Cotransmission of acetylcholine and GABA

 has been reported in the retina and cortex, and anatomical studies suggest that GABA cotransmission is a common feature of nearly all forebrain ACh-producing neurons.

Nitric Oxide: A Universal Modulator of Brain Function.

, serotonin, histamine in distinct brain areas.

Role of neurotransmitters in palate development and teratologic implications.

Mechanisms of action of benzodiazepines.

 synapse may account for alterations in the effects of other neurotransmitters, such as norepinephrine, serotonin, and 

An unusual cardiovascular adverse effect of donepezil

 and glycinergic inhibitory receptors by triggering vagal activity.

Hypothalamic-pituitary-adrenal regulation, neurotransmitters and affective disorders

Although some contradictory evidence exists, norepinephrine, opioids, and

Corelease of acetylcholine and GABA from cholinergic forebrain neurons

 has been reported within the cholinergic system, the full extent is unknown.

Differential Control by 5‐HT and 5‐HT1A, 2A, 2C Receptors of Phasic and Tonic GABAA Inhibition in the Visual Thalamus

Previous work in the cat and rat dLGN has shown that several neurotransmitters, including

, serotonin (5‐HT), dopamine, and norepinephrine can modulate vesicular 

 release from inhibitory interneurons, resulting in changes in phasic inhibition (IPSC frequency), primarily through presynaptic modulation of GABA release from dendro‐dendritic synapses 5.

Reciprocal cholinergic and GABAergic modulation of the small ventrolateral pacemaker neurons of Drosophila's circadian clock neuron network.

Our s-LN(v) experiments revealed the predicted excitatory responses to bath-applied cholinergic agonists and the predicted inhibitory effects of GABA and established that the antagonism of

 extends to their effects on cAMP signaling.

[Effects and mechanism of low frequency stimulation of pedunculopontine nucleus on spontaneous discharges of ventrolateral thalamic nucleus in rats].

Importantly, the VL neurons responding to

Endogenous GABA Levels in the Pontine Reticular Formation Are Greater during Wakefulness than during Rapid Eye Movement Sleep

The inverse relationship between changes in PRF levels of

 during REM sleep indicates that low GABAergic tone combined with high cholinergic tone in the PRF contributes to the generation of REM sleep.

Benzodiazepine receptor agonists cause drug-specific and state-specific alterations in EEG power and acetylcholine release in rat pontine reticular formation.

In the pontine reticular formation (PRF),

 inhibits rapid eye movement (REM) sleep and 

Effects of Z-338, a novel gastroprokinetic agent, on the actions of excitatory and inhibitory neurotransmitters on neurons in area postrema.

Iontophoretic applications of acetylcholine 

 suppressed the firing rates of AP neurons recorded by extracellular electrodes.

Neuronal and network activity in networks of cultured spinal motor neurons

Both spiking and network bursts are stimulated by GABA antagonists and

Paradigms for pharmacological characterization of C. elegans synaptic transmission mutants.

 transmission, loss of GABA transmission, or a failure to negatively regulate ACh release, confers hypersensitivity to aldicarb.

[Influence of microwave radiation on synaptic structure and function of hippocampus in Wistar rats].

The concentration of Ca(2+) in synapse (P<0.01) and tc of membrane proteins (P<….01) of synaptosome increased contents of glutamic acid and glycine (P<0.01) and release of

 increased the increase of … and release of 

, and activity of acetyl … (P<0.01) increased.

Muscarinic M2 and M1 receptors reduce GABA release by Ca2+ channel modulation through activation of PI3K/Ca2+ -independent and PLC/Ca2+ -dependent PKC.

 enhances the excitability of the … decreasing the release of 

 by inhibiting axonal V-dependent Ca(2+) channels, mostly through activation of presynaptic M(2)Rs/PI(3)K/… PKC pathway and-to a smaller extent-by the activation of M(1)/PLC/Ca(2+)-dependent PKC.

An electrophysiological investigation of the characteristics and function of GABAA receptors on bovine adrenomedullary chromaffin cells

 reduced the amplitude of depolarization and action potential discharge occurring in response to locally applied 

 (100 μM), but had no effect upon the underlying ACh-induced current.

Antagonism by γ-aminobutyric acid of the stimulant effect of angiotensin II on cardiac sympathetic ganglia in spinal dogs

The positive chronotropism induced by bethanechol (25, 50μg) and a small dose of

 (25μg) were significantly inhibited by a high dose (500μg) but not by a low dose (50μg) of 

Effect of Activators and Blockers of Ligand-Regulated Ion Channels on the Activity of the Cl−-Stimulated Mg2+-ATPase of the Plasma Membrane Fraction from Bream (Abramis brama L.) Brain

 and glycine activated “… activation by 

 and glutamate activated “basal” Mg2+-ATPase to a lesser extent and did not suppress the activation of the enzyme by Cl−.… neuromediators was decreased by blockers of the corresponding receptors (picrotoxin, strychnine, benztropine mesylate, and D-2-amino-5-phosphonovaleric acid).

