Electrophysiological examination of the ventral tegmental (A10) area in the rat

German, Dwight C.; Dalsass, Mario; Kiser, R. Sanford

doi:10.1016/0006-8993(80)91269-x

Cited by 97 publications

(15 citation statements)

References 17 publications

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“…That view is consistent with the mismatch between the characteristics of the directly stimulated reward substrate inferred from behavioral trade-off experiments and the properties of midbrain DA neurons observed in electrophysiological studies [47]. The findings of the present study strengthen the mismatch: it is unlikely that DA neurons, which have fine, unmyelinated axons [14], long refractory periods [48] and slow conduction velocities [49][50][51][52][53][54], could respond at the high frequencies required to account for the data presented here.…”

Section: The Stimulated Neurons Are Likely Non-dopaminergicsupporting

confidence: 88%

Psychophysical inference of frequency-following fidelity in the neural substrate for brain stimulation reward

Solomon

Trujillo-Pisanty

Conover

et al. 2015

Behavioural Brain Research

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Section: The Stimulated Neurons Are Likely Non-dopaminergicsupporting

confidence: 88%

Psychophysical inference of frequency-following fidelity in the neural substrate for brain stimulation reward

Solomon

Trujillo-Pisanty

Conover

et al. 2015

Behavioural Brain Research

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“…The A9 and A 10 cells exhibited the characteristic electrophysiological and pharmacological response properties of dopaminergic neurons previously reported for the mouse slice preparation (Sanghera et al, 1984), and for the rat in vivo (Bunney et al, 1973;German et al, 1979German et al, , 1980. The present data indicate that low concentrations of d-AMP can potently inhibit the firing rates of both A9 and A10 cells in the in vitro mouse brain slice preparation.…”

Section: Discussionsupporting

confidence: 58%

Amphetamine-induced and spontaneous release of dopamine from A9 and A10 cell dendrites: an in vitro electrophysiological study in the mouse

Bernardini

Viscardi

et al. 1991

J. Neural Transmission

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d-Amphetamine (d-AMP) is a potent releaser of dopamine (DA), and its central nervous system stimulant action is mediated primarily through its effect on the substantia nigra and ventral tegmental area dopaminergic neurons (nuclei A9 and A10, respectively). The purpose of the present experiment was to use electrophysiological techniques to examine dendritic release of DA in the in vitro slice preparation, and determine whether: (1) d-AMP inhibits the firing rates of both A9 and A10 cells; (2) the d-AMP-induced inhibition is mediated via the dendritic release of DA; and (3) there is spontaneous dendritic release of DA. Superfusion with d-AMP (2-100 microM) produced identical inhibitory dose-response curves for A9 and A10 cells, and a dose of 6.25 microM caused more than 50% inhibition in the cell firing rates. The d-AMP-induced inhibition was attenuated by blocking DA synthesis. Either D2 receptor blockade (sulpiride, 1 microM), or DA synthesis inhibition (alpha-methylparatyrosine, 50 microM) resulted in a marked increase in the firing rates of dopaminergic cells. These data suggest that d-AMP comparably releases DA from both A9 and A10 cell dendrites, that it releases newly-synthesized DA to inhibit cell firing, and that DA is tonically released to regulate cell firing rates via interactions with inhibitory D2 autoreceptors.

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“…Refractory periods were measured by using the twin-pulse test (19,20): once the minimum stimulating current sufficient to evoke an antidromic response (threshold current) was determined, two stimuli were delivered at an interval that was progressively reduced. The delay at which the second antidromic response disappeared corresponded to the relative refractory period of that particular unit.…”

Section: Methodsmentioning

confidence: 99%

Profound decrement of mesolimbic dopaminergic neuronal activity during ethanol withdrawal syndrome in rats: electrophysiological and biochemical evidence.

Diana

Pistis²,

Carboni³

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

280

199

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Activity of the mesolimbic dopaminergic system was investigated in rats withdrawn from chronic ethanol administration by single-cell extracellular recordings from dopaminergic neurons of the ventrotegmental area, coupled with antidromic identification from the nucleus accumbens, and by microdialysis-technique experiments in the nucleus accumbens. Spontaneous firing rates, spikes per burst, and absolute burst firing but not the number of spontaneously active neurons were found drastically reduced; whereas absolute and relative refractory periods increased in rats withdrawn from chronic ethanol treatment as compared with chronic saline-treated controls. Consistently, dopamine outflow in the nucleus accumbens and its acid metabolites were reduced after abruptly stopping chronic ethanol administration. All these changes, as well as ethanol-withdrawal behavioral signs, were reversed by ethanol administration. This reversal suggests that the abrupt cessation of chronic ethanol adminitration plays a causal role in the reduction of mesolimbic dopaminergic activity seen in the ethanol-withdrawal syndrome. Results indicate that during the ethanol-withdrawal syndrome the mesolimbic dopaminergic system is tonically reduced in activity, as indexed by electrophysiological and biochemical criteria. Considering the role of the mesolimbic dopaminergic system in the reinforcing properties of ethanol, the depressed activity of this system during the ethanol-withdrawal syndrome may be relevant to the dysphoric state associated with ethanol withdrawal in humans.Alcoholism is a major economic, social, and health problem (1). Indeed, alcohol is the most abused substance after nicotine in the Western world, and alcohol abuse and dependence ranked first of all psychiatric disorders in lifetime prevalence rates (2). As for many other abused drugs, this compulsive behavior seems to be elicited and maintained by the powerful reinforcing properties of the drug. Dopamine (DA) is one of the major candidates suggested to mediate reinforcement in animals (3): accordingly, rats will self-stimulate when electrodes are placed near DA neurons in the ventrotegmental area (VTA) (4, 5), and many addicting drugs, including ethanol, increase DA release in the nucleus accumbens (6) and increase DA firing in the VTA (7).The ethanol-withdrawal syndrome begins after cessation of prolonged ethanol administration. A symptom common to withdrawal syndromes, regardless of the substance abused, is the dysphoria associated with absence of the drug. In spite of the evidence linking an increase in dopaminergic transmission to the hedonic properties of ethanol (8), no study has tested in vivo whether the ethanol-withdrawal syndrome is associated with a decline in mesolimbic dopaminergic activity. However, a reduction of DA turnover has been reported The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.(9),...

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Electrophysiological examination of the ventral tegmental (A10) area in the rat

Cited by 97 publications

References 17 publications

Psychophysical inference of frequency-following fidelity in the neural substrate for brain stimulation reward

Psychophysical inference of frequency-following fidelity in the neural substrate for brain stimulation reward

Amphetamine-induced and spontaneous release of dopamine from A9 and A10 cell dendrites: an in vitro electrophysiological study in the mouse

Profound decrement of mesolimbic dopaminergic neuronal activity during ethanol withdrawal syndrome in rats: electrophysiological and biochemical evidence.

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