Dopamine‐independent action of cocaine on striatal and accumbal neurons

Kiyatkin, Eugene A.; Rebec, George V.

doi:10.1046/j.1460-9568.2000.00066.x

Cited by 38 publications

(26 citation statements)

References 43 publications

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“…In a recent in vivo study, cocaine was found to exert a preferential local-anaesthetic-like action on striatal neurons (Kiyatkin and Rebec 2000), suggesting that this kind of effect might in principle have occurred in our experimental condition. The quiescent behavior of spiny neurons in vitro, however, prevented the observation of cocaine effects on voltage dependent-sodium channels.…”

Section: Discussionmentioning

confidence: 68%

“…26, NO. 2 cently reported that cocaine modulates striatal neuron firing activity independently of a DA-mediated mechanism (Kiyatkin and Rebec 2000). To test whether the inhibitory effect of both cocaine and amphetamine on striatal GABAergic transmission was caused by the action of these drugs on DAergic nerve terminals of the striatum, we recorded striatal neurons from rats with 6-OHDA-induced lesion of the homolateral substantia nigra.…”

Section: Effects Of Da Denervation and Of Pharmacological Blockade Ofmentioning

confidence: 99%

“…Cocaine has been shown to cause a strong inhibition of striatal neurons in vivo (Qiao et al 1990;White et al 1993;Kiyatkin and Rebec 2000). This inhibitory effect was highly dependent on the activity state of the neuron (being generally undetectable in slow-firing cells and maximal in fast-firing neurons), and was attributed, at least in part, to a DA-independent local-anesthetic-like interaction with sodium transport (Kiyatkin and Rebec 2000).…”

Section: Comparison With Other Electrophysiological Studiesmentioning

confidence: 99%

“…Other mechanisms, however, might be involved in the pharmacological actions of cocaine and amphetamine in the striatum. Both drugs, in fact, facilitate serotonin and norepinephrine release (Barker and Blakely 1995;Johanson and Schuster 1995) and cocaine has been found to modulate striatal neuron firing activity in vivo independently of transmitter release but through a direct interaction with sodium channels (Kiyatkin and Rebec 2000).In the present in vitro study, therefore, we investigated the cellular and synaptic mechanisms implicated in the pharmacological actions of both cocaine and amphetamine on striatal neurons, addressing in detail the dependency of their effects upon the integrity of the DAergic system in this brain area. To achieve these goals we coupled whole-cell patch clamp recordings from striatal projection neurons to the focal stimulation of either corticostriatal glutamatergic or intrinsic GABAergic nerve terminals.…”

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Cocaine and Amphetamine Depress Striatal GABAergic Synaptic Transmission through D2 Dopamine Receptors

Centonze

Picconi

Baunez

et al. 2002

Neuropsychopharmacology

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The striatum is a brain area implicated in the pharmacological action of drugs of abuse. To test the possible involvement of both cocaine and amphetamine in the modulation of synaptic transmission in this nucleus, we coupled whole-cell patch clamp recordings from striatal spiny neurons to the focal stimulation of glutamatergic or GABAergic nerve terminals. We found that neither cocaine (1-600 M) nor amphetamine (0.3-300 M) significantly affected the glutamate-mediated EPSCs recorded from these cells. Conversely, both pharmacological agents depressed GABA-mediated IPSCs in a dose-dependent manner. This effect was mediated by the stimulation of dopamine (DA) D2 receptors since it was prevented by 3 M L-sulpiride (a DA D2-like receptor antagonist), mimicked by the DA D2-like receptor agonist quinpirole (0.3-30 M), and absent in mice lacking DA D2 receptors. A presynaptic mechanism was likely involved in this action since both cocaine and amphetamine depress GABAergic transmission by increasing paired-pulse facilitation. Cocaine and amphetamine failed to affect GABAergic IPSCs after 6-OHDA-induced nigral lesion, indicating that both drugsFollowing psychostimulant administration, markers of brain activity are altered in many areas (Stein and Fuller 1993;Lyons et al. 1996;Breiter et al. 1997), suggesting that the diverse cognitive, emotional, and motor effects of these drugs are caused by the interaction with multiple neuronal systems in the central nervous system. Increasing evidence indicates that not only cortical but also subcortical areas play a role in the cocaine-and amphetamine-mediated effects. In particular, the increased locomotor activity and stereotypy caused by psychostimulants seem to involve specifically the nucleus striatum (Kelly et al. 1975;Amalric and Koob 1993;Berke and Hyman 2000), a structure that receives virtually all the cortical information directed to the basal ganglia (Penney and Young 1983;Albin et al. 1989;McGeorge and Faull 1989;Calabresi et al. 1996 Kaneko et al. 2000). The nucleus striatum also receives profuse dopaminergic innervation from the substantia nigra and has a very high density of D1 and D2 dopamine (DA) receptors but also of D3, D4 and D5 receptors (Mansour and Watson 1995;Surmeier et al. 1996;Bordet et al. 1997;LaHoste et al. 2000). Amphetamine and cocaine cause in the striatum rapid induction of c-fos, a commonly used molecular marker for neuronal activity. Interestingly, this effect is sensitive to dopamine (DA) receptor blockade (Graybiel et al. 1990;Moratalla et al. 1993), suggesting that increased release of DA in the striatum is responsible, at least in part, for the action of these drugs. In this regard, while the full diversity of drug effects is mediated by multiple neurotransmitters acting in multiple brain regions, most drugs abused by humans share the common property of increasing DA release in this brain area (Di Chiara and Imperato 1988; Kuczenshi et al. 1991;Yamamoto and Spanos 1988;Koob et al. 1998;Ito et al. 2000). Cocaine increases DA availability in th...

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Section: Discussionmentioning

confidence: 68%

Section: Effects Of Da Denervation and Of Pharmacological Blockade Ofmentioning

confidence: 99%

Section: Comparison With Other Electrophysiological Studiesmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Cocaine and Amphetamine Depress Striatal GABAergic Synaptic Transmission through D2 Dopamine Receptors

Centonze

Picconi

Baunez

et al. 2002

Neuropsychopharmacology

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Locomotor inhibition induced by procaine injections into the nucleus accumbens core, but not the medial ventral striatum: Implication for cocaine‐induced locomotion

Ikemoto

Witkin

2002

Synapse

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We examined whether injections of the local anesthesia procaine into the nucleus accumbens core disrupts locomotion more readily than those into the medial ventral striatum. Spontaneous locomotion decreased during the first 10 min immediately following injections of procaine into the core. When procaine was co-administered with d-amphetamine into the core, the injections also decreased amphetamine-induced locomotion during the initial 10 min. On the other hand, no detectable effect on spontaneous or amphetamine-induced locomotion was found when procaine was injected into the medial ventral striatum, including the medial shell and medial olfactory tubercle. We replicated our recent finding that cocaine injections into the core induced delayed, modest locomotion, while cocaine injections into the medial ventral striatum induced immediate, vigorous locomotion. Injections of amphetamine into the core induced as equally vigorous locomotion as that of the medial ventral striatum. These results show that the neurons of the core involved in locomotion are more vulnerable to local anesthesia than the neurons of the medial ventral striatum. In other words, cocaine at the doses inducing vigorous locomotion in the medial ventral striatum induces local anesthesia when applied to the core.

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