Regulation of endogenous dopamine release in amphibian retina by gamma-aminobutyric acid and glycine

AbstractEndogenous dopamine release in the retina of the African clawed frog (Xenopus laevis) increases in light and decreases in darkness. The roles of the inhibitory amino acid transmitters gamma-aminobutyric acid (GABA) and glycine in regulating this light/dark difference in dopamine release were explored in the present study. Exogenous GABA, the GABA-A receptor agonist muscimol, the GABA-B receptor agonist baclofen, and the GABA-C receptor agonist cis-aminocrotonic acid (CACA) suppressed light-evoked dopamine overflow from eyecups. The effects of GABA-A and -B receptor agonists were selectively reversed by their respective receptor-specific antagonists, whereas the effect of CACA was reversed by the competitive GABA-A receptor antagonist bicuculline. The benzodiazepine diazepam enhanced the effect of muscimol on light-evoked dopamine release. Both GABA-A and -B receptor antagonists stimulated dopamine release in light or darkness. Bicuculline was more potent in light than in darkness. These data suggest that retinal dopaminergic neurons are inhibited by GABA-A and -B receptor activation in both light and darkness but that GABA-mediated inhibitory tone may be greater in darkness than in light.Exogenous glycine inhibited light-stimulated dopamine release in a concentration-dependent and strychnine-sensitive manner. However, strychnine alone did not increase dopamine release in light or darkness, nor did it augment bicuculline-stimulated release in darkness. Additionally, both strychnine and 7-chlorokynurenate, an antagonist of the strychnine-insensitive glycine-binding site of the N-methyl-D-aspartate subtype of glutamate receptor, suppressed light-evoked dopamine release. Thus, the role of endogenous glycine in the regulation of dopamine release remains unclear.

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Regulation of endogenous dopamine release in amphibian retina by melatonin: The role of GABA

Visual Neuroscience ◽

10.1017/s0952523800003941 ◽

1994 ◽

Vol 11 (5) ◽

pp. 1013-1018 ◽

Cited By ~ 62

Author(s):

Jeffrey H. Boatright ◽

Nara M. Rubim ◽

P. Michael Iuvone

Keyword(s):

Dopamine Release ◽

Rank Order ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Gaba A ◽

Endogenous Dopamine ◽

Frog Retina ◽

Endogenous Dopamine Release ◽

Clawed Frog

AbstractIn the retina of the African clawed frog (Xenopus laevis), endogenous dopamine release increases in light and decreases in darkness. Exogenous melatonin and several chemical analogs of melatonin suppressed light-evoked dopamine release from frog retina in a concentration-dependent manner. The rank order of potency for inhibition of light-evoked dopamine release was melatonin » 5-methoxytryptamine ≥ N-acetylserotonin > 5-methoxytryptophol ⋙ serotonin. Melatonin did not suppress dopamine release below levels seen in darkness. The putative melatonin receptor antagonist luzindole inhibited the effect of melatonin. Luzindole enhanced dopamine release in darkness but had little effect in light. These data suggest a role for endogenous melatonin in dark-induced suppression of retinal dopamine.Picrotoxin and bicuculline, GABA-A receptor antagonists, blocked melatonin-induced suppression of dopamine release. In the presence of melatonin, bicuculline was significantly less potent in stimulating dopamine release. These results suggest that melatonin enhances GABAergic inhibition of light-evoked dopamine release. This mechanism may underlie the light/dark difference in dopamine release in vertebrate retina.

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?Real time? measurement of endogenous dopamine release during short trains of pulses in slices of rat neostriatum and nucleus accumbens : role of autoinhibition

Naunyn-Schmiedeberg s Archives of Pharmacology ◽

10.1007/bf00174745 ◽

1991 ◽

Vol 344 (6) ◽

Cited By ~ 50

Author(s):

Norbert Limberger ◽

StephenJ. Trout ◽

ZygmuntL. Kruk ◽

Klaus Starke

Keyword(s):

Nucleus Accumbens ◽

Real Time ◽

Dopamine Release ◽

Time Measurement ◽

Endogenous Dopamine ◽

Real Time Measurement ◽

Endogenous Dopamine Release

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MK212, a 5-hydroxytryptamine 2C receptor agonist, inhibits conditioned avoidance responses independent of blocking endogenous dopamine release in rats

Progress in Neuro-Psychopharmacology and Biological Psychiatry ◽

10.1016/j.pnpbp.2018.08.022 ◽

2019 ◽

Vol 89 ◽

pp. 16-22

Author(s):

Xiaqing Wang ◽

Meng Sun ◽

Lu Gan ◽

Weihai Chen

Keyword(s):

Receptor Agonist ◽

Dopamine Release ◽

Conditioned Avoidance ◽

Endogenous Dopamine ◽

Endogenous Dopamine Release ◽

Avoidance Responses

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Modulation of Recombination Human γ-Aminobutyric Acid-A Receptors by Isoflurane

Anesthesiology ◽

10.1097/00000542-199801000-00029 ◽

1998 ◽

Vol 88 (1) ◽

pp. 206-217 ◽

Cited By ~ 24

Author(s):

