobe (IL) we are investigating how GABA modulates stimulus-secretion coupling in the hypophysis. Two classes of GABA receptors have been described: GABA-A and GABA-B. We have characterised the GABA-A receptor using the patch clamp technique (Whole Cell Recording). GABA (10-100 microM) and isoguvacine (50 microM) a specific GABA-A agonist elicit an inward current with an equilibrium potential that coincides with Ecl-, this could explain the depolarising action of GABA-A agonists. When applying baclofen, the specific GABA-B agonist, no modifications of membrane potential were seen. Perfusion studies on alpha MSH release showed GABA (50 microM) and isoguvacine (50 microM) to potentiate Ba++-evoked secretion. The effects were antagonised by bicuculline and SR 95103, confirming GABA-A receptor action. Baclofen stereospecifically inhibited both basal and Ba++-evoked release. Together the results suggest the co-existence of the two classes of GABA receptors on the endocrine cells of the IL.

Animals↗
PubMed1998

Changes in GABAB modulation during a theta cycle may be analogous to the fall of temperature during annealing.

Changes in GABA modulation may underlie experimentally observed changes in the strength of synaptic transmission at different phases of the theta rhythm (Wyble, Linster, & Hasselmo, 1997). Analysis demonstrates that these changes improve sequence disambiguation by a neural network model of CA3. We show that in the framework of Hopfield and Tank (1985), changes in GABA suppression correspond to changes in the effective temperature and the relative energy of data terms and constraints of an analog network. These results suggest that phasic changes in the activity of inhibitory interneurons during a theta cycle may produce dynamics that resemble annealing. These dynamics may underlie a role for the theta cycle in improving sequence retrieval for spatial navigation.

Animals↗
PubMed2001

Modulation of recombinant GABA receptor/channel subunits by domain-specific antibodies in Xenopus oocytes.

To study interaction of specific antibodies with the GABA receptor/channel, antisera were raised against the extracellular domains of the GABAA receptor/channel beta2 subunit, gamma2 subunit and the GABAC receptor/channel rho1 subunit. The specificity of the antibodies was characterized by immunocytochemistry and by Western blotting of transfected FDC-P1 cells expressing recombinant GABA receptor/channel subunits. The effects of the antibodies on whole-cell currents in Xenopus laevis oocytes expressing homomeric recombinant GABA receptor/channel beta2, gamma2, and rho1 were studied using two-microelectrode voltage clamp. In the absence of GABA, anti-alpha2, anti-gamma2, and anti-rho1 antisera elicited whole-cell currents in oocytes expressing beta2, gamma2, and rho1 subunits, respectively. The effect of antibody on channel activation was concentration-dependent. The whole-cell currents induced by anti-beta2 and anti-gamma2 were several-fold greater than those induced by application of 100 microm GABA. In Xenopus oocytes expressing recombinant rho1 subunits, GABA-induced whole-cell currents were inhibited by the anti-rho1 antibody. In contrast, the GABA-induced whole-cell currents were potentiated several-fold by anti-beta2 and anti-gamma2 antibodies in Xenopus oocytes expressing homomeric beta2 and gamma2 subunits. Our studies indicate that antibodies specific to the N-terminal domain of GABA receptor/channel subunits can modulate the neurotransmitter receptor function.

Animals↗
PubMed2006

Pharmacological and computational analysis of alpha-subunit preferential GABA(A) positive allosteric modulators on the rat septo-hippocampal activity.

