Synaptic input and output of parvalbumin-immunoreactive neurons in the neostriatum of the rat

Bennett, Ben D.; Bolam, J. Paul

doi:10.1016/0306-4522(94)90471-5

Cited by 245 publications

(184 citation statements)

References 50 publications

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“…GABAergic innervation of striatal neurons is entirely intrinsic, originating from axonal collaterals of projection cells (95% of striatal neuronal population) or from GABA interneurons (41)(42)(43)(44)(45)(46). Our electrophysiologic data pointed toward a presynaptic site for increased GABA transmission in mice lacking FMRP and BC1 RNA, implying that both molecules are present in axons of striatal cells.…”

Section: Fmrp and Bc1 Rna Partially Colocalize In Striatal Axonal Bunmentioning

confidence: 68%

Abnormal Striatal GABA Transmission in the Mouse Model for the Fragile X Syndrome

Centonze

Rossi

Mercaldo

et al. 2008

Biological Psychiatry

153

134

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Section: Fmrp and Bc1 Rna Partially Colocalize In Striatal Axonal Bunmentioning

confidence: 68%

Abnormal Striatal GABA Transmission in the Mouse Model for the Fragile X Syndrome

Centonze

Rossi

Mercaldo

et al. 2008

Biological Psychiatry

153

134

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“…One possibility is that an increase in NAc GABA levels may hyperpolarize NAc medium spiny (GABAergic) neurons, and therefore desensitize NAc neuronal responses to cocaine-induced increases in NAc DA and inhibit cocaine-triggered reinstatement. However, this is unlikely because our previous studies have shown that selective elevation of NAc GABA levels by microinjection of GVG into the NAc failed to inhibit heroin self-administration (Xi and Stein, 2000), while microinjections of GVG into the ventral tegmental area (VTA) or the ventral palladium (VP), the primary NAc GABAergic projection area (Smith and Bolam, 1990;Bennett and Bolam, 1994), almost completely inhibit heroin self-administration (Xi and Stein, 2000). These data suggest that GVG-induced increases in extracellular GABA in the VTA or VP, but not in the NAc, may play a critical role in attenuating heroin's rewarding effects.…”

Section: Gabaergic Mediation Of Gvg's Inhibition Of Drug-seeking Behamentioning

confidence: 99%

Gamma-vinyl GABA inhibits cocaine-triggered reinstatement of drug-seeking behavior in rats by a non-dopaminergic mechanism

Peng

Gilbert

et al. 2008

Drug and Alcohol Dependence

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Relapse to drug use is a core feature of addiction. Previous studies demonstrate that γ-vinyl GABA (GVG), an irreversible GABA transaminase inhibitor, attenuates the acute rewarding effects of cocaine and other addictive drugs. We here report that systemic administration of GVG (25-300 mg/ kg) dose-dependently inhibits cocaine-or sucrose-induced reinstatement of reward-seeking behavior in rats. In vivo microdialysis data indicated that the same doses of GVG dose-dependently elevate extracellular GABA levels in the nucleus accumbens (NAc). However, GVG, when administered systemically or locally into the NAc, failed to inhibit either basal or cocaine-priming enhanced NAc dopamine in either naïve rats or cocaine extinction rats. These data suggest that: (1) GVG significantly inhibits cocaine-or sucrose-triggered reinstatement of reward-seeking behavior; and (2) a GABAergic-, but not dopaminergic-, dependent mechanism may underlie the antagonism by GVG of cocaine-triggered reinstatement of drug-seeking behavior, at least with respect to GVG's action on the NAc.

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“…Moreover, interneurons are prone to fire repetitively and tend to synchronize one another through gap junctions (Koos and Tepper, 1999), and each terminal bouton tends to have more than one active zone (Bevan et al, 1998). In addition, the FS interneurons preferentially target the perisomatic region and not only the dendrites of projection cells (Bennett and Bolam, 1994;Koos and Tepper, 1999;Kubota and Kawaguchi, 2000). Therefore, a striatal field stimulus will be biased toward interneurons and a larger IPSC (Jaeger et al, 1994).…”

Section: Ipscs From Axon Collateralsmentioning

confidence: 99%

“…Inhibition comes from two main sources: interneurons (Kita, 1993;Bennett and Bolam, 1994;Jaeger et al, 1994;Kawaguchi et al, 1995;Koos and Tepper, 1999) and recurrent axon collaterals interconnecting projection neurons (Park et al, 1980;Wilson and Groves, 1980;Somogyi et al, 1981;Bishop et al, 1982;Groves, 1983;Aronin et al, 1986;Bolam and Izzo, 1988;Czubayko and Plenz, 2002;Koos et al, 2002;Tunstall et al, 2002). We asked whether dopamine regulates the strength of synapses between projection neurons.…”

Section: Introductionmentioning

confidence: 99%

Dopaminergic Modulation of Axon Collaterals Interconnecting Spiny Neurons of the Rat Striatum

et al. 2003

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Dopamine is a critical modulator of striatal function; its absence produces Parkinson's disease. Most cellular actions of dopamine are still unknown. This work describes the presynaptic actions of dopaminergic receptor agonists on GABAergic transmission between neostriatal projection neurons. Axon collaterals interconnect projection neurons, the main axons of which project to other basal ganglia nuclei. Most if not all of these projecting axons pass through the globus pallidus. Thus, we lesioned the intrinsic neurons of the globus pallidus and stimulated neostriatal efferent axons antidromically with a bipolar electrode located in this nucleus. This maneuver revealed a bicuculline-sensitive synaptic current while recording in spiny cells. D 1 receptor agonists facilitated whereas D 2 receptor agonists depressed this synaptic current. In contrast, a bicuculline-sensitive synaptic current evoked by field stimulation inside the neostriatum was not consistently modulated, in agreement with previous studies. The data are discussed in light of the most recent experimental and modeling results. The conclusion was that inhibition of spiny cells by axon collaterals of other spiny cells is quantitatively important; however, to be functionally important, this inhibition might be conditioned to the synchronized firing of spiny neurons. Finally, dopamine exerts a potentially important role regulating the extent of lateral inhibition.

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Synaptic input and output of parvalbumin-immunoreactive neurons in the neostriatum of the rat

Cited by 245 publications

References 50 publications

Abnormal Striatal GABA Transmission in the Mouse Model for the Fragile X Syndrome

Abnormal Striatal GABA Transmission in the Mouse Model for the Fragile X Syndrome

Gamma-vinyl GABA inhibits cocaine-triggered reinstatement of drug-seeking behavior in rats by a non-dopaminergic mechanism

Dopaminergic Modulation of Axon Collaterals Interconnecting Spiny Neurons of the Rat Striatum

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