George Lees ◽

Michelle D. Edwards

Keyword(s):

Physiological Role ◽

Aminobutyric Acid ◽

Maximal Response ◽

Xenopus Laevis Oocytes ◽

Gamma Aminobutyric Acid ◽

Gaba A ◽

Anesthetic Agents ◽

Subunit Expression ◽

Delta Subunit

Background The gamma-aminobutyric acid (GABA)A receptor/chloride channel has a broad-spectrum anesthetic sensitivity and is a key regulator of arousal. Each receptor/channel complex is an assembly of five protein subunits. Six subunit classes have been identified, each containing one to six members; many combinations are expressed throughout the brain. Benzodiazepines and intravenous anesthetic agents are clearly subunit dependent, but the literature to date suggests that volatile anesthetics are not. The physiological role of the delta subunit remains enigmatic, and it has not been examined as a determinant of anesthetic sensitivity. Methods Combinations of GABA(A) receptor subunit cDNAs were injected into Xenopus laevis oocytes: alpha1beta1, alpha1beta1gamma2L, alpha1beta1delta, and alpha1beta1gamma2Ldelta. Expression of functional ion channels with distinct signalling and pharmacologic properties was demonstrated within 1-4 days by established electrophysiological methods. Results Co-expression of the delta subunit produced changes in receptor affinity; current density; and the modulatory efficacy of diazepam, zinc, and lanthanum; it also produced subtle changes in the rate of desensitization in response to GABA. Isoflurane enhanced GABA-induced responses from all combinations: alphabeta delta (>10-fold) > alphabeta > alphabeta gamma > or = alphabeta gammadelta (approximately 5-fold). Dose-response plots were bell shaped. Compared with alphabeta gamma receptors (EC50 = 225 microM), both alphabeta delta (EC50 = 372 microM) and alphabeta gammadelta (EC50 = 399 microM) had a reduced affinity for isoflurane. Isoflurane (at a concentration close to the EC50 for each subunit) increased the affinity of GABA for its receptor but depressed the maximal response (alphabeta gamma and alphabeta gammadelta). In contrast, the small currents through alphabeta delta receptors were enhanced, even at saturating agonist concentrations. Conclusions Delta subunit expression alters GABA(A) receptor function but is not an absolute determinant of anesthetic sensitivity.

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Alterations in Rat Accumbens Dopamine, Endocannabinoids and GABA Content During WIN55,212-2 Treatment: The Role of Ghrelin

International Journal of Molecular Sciences ◽

10.3390/ijms22010210 ◽

2020 ◽

Vol 22 (1) ◽

pp. 210

Author(s):

Chrysostomos Charalambous ◽

Marek Lapka ◽

Tereza Havlickova ◽

Kamila Syslova ◽

Magdalena Sustkova-Fiserova

Keyword(s):

Nucleus Accumbens ◽

Food Intake ◽

Dopamine Release ◽

Brain Regions ◽

Aminobutyric Acid ◽

Gamma Aminobutyric Acid ◽

Nucleus Accumbens Shell ◽

Gaba Content ◽

Dopamine Efflux

The endocannabinoid/CB1R system as well as the central ghrelin signalling with its growth hormone secretagogoue receptors (GHS-R1A) are importantly involved in food intake and reward/reinforcement processing and show distinct overlaps in distribution within the relevant brain regions including the hypothalamus (food intake), the ventral tegmental area (VTA) and the nucleus accumbens (NAC) (reward/reinforcement). The significant mutual interaction between these systems in food intake has been documented; however, the possible role of ghrelin/GHS-R1A in the cannabinoid reinforcement effects and addiction remain unclear. Therefore, the principal aim of the present study was to investigate whether pretreatment with GHS-R1A antagonist/JMV2959 could reduce the CB1R agonist/WIN55,212-2–induced dopamine efflux in the nucleus accumbens shell (NACSh), which is considered a crucial trigger impulse of the addiction process. The synthetic aminoalklylindol cannabinoid WIN55,212-2 administration into the posterior VTA induced significant accumbens dopamine release, which was significantly reduced by the 3 mg/kg i.p. JMV2959 pretreatment. Simultaneously, the cannabinoid-increased accumbens dopamine metabolic turnover was significantly augmented by the JMV2959 pretreament. The intracerebral WIN55,212-2 administration also increased the endocannabinoid arachidonoylethanolamide/anandamide and the 2-arachidonoylglycerol/2-AG extracellular levels in the NACSh, which was moderately but significantly attenuated by the JMV2959 pretreatment. Moreover, the cannabinoid-induced decrease in accumbens γ-aminobutyric acid/gamma-aminobutyric acid levels was reversed by the JMV2959 pretreatment. The behavioural study in the LABORAS cage showed that 3 mg/kg JMV2959 pretreatment also significantly reduced the systemic WIN55,212-2-induced behavioural stimulation. Our results demonstrate that the ghrelin/GHS-R1A system significantly participates in the rewarding/reinforcing effects of the cannabinoid/CB1 agonist that are involved in cannabinoid addiction processing.

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