Clinically most active anxiolytic drugs are positive allosteric modulators (PAMs) of GABA(A) receptors, represented by benzodiazepine compounds. Due to their non-selective profile, however, they potently modulate several sup-type specific GABA(A) receptors, contributing to their broad-range side effects. Based on observations in genetically altered mice, however, it has been proposed that anxiolytic action of benzodiazepines is predominantly mediated by GABA(A) alpha2/3 subunit-containing receptors. In the present study we analyzed the actions of the preferential GABA(A) alpha1 and alpha2/3 PAMs, zolpidem and L-838417, respectively on hippocampal EEG and medial septum neuronal activity in anesthetized rats. In parallel, a computational model was constructed to model pharmacological actions of these compounds on the septo-hippocampal circuitry. The present results demonstrated that zolpidem inhibited theta oscillation both in the hippocampus and septum, and profoundly inhibited firing activity of septal neurons. L-838417 also inhibited hippocampal and septal theta oscillation, however, it did not significantly alter firing rate activity of septal neurons. Our computational model showed that cessation of periodic firing of hippocampo-septal neurons, representing absence of hippocampal theta activity, disrupted oscillation of septal units, without altering their overall firing activity, similar to changes observed in our in vivo experiments following administration of L-838417. Understanding the correlation between changes in septo-hippocampal activity and actions of selective modulators of GABA(A) subtype receptor modulators would further advance design of anxiolytic drugs.

Action Potentials↗
PubMed1993

Insulin resistance syndrome: defective GABA neuromodulation as a possible hereditary pathogenetic factor (the 'GABA hypothesis').

The origin of the insulin resistance syndrome which, mostly through its cardiovascular implications, is characterized by a high incidence of death, is still practically unknown. Energy and glucose homeostasis are under the control of CNS centers and the neurotransmitter GABA modulates the activity of these centers. Alteration of the biochemical structure of GABA receptors is suggested as an interpretation of the origin of the syndrome.

Animals↗
PubMed1999

Waglerin-1 inhibits GABA(A) current of neurons in the nucleus accumbens of neonatal rats.

The effect of Waglerin-1, a 22-amino acid peptide purified from the venom of Wagler's pit viper on the whole cell current response (I(GABA)) to gamma-aminobutyric acid (GABA) was examined for neurons freshly isolated from the nucleus accumbens of 3- to 7-day-old rats. Waglerin-1 depressed I(GABA) induced by subsaturating concentrations of GABA; the IC(50) for I(GABA) induced by 10 microM GABA was 2.5 microM Waglerin-1. This concentration of Waglerin-1 shifted the GABA concentration-response curve to the right in a parallel manner, increasing the GABA EC(50) from 12+/-3 to 27+/-5 microM. The depressant effect of Waglerin-1 was greater at negative holding potentials. Zn(2+) also inhibited I(GABA) with an IC(50) of 0.3 microM. Phosphorylation state appeared to modulate GABA(A) receptor sensitivity to the inhibitory effect of Waglerin-1 since dialysis of neurons with N-[2-((p-bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide HCl (H-89), an inhibitor of protein kinase A, prevented inhibition. The data are discussed in terms of developmental influences on the subunit composition of GABA(A) receptors in neurons of the nucleus accumbens.

Amino Acid Sequence↗
PubMed2004

The heptahelical domain of GABA(B2) is activated directly by CGP7930, a positive allosteric modulator of the GABA(B) receptor.

The gamma-aminobutyric acid, type B (GABA(B)) receptor is well recognized as being composed of two subunits, GABA(B1) and GABA(B2). Both subunits share structural homology with other class-III G-protein-coupled receptors. They are composed of two main domains: a heptahelical domain (HD) typical of all G-protein-coupled receptors and a large extracellular domain (ECD). Although GABA(B1) binds GABA, GABA(B2) is required for GABA(B1) to reach the cell surface. However, it is still not demonstrated whether the association of these two subunits is always required for function in the brain. Indeed, GABA(B2) plays a major role in the coupling of the heteromer to G-proteins, such that it is possible that GABA(B2) can transmit a signal in the absence of GABA(B1). Today only ligands interacting with GABA(B1) ECD have been identified. Thus, the compounds acting exclusively on the GABA(B2) subunit will be helpful in analyzing the specific role of this subunit in the brain. Here, we explored the mechanism of action of CGP7930, a compound described as a positive allosteric regulator of the GABA(B) receptor. We showed that it activates the wild type GABA(B) receptor but with a low efficacy. The GABA(B2) HD is necessary for this effect, although one cannot exclude that CGP7930 could also bind to GABA(B1). Of interest, CGP7930 could activate GABA(B2) expressed alone and is the first described agonist of GABA(B2). Finally, we show that CGP7930 retains its agonist activity on a GABA(B2) subunit deleted of its ECD. This demonstrates that the HD of GABA(B2) behaves similar to a rhodopsin-like receptor, because it can reach the cell surface alone, can couple to G-protein, and be activated by agonists. These data open new strategies for studying the mechanism of activation of GABA(B) receptor and examine any possible role of homomeric GABA(B2) receptors.