GABAergic modulation of catecholamine release from cultured bovine adrenal chromaffin cells. Evidence for the involvement of Cl−-dependent Ca2+ entry

 (ACh) were simultaneously applied, additive increase in 45Ca uptake was observed.

Modulation by GABA of neuroplasticity in the central and peripheral nervous system

 from preganglionic nerve terminals and changes, at least transiently, the neurochemical markers of cholinergic innervation (acetylcholinesterase and nicotinic receptors).

Synaptic interactions involving acetylcholine, glutamate, and GABA in rat auditory cortex

In support of this, preincubation of slices in NMDA (10–20 … permit three conclusions of relevance to cortical information processing: (1) spontaneous

; (2) ACh depresses responses to weak inputs to a greater degree than responses … that could place regulation of local ACh release under glutamatergic afferent control.

Multiple modes of GABAergic inhibition of rat cerebellar granule cells

 (ACh) evokes a large Ca2+‐dependent but action potential‐independent release of 

, which activates α6 subunit‐containing GABAA receptors.

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

These results provide evidence that serotonin exerts a complex modulation on the GABAergic system, via 5-HT4 receptors, and suggest that the amine releases

 which, in turn, bidirectionally modulates 

Acetylcholine attenuates synaptic GABA release to supraoptic neurons through presynaptic nicotinic receptors

These results suggest that the excitatory effect of

 on the SON neurons is mediated, at least in part, by inhibition of presynaptic 

Differences in time course of ACh and GABA modulation of excitatory synaptic potentials in slices of rat hippocampus.

In brain slice preparations of hippocampal region CA1, we have explored the time course of suppression of extracellularly recorded synaptic potentials after pressure pulse application of

Muscarinic modulation of GABAergic transmission to neurons in the rat subfornical organ.

 release through muscarinic receptors located on the presynaptic terminals.

Postsynaptic mechanism may contribute to inhibitory acetylcholine effect on GABAergic synaptic transmission in hippocampal cell cultures

 responses, indicating that postsynaptic mechanisms may also contribute to the inhibitory ACh effect on GABAergic transmission.

The relationship between GABA-containing cells and the cholinergic circuitry in the rabbit retina

Taken together, our results suggest that some GABAergic amacrine cells are cholinoceptive, raising the possibility that

, acting through nAChRs, can modulate the release of 

Local GABAergic modulation of acetylcholine release from the cortex of freely moving rats

 agonists and antagonists modulates the spontaneous release of 

Modulation of acetylcholine release via GABAA and GABAB receptors in rat striatum

 release through stimulation of GABAB receptors located on non-cholinergic neuronal elements in the striatum.

Muscarinic receptor modulation of GABA‐mediated giant depolarizing potentials in the neonatal rat hippocampus

, through the activation of M1 receptors, enhances the release of γ‐aminobutyric acid (

Contribution of nicotinic receptors to the function of synapses in the central nervous system: The action of choline as a selective agonist of α7 receptors

Experiments carried out in cultured hippocampal neurons not only confirmed that preterminal alpha 7 and … nAChRs modulate the TTX-sensitive release of GABA, but also demonstrated that evoked release of

 (ACh, 10 microM-1 mM) in … muscarinic receptor antagonist atropine (1 microM).

GABA(A) receptor modulates the activity of inner hair cell afferents in guinea pig cochlea.

Application of GABA had little effect on spontaneous activity whereas the glutamate or

 induced firing rate could be depressed by 


 N-Methyl-d-aspartate-evoked release of [3H]acetylcholine in striatal compartments of the rat: regulatory roles of dopamine and GABA

 in the control of …-aspartate-evoked release of 

, in the presence of bicuculline, (-)-sulpiride and SCH23390 alone or in combination enhanced, in both compartments, the responses … by 1 mM N-methyl-D-aspartate+D-serine, but also by 50 microM N-methyl-D-aspartate.

[Influences of acetylcholine, glutamic acid and GABA on the neuronal firings in ventromedial thalamic nucleus].

Contributions of GABAA receptors and GABAC receptors to acetylcholine release and directional selectivity in the rabbit retina.

 and strongly potentiated by GABA antagonists.

Roles of GABA, glutamate, acetylcholine and STN stimulation on thalamic VM in rats

, when applied iontophoretically, inhibited VM neuronal activity while bicuculline, L-glutamic acid and 

 enhanced the firing rates of the same VM neurons.

Selective cholinergic modulation of cortical GABAergic cell subtypes.

 (GABA) from intracortical inhibitory interneurons exert strong influence on the cortical activity and may interact with each other.

