Release of endogenous and labeled GABA from isolated guinea pig ileum

1983 ◽  
Vol 245 (5) ◽  
pp. G717-G721 ◽  
Author(s):  
K. Taniyama ◽  
Y. Miki ◽  
M. Kusunoki ◽  
N. Saito ◽  
C. Tanaka
Keyword(s):  
Guinea Pig ◽  
Gaba Release ◽  
Ringer Solution ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Tetraacetic Acid ◽  
Spontaneous Release ◽  
Guinea Pig Ileum ◽  
Fractional Rate ◽  
Endogenous Gaba

The release of gamma-aminobutyric acid (GABA) was studied by comparing the properties of labeled GABA released from preloaded preparations to those of endogenous GABA released from the isolated guinea pig ileum. The spontaneous release of endogenous GABA was 4.46 +/- 0.10 pmol X min-1 X g wet wt-1, and the fractional rate of endogenous GABA release was much lower. The ratio of evoked to spontaneous release of endogenous GABA was high compared with that of labeled GABA. The electrical transmural stimulation-evoked release of labeled and endogenous GABA was inhibited by superfusion with tetrodotoxin and Ca2+-free Krebs-Ringer solution containing 1 mM ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid. Thus the nature of the stimulation-evoked release of labeled GABA was similar to that of endogenous GABA. These results indicate that the released GABA is neuronal in origin and provide additional evidence for the presence of GABA-ergic neurons in the guinea pig ileum.

scholarly journals Substance P induces endogenous GABA release from guinea pig ileum

1984 ◽  
Vol 36 ◽  
pp. 87
Author(s):  
Kohtaro Taniyama ◽  
Yukiko Miki ◽  
Masato Kusunoki ◽  
Naoaki Saito ◽  
Chikako Tanaka
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Gaba Release ◽  
Guinea Pig Ileum ◽  
Endogenous Gaba

Uptake and release of gamma-aminobutyric acid in guinea pig gallbladder

1985 ◽  
Vol 249 (2) ◽  
pp. G192-G196 ◽  
Author(s):  
N. Saito ◽  
K. Taniyama ◽  
C. Tanaka
Keyword(s):  
Guinea Pig ◽  
Ganglion Cells ◽  
Regional Distribution ◽  
Gaba Release ◽  
Aminobutyric Acid ◽  
Transport Systems ◽  
Gamma Aminobutyric Acid ◽  
Beta Alanine ◽  
High Affinity ◽  
Uptake And Release

The presence of gamma-aminobutyric acid (GABA)-ergic neuron in guinea pig gallbladder was investigated by measuring GABA contents and glutamate decarboxylase (GAD) activity and by demonstrating the uptake and release of [3H]GABA. GABA and GAD are both present in the gallbladder, and a positive correlation in regional distribution was observed among GABA, GAD, and the number of ganglion cells. The uptake of [3H]GABA by the gallbladder showed two saturable components; a high-affinity component (Km = 23.3 microM, Vmax = 7.63 nmol X g-1 X 10 min-1) and a low-affinity component (Km = 515 microM, Vmax = 57.1 nmol X g-1 X 10 min-1). These high-affinity and low-affinity transport systems corresponded to those obtained in the presence of beta-alanine and L-2,4-diaminobutyric acid, respectively, thereby suggesting the presence of neuronal and nonneuronal GABA transport systems in this tissue. Electrical transmural stimulation produced an increase in [3H]-GABA release from the isolated gallbladder preloaded with [3H]GABA, in the presence of beta-alanine. The stimulation-evoked release of [3H]GABA was prevented by calcium-free medium containing 1 mM EGTA and tetrodotoxin, thereby indicating that the released GABA originates from the nerve terminals. These results provide evidence for the presence of GABA-ergic neurons in the guinea pig gallbladder.

Regulation of [3H]GABA release from strips of guinea pig urinary bladder

1988 ◽  
Vol 255 (6) ◽  
pp. R888-R893
Author(s):  
J. Shirakawa ◽  
K. Taniyama ◽  
S. Iwai ◽  
C. Tanaka
Keyword(s):  
Urinary Bladder ◽  
Guinea Pig ◽  
Adrenergic Receptors ◽  
Gaba Release ◽  
Inhibitory Effect ◽  
Atropine Sulfate ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
High K ◽  
M1 Muscarinic

The presence of receptors that regulate the release of gamma-aminobutyric acid (GABA) was studied in strips of the guinea pig urinary bladder. GABA (10(-8)-10(-5) M) and muscimol (10(-8)-10(-5) M), but not baclofen (10(-5) M), reduced the Ca2+-dependent, tetrodotoxin-resistant release of [3H]GABA evoked by high K+ from the urinary bladder strips preloaded with [3H]GABA. The inhibitory effect of muscimol was antagonized by bicuculline and potentiated by diazepam, clonazepam, and pentobarbital sodium. The potentiating effect of clonazepam was antagonized by Ro 15-1788. Acetylcholine (ACh) inhibited the high K+-evoked release of [3H]GABA. The inhibitory effect of ACh was antagonized by atropine sulfate and pirenzepine but not by hexamethonium. Norepinephrine (NE) inhibited the evoked release of [3H]GABA. The inhibitory effect of NE was mimicked by clonidine, but not by phenylephrine, and was antagonized by yohimbine but not by prazosin. These results provide evidence that the release of GABA from strips of guinea pig urinary bladder is regulated via the bicuculline-sensitive GABAA receptor, M1-muscarinic, and alpha 2-adrenergic receptors.