Allosteric Regulation↗
PubMedDate not supplied

An open-label study of tiagabine as augmentation therapy for anxiety.

BACKGROUND: At least 50% of patients with anxiety disorders experience only partial response to pharmacotherapy and require augmentation therapy. Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the CNS, and agents that modulate GABA neurotransmission have shown promise in the treatment of anxiety disorders and are often used as augmentation agents. OBJECTIVE: This study evaluated tiagabine, a selective GABA reuptake inhibitor (SGRI), as augmentation therapy. METHODS: This 8-week, open-label study enrolled patients who remained symptomatic despite adequate drug trials for treatment of anxiety symptoms. Tiagabine augmentation therapy was initiated at 4 mg/d (taken in 2 doses; one in the morning with breakfast and one in the evening with a snack) for 2 days and increased to 8 mg/d for 10 days. Dose was then adjusted according to efficacy/tolerability in increments of 2 mg every 3 days up to a maximum of 20 mg/d. Effect was assessed using the Hamilton Rating Scale for Anxiety (HAM-A), Beck Anxiety Inventory (BAI), Clinical Global Impression (CGI) scale, Pittsburgh Sleep Quality Index (PSQI), and 36-item Short-Form Health Survey (SF-36). RESULTS: Of the 18 patients enrolled, 17 were included in the efficacy analysis; one withdrew due to an adverse event prior to post-baseline assessment. Mean final dose of tiagabine was 13 mg/d. Tiagabine as augmentation therapy further reduced anxiety symptoms, as shown by significant decreases in mean HAM-A total and BAI scores at Week 8 (P<0.001). Thirteen patients (76%) responded (> or =50% reduction in HAM-A total score), and 10 patients (59%) achieved remission (HAM-A total score < or =7) at Week 8. Tiagabine improved sleep quality, with a significant reduction seen in PSQI global score at Week 8 (P=.001). Augmentation therapy with tiagabine was generally well tolerated. CONCLUSION: These preliminary findings suggest that the SGRI tiagabine may be an effective and generally well tolerated augmentation therapy in patients with anxiety who remain symptomatic despite adequate drug trials for treatment of anxiety symptoms.

Adult↗
PubMed1989

Release of taurine and GABA from cerebellar slices from developing and adult mice.

The properties of the release of exogenous radioactive taurine and GABA from cerebellar slices from developing and adult mice were investigated using a superfusion system. Potassium stimulation (50 mM K+) caused, approximately, a 1.4-fold enhancement in the release of preloaded taurine from slices from adult mice, while the response to potassium in 7-day-old mice was about 6-fold. The potassium stimulation caused, approximately, a 3-fold increase in the release of preloaded GABA from cerebellar slices from 7-day-old mice, whereas the enhancement was about 10-fold in the adult. The actual molar amount of taurine released from the immature cerebellum was strikingly large, about 16 times larger than the amount of GABA released upon the same stimulus. Spontaneous taurine efflux was potentiated by taurine and GABA, the responses being more pronounced in the 7-day-old cerebellum, suggesting that the immature cerebellum is more prone to stimulation by homo- and heteroexchange than the mature cerebellum. Potassium-stimulated taurine release was inhibited by GABAergic substances in the adult but not in the developing cerebellum. Potassium-stimulated GABA release from the adult cerebellum was greatly increased by GABA and also moderately by muscimol and bicuculline, the effect of the latter being antagonized by taurine and hypotaurine. Taurine was thus able to modulate GABA release through bicuculline-sensitive receptors, but this modulation was not evident in cerebellar slices from 7-day-old mice. An exposure of the slices to sodium-free media greatly enhanced taurine and GABA release in both age groups. The stimulated release of GABA generally exhibited a similar calcium dependency in the adult and 7-day-old cerebella but in 7-day-old mice the stimulated release of taurine was not strictly calcium-dependent.

Aging↗