Role of External and Internal Calcium on Heterocarrier‐Mediated Transmitter Release

 and [3H]noradrenaline from rat hippocampal synaptosomes and of [3H]dopamine from striatal synaptosomes.

Effect of gamma-aminobutyric acid on the carnitine metabolism in neural cells.

A postulated involvement of this enzyme in delivering acetyl moieties for acetylcholine synthesis would suggest a negative feedback between

The effects of a purified toxic extract of Prymnesium patelliferum on transport of ions through the plasma membrane of synaptosomes.

It inhibits the sodium dependent uptake of L-glutamate and

 and enhances the calcium-dependent release of 

GABA‐activated Chloride Currents of Postnatal Mouse Retinal Ganglion Cells are Blocked by Acetylcholine and Acetylcarnitine: How Specific are Ion Channels in Immature Neurons?

 induced a rightward shift in the dose ‐ response curve for 

Taken together, these results indicate that

 and acetylcarnitine can act directly at the GABAA binding site and thereby reduce the action of 

GABAA and GABAB receptors differentially regulate striatal acetylcholine release in vivo

 release primarily through stimulation of inhibitory GABAA receptors.

In vivo modulation of acetylcholine in the nucleus accumbens of freely moving rats: II. Inhibition by γ-aminobutyric acid

 and its agonists dose-dependently decreased extracellular levels of 

The results demonstrate an inhibitory action of

 in the nucleus accumbens involving both GABAA and GABAB receptor subtypes.

[The postradiation effect of acetylcholine and GABA on the active potassium uptake by slices of rat cerebral cortex].

Radiation made the effects of neuromediators on active K+ transport be differently directed:

 enhanced the inhibitory effect of radiation and 

Activation of Protein Kinase C Suppresses the γ‐Aminobutyric AcidB Receptor‐Mediated Inhibition of the Vesicular Release of Noradrenaline and Acetylcholine

 inhibited the high K+‐evoked release of NA and 

, but not the ouabain‐evoked Ca2+‐independent release.

Distinct muscarinic receptors inhibit release of gamma-aminobutyric acid and excitatory amino acids in mammalian brain.

 and excitatory amino acids, but measurements of the dissociation equilibrium constants for the antagonists pirenzepine, 11-(2-[(diethylamino)methyl]-1-piperidinyl)acetyl-5,…-b][1,4]benzodiazepine-6-one, methoctramine, and hexahydrosiladifenidol indicated clearly that different muscarinic receptors were involved (M1 and probably M3, respectively).

Very low concentrations of acetylcholine and GABA modulate transmitter responses.

 cause a reduction of the response to both acetylcholine and 

, while low concentrations of GABA cause a facilitation of responses to both acetylcholine and GABA.

[The cross desensitization and modulation of Cl currents activated by gamma-aminobutyric acid and L-glutamate in the isolated neurons of Aplysia].

It has been found that very low concentrations of

 (10(-8) to 10(-14) M) which have no electrophysiologic responses of their own, modulate the response to a constant application of 

Bis-oxonol experiment on plasma membrane potentials of bovine adrenal chromaffin cells: Depolarizing stimuli and their possible interaction

 or veratridine not only simultaneously but also pretreatedly caused an additive increment of bis-oxonol fluorescence.

Cholinergic and GABAergic modulation of medial septal area: effect on working memory.

The data support a role for the septohippocampal projection in working memory and suggest that

 may have opposing influences on neurons in the MSA.

Muscarinic receptors mediating inhibition of gamma-aminobutyric acid release in rat corpus striatum and their pharmacological characterization.

 also inhibited the K(+)-evoked release of endogenous 

Acetylcholine and GABA mediate opposing actions on neuronal chloride channels in crayfish.

In tangential cells of crayfish optic lobes, a hyperpolarizing, biphasic synaptic potential is produced by the concurrent action of

Presynaptic regulation of acetylcholine release in the CNS.

In particular it will be shown: 1) that the release of the cholinergic transmitter can be inhibited through muscarinic receptors of … ACh by depressing ACh release through the activation of receptors of the 5-HT1B subtype; 3) that the release of

 by a novel … the cholinergic terminals.

Disinhibition in the rat septum mediated by M1 muscarinic receptors

, acting on M1 muscarinic receptors leads to disinhibition by decreasing 

 within the dorsolateral septal nucleus of the rat to examine its actions within this nucleus, specifically how it may interact to modulate the inhibitory action of 

 (GABA), the known inhibitory transmitter in this area.

Inversion of the alpha-2 and alpha-1 noradrenergic control of the cortical release of acetylcholine and gamma-aminobutyric acid in morphine-tolerant guinea pigs.