Cholinergic modulation of synaptic inhibition in the guinea pig hippocampus in vitro: excitation of GABAergic interneurons and inhibition of GABA-release

1993 ◽  
Vol 69 (2) ◽  
pp. 626-629 ◽  
Author(s):  
J. C. Behrends ◽  
G. ten Bruggencate
Keyword(s):  
Guinea Pig ◽  
Synaptic Transmission ◽  
Pyramidal Neurons ◽  
Gaba Release ◽  
Cholinergic Receptor ◽  
Receptor Activation ◽  
Release Mechanism ◽  
Gabaergic Interneurons ◽  
Gamma Aminobutyric Acid

1. The effect of cholinergic receptor activation on gamma-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission was investigated in voltage-clamped CA1 pyramidal neurons (HPNs) in the guinea pig hippocampal slice preparation. 2. The cholinergic agonist carbachol (1-10 microM) induced a prominent and sustained increase in the frequency and amplitudes of spontaneous inhibitory postsynaptic currents (IPSCs) in Cl(-)-loaded HPNs. The potentiation of spontaneous IPSCs was not dependent on excitatory synaptic transmission but was blocked by atropine (1 microM). 3. Monosynaptically evoked IPSCs were reversibly depressed by carbachol (10 microM). 4. The frequency of miniature IPSCs recorded in the presence of tetrodotoxin (0.6 or 1.2 microM) was reduced by carbachol (10 or 20 microM) in an atropine-sensitive manner. 5. We conclude that, while cholinergic receptor activation directly excites hippocampal GABAergic interneurons, it has, in addition, a suppressant effect on the synaptic release mechanism at GABAergic terminals. This dual modulatory pattern could explain the suppression of evoked IPSCs despite enhanced spontaneous transmission.

GABA release in posterior hypothalamus across sleep-wake cycle

1996 ◽  
Vol 271 (6) ◽  
pp. R1707-R1712 ◽  
Author(s):  
D. Nitz ◽  
J. M. Siegel
Keyword(s):  
Receptor Agonist ◽  
High Performance ◽  
Slow Wave Sleep ◽  
Gaba Release ◽  
Posterior Hypothalamus ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Rapid Eye Movement Sleep ◽  
Unit Discharge ◽  
Selective Increase

The activity of neurons in the posterior hypothalamus (PH) is thought to contribute to the production of wakefulness and electroencephalograph desynchronization. Inactivation of neuronal activity in this area is known to induce sleep. Most PH neurons decrease unit discharge during slow-wave sleep (SWS) relative to wake and rapid eye movement sleep. In the present study, we sought to examine potential sources of inhibition or disfacilitation underlying the reduction of PH unit activity during SWS in the cat. We employed the microdialysis technique in conjunction with high-performance liquid chromatography methods for the quantification of glutamate, glycine, and gamma-aminobutyric acid (GABA) release. We found a selective increase in GABA release during SWS in the PH. Glutamate and glycine levels were unchanged across the sleep-wake cycle. microinjection of the GABAA-receptor agonist muscimol, into the same areas from which microdialysis samples were collected, increased SWS time. Our studies support the hypothesis that GABA release in the posterior hypothalamus mediates inhibition of posterior hypothalamic neurons, thereby facilitating SWS.

scholarly journals Evidence that γ-Aminobutyric Acid Is Part of the Neural Circuit Mediating Estradiol Negative Feedback in Anestrous Ewes

Endocrinology ◽  
2008 ◽  
Vol 149 (6) ◽  
pp. 2762-2772 ◽  
Author(s):  
Adrienne L. Bogusz ◽  
Steven L. Hardy ◽  
Michael N. Lehman ◽  
John M. Connors ◽  
Stanley M. Hileman ◽  
...  
Keyword(s):  
Negative Feedback ◽  
Gaba Receptor ◽  
Receptor Agonist ◽  
Neural Circuit ◽  
Gabab Receptor ◽  
Gaba Release ◽  
Aminobutyric Acid ◽  
Receptor Ligands ◽  
Endogenous Gaba ◽  
Lh Secretion

Seasonal anestrus in ewes is driven by an increase in response to estradiol (E2) negative feedback. Compelling evidence indicates that inhibitory A15 dopaminergic (DA) neurons mediate the increased inhibitory actions of E2 in anestrus, but these neurons do not contain estrogen receptors. Therefore, we have proposed that estrogen-responsive afferents to A15 neurons are part of the neural circuit mediating E2 negative feedback in anestrus. This study examined the possible role of afferents containing γ-aminobutyric acid (GABA) and nitric oxide (NO) in modulating the activity of A15 neurons. Local administration of NO synthase inhibitors to the A15 had no effect on LH, but GABA receptor ligands produced dramatic changes. Administration of either a GABAA or GABAB receptor agonist to the A15 increased LH secretion in ovary-intact ewes, suggesting that GABA inhibits A15 neural activity. In ovariectomized anestrous ewes, the same doses of GABA receptor agonist had no effect, but combined administration of a GABAA and GABAB receptor antagonist to the A15 inhibited LH secretion. These data are consistent with the hypothesis that endogenous GABA release within the A15 is low in ovary-intact anestrous ewes and elevated after ovariectomy. Using dual immunocytochemistry, we observed that GABAergic varicosities make close contacts on to A15 neurons and that A15 neurons contain both the GABAA-α1 and the GABAB-R1 receptor subunits. Based on these data, we propose that in anestrous ewes, E2 inhibits release of GABA from afferents to A15 DA neurons, increasing the activity of these DA neurons and thus suppressing episodic secretion of GnRH and LH.

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