Permeation and block of dopamine-modulated potassium channels on rat striatal neurons by cesium and barium ions

Lin, Youping; Greif, Gabriela J.; Freedman, Jonathan E.

doi:10.1152/jn.1996.76.3.1413

Cited by 14 publications

(8 citation statements)

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“…The enhancement of paired pulse facilitation, together with the lack of any postsynaptic action of these compounds on IPSC reversal potential, holding current and membrane conductance, all point to a presynaptic site for this action. Accordingly, although DA receptors are abundantly expressed postsynaptically on striatal neurons (Surmeier et al 1996), their activation is known to modulate membrane conductances operating in voltage ranges far from the values chosen in this study to evoke synaptic events (Ϫ80 mV and Ϫ40 mV) (Schiffmann et al 1995;Surmeier et al 1995;Lin et al 1996;Hernandez-Lopez et al 2000). This observation, therefore, further confirms that the postsynaptic effects of DA receptor activation cannot be responsible for the observed modulation of striatal IPSCs.…”

Section: Discussionsupporting

confidence: 78%

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: Discussionsupporting

confidence: 78%

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

Centonze

Picconi

Baunez

et al. 2002

Neuropsychopharmacology

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“…According to the Goldman-HodgkinKatz equation, this shift is compatible with an approximately 2-fold permeability preference for K ϩ over Na ϩ . However, this value may not be exact, because of the possibility of mole-fraction effects (19,20). Channel fractional open probability was independent of membrane potential at voltages negative to the reversal potential, but outward currents were not resolvable (Fig.…”

Section: Resultsmentioning

confidence: 99%

Altered gating of opiate receptor-modulated K ⁺ channels on amygdala neurons of morphine-dependent rats

Chen

Marrero

Murphy

et al. 2000

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

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The molecular mechanism of tolerance to opiate drugs is poorly understood. We have used single-channel patch-clamp recordings to study opiate receptor effects on dissociated neurons from rat amygdala, a limbic region implicated in addiction processes. A 130-pS inwardly rectifying K ؉ -preferring cation channel was activated by opioid receptors in a membrane-delimited manner. After chronic treatment of the rats with morphine, channel gating changed markedly, with an approximately 100-fold decrease in open probability at a given morphine concentration. The change in channel gating correlated both in time course and in dose of morphine treatment with the development of functional opiate dependence and appeared to arise at a step after G-protein activation and before channel permeation by K ؉ . This decreased receptor-channel coupling appears to be large enough to account quantitatively for opiate tolerance and may represent one of the mechanisms through which tolerance occurs. D rug addiction is a complex process that includes tolerance (the need for increasing drug dosage to achieve the same effect) and dependence (the appearance of adverse effects on drug withdrawal). Human heroin addicts experience tolerance of more than 100-fold if drug availability is unlimited (1). Changes in the number, affinity, or membrane trafficking of opioid receptors (2-6), in the coupling of receptors to Gproteins (7, 8), or in associated second messenger systems (9) have been implicated in opiate tolerance mechanisms; however, these effects are usually on the order of 10 -20% and therefore appear unable to account quantitatively for tolerance. Consequently, the molecular basis of opiate tolerance remains poorly understood.We have used patch-clamp electrophysiology to resolve single ion channels that are activated by opioid receptors and to study changes in channel properties after chronic opiate treatment. We performed these studies by using freshly dissociated neurons from the amygdalohippocampal area (AHA) of 30-to 45-day-old rats. The AHA is an output nucleus of the amygdala (10, 11) and as such is part of a limbic region implicated in the motivational effects of opiates and other drugs of abuse (10-15). AHA neurons are known to display inhibitory responses to opiates in vivo (14). Furthermore, these cells exhibit a decreased inhibition by morphine after chronic treatment, consistent with tolerance, as well as an activation of firing after precipitated withdrawal, consistent with dependence (14). We now describe a K ϩ -permeable channel that is activated by opioid receptors and show that its gating undergoes changes after chronic morphine treatment in a manner that may account for opiate tolerance in limbic neurons. MethodsCell Preparation. Coronal 300-m sections of the posteriodorsal amygdala were cut on a vibrating tissue slicer under an ice-cold Pipes-buffered solution previously described (16) and were blocked to include the AHA (10) and some underlying amygdaloid nuclei, but excluded the hippocampus. After slowly warming the ...

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“…In substantia nigra and striatal neurons inwards rectifier (Kir) channels have been identified [10,37,65]. The Mcurrent has been shown in the mouse neuroblastomarat glioma hybrid cells NG108-15 [40,42], in rat cerebral neurons [42], in rat sympathetic neurons [7,35] and in the amygdala [70].…”

Section: Discussionmentioning

confidence: 99%

Functional coupling between heterologously expressed dopamine D2 receptors and KCNQ channels

Ljungstrøm

Grunnet

Jensen

et al. 2003

Pflugers Arch - Eur J Physiol

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Activation of KCNQ potassium channels by stimulation of co-expressed dopamine D(2) receptors was studied electrophysiologically in Xenopus laevis oocytes and in mammalian cells. To address the specificity of the interaction between D(2)-like receptors and KCNQ channels, combinations of KCNQ1-5 channels and D(2)-like receptors (D(2L), D(3), and D(4)) were investigated in Xenopus oocytes. Activation of either receptor with the selective D(2)-like receptor agonist quinpirole (100 nM) stimulated all the KCNQ currents, independently of the subunit combination, indicating a common pathway of receptor-channel interaction. The KCNQ4 current was investigated in further detail and was increased by 19.9+/-1.6% ( n=20) by D(2L) receptor stimulation. The effect could be mimicked by injection of GTPgammaS and prevented by injection of Bordetella pertussis toxin, indicating that channel stimulation was mediated via a G protein of the G(alphai/o) subtype. Cells of the human neuroblastoma line SH-SY5Y were co-transfected transiently with KCNQ4 and D(2L) receptors. Stimulation of D(2L) receptors increased the KCNQ4 current ( n=6) as determined in whole-cell patch-clamp recordings. The specificity of the dopaminergic activation of the KCNQ channels was confirmed by co-expression of other neuronal K(+) channels (BK, K(V)1.1, and K(V)4.3) with the D(2L) receptor in Xenopus oocytes. None of these K(+) channels responded to stimulation of the D(2L) receptor. In the mammalian brain, dopamine D(2) receptors and KCNQ channels co-localise postsynaptically in several brain regions, so modulation of neuronal excitability by dopamine release could in part be mediated via an effect on KCNQ channels.

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Permeation and block of dopamine-modulated potassium channels on rat striatal neurons by cesium and barium ions

Cited by 14 publications

References 0 publications

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

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

Altered gating of opiate receptor-modulated K ⁺ channels on amygdala neurons of morphine-dependent rats

Functional coupling between heterologously expressed dopamine D2 receptors and KCNQ channels

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Permeation and block of dopamine-modulated potassium channels on rat striatal neurons by cesium and barium ions

Cited by 14 publications

References 0 publications

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

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

Altered gating of opiate receptor-modulated K + channels on amygdala neurons of morphine-dependent rats

Functional coupling between heterologously expressed dopamine D2 receptors and KCNQ channels

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Altered gating of opiate receptor-modulated K ⁺ channels on amygdala neurons of morphine-dependent rats