Release of dopamine from dendrites in rat substantia nigra

Geffen, L. B.; Jessell, Thomas M.; Cuello, A. Claudio; Ll, Iversen

doi:10.1038/260258a0

Cited by 624 publications

(226 citation statements)

References 11 publications

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“…Midbrain DA neurons in the SNc and VTA also release DA from their somata and dendrites [13][14][15][16][17][18][19][20][21][22][23][24][25][26]. The term 'somatodendritic' accurately describes evoked DA release in the SNc and VTA, in which somata and dendrites intermingle (figure 1), so that somatic and dendritic release cannot readily be distinguished.…”

Section: Introductionmentioning

confidence: 99%

Somatodendritic dopamine release: recent mechanistic insights

Rice

Patel

2015

Phil. Trans. R. Soc. B

101

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One contribution of 16 to a discussion meeting issue 'Release of chemical transmitters from cell bodies and dendrites of nerve cells'. Dopamine (DA) is a key transmitter in motor, reward and cogitative pathways, with DA dysfunction implicated in disorders including Parkinson's disease and addiction. Located in midbrain, DA neurons of the substantia nigra pars compacta project via the medial forebrain bundle to the dorsal striatum (caudate putamen), and DA neurons in the adjacent ventral tegmental area project to the ventral striatum (nucleus accumbens) and prefrontal cortex. In addition to classical vesicular release from axons, midbrain DA neurons exhibit DA release from their cell bodies and dendrites. Somatodendritic DA release leads to activation of D2 DA autoreceptors on DA neurons that inhibit their firing via G-protein-coupled inwardly rectifying K þ channels. This helps determine patterns of DA signalling at distant axonal release sites. Somatodendritically released DA also acts via volume transmission to extrasynaptic receptors that modulate local transmitter release and neuronal activity in the midbrain. Thus, somatodendritic release is a pivotal intrinsic feature of DA neurons that must be well defined in order to fully understand the physiology and pathophysiology of DA pathways. Here, we review recent mechanistic aspects of somatodendritic DA release, with particular emphasis on the Ca 2þ dependence of release and the potential role of exocytotic proteins.

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Section: Introductionmentioning

confidence: 99%

Somatodendritic dopamine release: recent mechanistic insights

Rice

Patel

2015

Phil. Trans. R. Soc. B

101

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“…Since their report, considerable effort has been expended in establishing that the transmitter is physiologically and pharmacologically releasable from this pool (Cheramy et al, 1981;Geffen et al, 1976;Korfet al, 1976;Nieoullon et al, 1977) and, more recently, in elucidating the physiological consequences of this release. It has long been recognized that dendritically released dopamine might exert autoregulatory influences on the dopamine neurons themselves.…”

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confidence: 99%

Endogenous dopamine can modulate inhibition of substantia nigra pars reticulata neurons elicited by GABA iontophoresis or striatal stimulation

Waszczak¹,

Walters²

1986

J. Neurosci.

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Previous reports from this laboratory have described an ability of iontophoretically applied dopamine to attenuate the inhibitory effects of iontophoresed GABA on neurons of the substantia nigra pars reticulata. This finding raised the question of whether endogenous dopamine, released from dendrites of neighboring pars compacta dopamine neurons, might act as a neuromodulator which diminishes the inhibition of pars reticulata neurons evoked by either GABA iontophoresis or electrical stimulation of the striatonigral GABAergic pathway. Extracellular, single-unit activity of pars reticulata neurons was recorded in male rats anesthetized with chloral hydrate. In one set of studies, d-amphetamine, a drug reported to release dopamine from nigral dendrites, was administered intravenously (1.6 mg/kg) during regular, intermittent iontophoretic pulses of GABA. As had been previously observed with iontophoresed dopamine, i.v. amphetamine significantly lessened the inhibition of reticulata neurons produced by GABA application. This change was reflected by a decrease in GABA's inhibitory potency by 22% relative to the control level of inhibition achieved prior to amphetamine administration. Amphetamine caused no decreases in GABA's effectiveness, however, in animals that had previously received treatments that depleted or destroyed nigral dopamine stores, i.e., in rats pretreated with reserpine and alpha- methyl-p-tyrosine, or in rats with 6-hydroxydopamine lesions of the nigrostriatal dopamine pathway. In a second set of experiments, amphetamine or dopamine was delivered iontophoretically while monitoring the GABA-mediated (bicuculline-reversible) inhibition of reticulata neurons that can be elicited by striatal stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Response levers were inserted into the testing chambers at the end of the 10-min period of intermittent footshock. Ventral tegmental glutamate and heroin seeking B Wang et al region; these neurons release dopamine from their dendrites (Geffen et al, 1976) when activated (Legault et al, 1999(Legault et al, , 2000(Legault et al, , 2001. Rats exposed to the conditions of selfadministration but offered saline rather than a rewarding drug show no significant glutamate or dopamine response to the lever insertion or cue light presentation we used in similar experiments with cocaine .…”

Section: Discussionmentioning

confidence: 99%

Heroin Self-Administration Experience Establishes Control of Ventral Tegmental Glutamate Release by Stress and Environmental Stimuli

Wang

You

Wise

2012

Neuropsychopharmacol

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Heroin and cocaine have very different unconditioned receptor-mediated actions; however, in the brain circuitry of drug-reward and motivation, the two drugs establish common conditioned consequences. A single experience with either drug can change the sensitivity of ventral tegmental area (VTA) dopamine neurons to glutamatergic input. In the case of cocaine, repeated intravenous selfadministration establishes de novo VTA glutamate release and dopaminergic activation in response to conditioned stimuli and mild footshock stress. Here we determined whether repeated self-administration of heroin would establish similar glutamate release and dopaminergic activation. Although self-administration of heroin itself did not cause VTA glutamate release, conditioned glutamate release was seen when rats expecting rewarding heroin were given nonrewarding saline in its place. Mild footshock stress also caused glutamate release in heroin-trained animals. In each case, the VTA glutamate release was accompanied by elevations in VTA dopamine levels, indicative of dopaminergic activation. In each case, infusion of the ionotropic glutamate antagonist kynurenic acid blocked the VTA dopamine release associated with VTA glutamate elevation. Although glutamate levels in the extinction and reinstatement tests were similar to those reported in cocaine studies, the effects of heroin self-administration itself were quite different from what has been seen during cocaine self-administration.

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Release of dopamine from dendrites in rat substantia nigra

Cited by 624 publications

References 11 publications

Somatodendritic dopamine release: recent mechanistic insights

Somatodendritic dopamine release: recent mechanistic insights

Endogenous dopamine can modulate inhibition of substantia nigra pars reticulata neurons elicited by GABA iontophoresis or striatal stimulation

Heroin Self-Administration Experience Establishes Control of Ventral Tegmental Glutamate Release by Stress and Environmental Stimuli

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