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

 (ACh) inhibited the high K+-evoked release of 

Effect of gamma-aminobutyric acid on neurally mediated contraction of guinea pig trachealis smooth muscle.

 decreases the contractile response of airway smooth muscle to cholinergic nerve stimulation by inhibiting the evoked release of 

 and that this effect is exerted by activating Cl-dependent, bicuculline-sensitive GABA receptors.

Presynaptic muscarinic and α‐adrenoceptor‐mediated regulation of GABA release from my enteric neurones of the guinea‐pig small intestine

 and oxotremorine, at concentrations ranging from 10−9 to 10−6 M inhibited the evoked release of 

 in a concentration‐dependent manner, while nicotine was without effect.

Comparative actions of GABA and acetylcholine on the Xenopus laevis lateral line.

 (1.25-80 microM) and carbachol (1.25-40 microM) increased spontaneous activity.

Dual effect of GABA on the contractile activity of the guinea-pig isolated urinary bladder.

 the contractile effect of both DMPP (TTX-sensitive) and 

 (ACh, TTX-insensitive) were significantly reduced.

Pantoyl-gamma-aminobutyric acid facilitates cholinergic function in the central nervous system.

 and P-GABA enhanced K+ (25 mM)-induced release of 

 from slices of the cerebral cortex and hippocampus dose-dependently, and their effects were antagonized by bicuculline but not by tetrodotoxin.

The modulation of cortical acetylcholine release by GABA, GABA-like drugs and benzodiazepines in freely moving guinea-pigs

prevented the behavioural activation and the increased release of

, unmasked the depression due to subthreshold doses of diazepam (i.c.v.,

GABA modulation of cholinergic transmission in rat oviduct.

ACh produced contractions related to its concentration which were maximal at the diestrous-1 phase when

Inhibition of calcium spikes and transmitter release by γ‐aminobutyric acid in the guinea‐pig myenteric plexus

 and the transmitter mediating the slow e.p.s.p.

Pyroglutamic acid administration modifies the electrocorticogram and increases the release of acetylcholine and GABA from the guinea-pig cerebral cortex.

 increases, as previously demonstrated, the cortical 

 release and causes mild sedation and E.Co.

gamma-Aminobutyric acid and cholinergic transmission in the guinea-pig ileum.

 (1 - 300 microM) inhibited both release of 

 and contractions evoked by electrical stimulation.

, and in turn intestinal motility via two receptors with different pharmacological properties.

Modulation of cortical acetylcholine and gamma-aminobutyric acid release in freely moving guinea pigs: effects of clonidine and other adrenergic drugs.

On the role of neurotransmitters in palate development

It has been shown that they a f f ec t the reor ien ta t ion process in embryo culture: serotonin (SHT) s t imulates the anter ior end,

Physiology of neuroactive peptides in vertebrate retina.

 analogues muscimol and 3-APS also reduced the light-evoked release of 

 but were several thousand times more potent than GABA itself.

A tonic gamma-aminobutyric acid-mediated inhibition of cholinergic amacrine cells in rabbit retina

 (GABA) inhibited the light-evoked release of 

 (IC50 congruent to 1 mM), but the GABA antagonists bicuculline (5 micro M) and picrotoxin (20 micro M) potentiated the light-evoked release and markedly increased the resting release of ACh.

Electrophysiologic Evidence for Involvement of Acetylcholine as a Neurotransmitter in the Lateral Vestibular Nucleus

Atropine inhibited acetylcholine-induced firing without affecting glutamate-induced firing, while

Intracellular observations on the disinhibitory action of acetylcholine in the hippocampus

Since acetylcholine did not depress the inhibitory potency of iontophoretic applications of γ-aminobutyrate, it was concluded that

 either by a direct action on inhibitory terminals or by inhibition of inhibitory interneurons.

Gamma aminobutyric acid effect on acetylcholine level and metabolism in rat cerebral cortex.

 injected into the lateral brain ventricle of white rats in doses of 0.6, 0.8 and 1.6 mg raised the level of 

 and in doses of 0.2, 0.4, 0.6, 0.8 and 1.6 mg increased acetylcholine synthesis.

Gamma-aminobutyric acid and bicuculline effects on acetylcholine metabolism in the striatum in rats.

) injected into the lateral ventricles of rat bran in a dose of 600 microgram raised the level and increased the synthesis of 

 (ACh) raising also the activity of choline acetyltransferase (ChAc) but had no effect on the activity of cholinesterase (AChE) in rat striatum.

Stimulation of acetilcholine (ACh) output from isolated brain slices by anticholinergic drugs: influence of septal lesion, changes in ionic environment and GABA.

 (1×10 −3 M) facilitated the K + 17mM evoked release of 

 and potently enhanced the stimulating action of hyoscine.

supp.ai

Discover Supplement-Drug Interactions

Possible Interaction: Acetylcholine and Gamma-Aminobutyric Acid

Share:

Acetylcholine

Gamma-Aminobutyric Acid

Research Papers that Mention the Interaction