Unilateral Dopamine Denervation Blocks Corticostriatal LTP

Centonze, Diego; Gubellini, Paolo; Picconi, Barbara; Calabresi, Paolo; Giacomini, Patrizia; Bernardi, Giorgio

doi:10.1152/jn.1999.82.6.3575

Cited by 192 publications

(133 citation statements)

References 41 publications

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“…Striatal cells were silent at rest and showed membrane rectification and tonic firing activity during depolarizing current pulses. These features closely resembled the electrical activity described previously for rat and mouse spiny neurons (Calabresi et al, 1997b(Calabresi et al, , 2000Centonze et al, 1999;Picconi et al, 2003) (Fig. 3 A, B).…”

Section: Corticostriatal Synaptic Plasticity After Haloperidol Treatasupporting

confidence: 88%

“…In fact, ipsilateral nigral lesions and pharmacological or genetic inactivation of D1 receptors prevent LTP induction (Centonze et al, 1999(Centonze et al, , 2003bCalabresi et al, 2000;Kerr and Wickens, 2001), whereas pharmacological or genetic inactivation of D2L receptors enhances this process (Calabresi et al, 1997b; present study). The differential effects of D1 and D2L (but not D2S) receptors in LTP induction might rely on their opposite actions on the phosphorylation of DARPP-32, a phosphoprotein particularly enriched in dopaminoceptive neurons of the striatum that acts as a potent inhibitor of protein phosphatase-1 (Greengard et al, 1999).…”

Section: Discussionmentioning

confidence: 44%

“…In particular, haloperidoltreated animals (1 and 20 d), and D2RϪ/Ϫ, D2LϪ/Ϫ, and D2RϪ/Ϫ; D2LϪ/Ϫ mice were used along with their respective counterparts (shamtreated rats or WT mice). Corticostriatal coronal slices (200 -300 m) were prepared from tissue blocks of the brain with the use of a vibratome (Calabresi et al, 1992a(Calabresi et al, , 1997b(Calabresi et al, , 2000Centonze et al, 1999). A single slice was then transferred to a recording chamber and submerged in a continuously flowing Krebs solution (35°C; 2-3 ml/min) gassed with 95% O 2 -5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

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Chronic Haloperidol Promotes Corticostriatal Long-Term Potentiation by Targeting Dopamine D2L Receptors

Centonze¹,

Usiello²,

Costa³

et al. 2004

J. Neurosci.

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Reduced glutamate-mediated synaptic transmission has been implicated in the pathophysiology of schizophrenia. Because antipsychotic agents might exert their beneficial effects against schizophrenic symptoms by strengthening excitatory transmission in critical dopaminoceptive brain areas, in the present study we have studied the effects of acute and chronic haloperidol treatment on striatal synaptic plasticity. Repetitive stimulation of corticostriatal terminals in slices induced either long-term depression or long-term potentiation (LTP) of excitatory transmission in control rats, whereas it invariably induced NMDA receptor-dependent LTP in animals treated chronically with haloperidol. Haloperidol effects were mimicked and occluded in mice lacking both D2L and D2S isoforms of dopamine D2 receptors (D2RϪ/Ϫ), in mice lacking D2L receptors and expressing normal levels of D2S receptors (D2RϪ/Ϫ;D2LϪ/Ϫ), and in mice lacking D2L receptors and overexpressing D2S receptors (D2LϪ/Ϫ). These data indicate that the blockade of D2L receptors was responsible for the LTP-favoring action of haloperidol in the striatum. In contrast, overexpression of D2S receptors uncovered a facilitatory role of this receptor isoform in LTP formation because LTP recorded from D2LϪ/Ϫ mice, but not those recorded from wild-type, D2RϪ/Ϫ, and D2RϪ/Ϫ;D2LϪ/Ϫ mice, was insensitive to the pharmacological blockade of D1 receptors.The identification of the cellular, molecular, and receptor mechanisms involved in the action of haloperidol in the brain is essential to understand how antipsychotic agents exert their beneficial and side effects.

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Section: Corticostriatal Synaptic Plasticity After Haloperidol Treatasupporting

confidence: 88%

Section: Discussionmentioning

confidence: 44%

Section: Methodsmentioning

confidence: 99%

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Chronic Haloperidol Promotes Corticostriatal Long-Term Potentiation by Targeting Dopamine D2L Receptors

Centonze¹,

Usiello²,

Costa³

et al. 2004

J. Neurosci.

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“…The preparation and maintenance of coronal slices have been described previously (Calabresi et al 1997;Centonze et al 1999). Briefly, coronal slices were prepared from tissue blocks of the brain with the use of a vibratome.…”

Section: Methodsmentioning

confidence: 99%

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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“…1a bottom). Median durations of licking (50th percentile) during a 2.0-s period after stimulus onset were 0 ms after stimulus X but 323 ms after Y (400 trials; P , 0:0001; Wilcoxon test; X and Y tested 1 Published in "Nature 412: [43][44][45][46][47][48] 2001" which should be cited to refer to this work. …”

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confidence: 99%

Dopamine responses comply with basic assumptions of formal learning theory

Waelti

Dickinson

Schultz

2001

Nature

947

749

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According to contemporary learning theories, the discrepancy, or error, between the actual and predicted reward determines whether learning occurs when a stimulus is paired with a reward. The role of prediction errors is directly demonstrated by the observation that learning is blocked when the stimulus is paired with a fully predicted reward. By using this blocking procedure, we show that the responses of dopamine neurons to conditioned stimuli was governed differentially by the occurrence of reward prediction errors rather than stimulus±reward associations alone, as was the learning of behavioural reactions. Both behavioural and neuronal learning occurred predominantly when dopamine neurons registered a reward prediction error at the time of the reward. Our data indicate that the use of analytical tests derived from formal behavioural learning theory provides a powerful approach for studying the role of single neurons in learning.Classic theories assume that predictive learning occurs whenever a stimulus is paired with a reward or punishment 1,2 . However, more recent analyses of associative learning argue that simple temporal contiguity between a stimulus and a reinforcer is not suf®cient for learning and that a discrepancy between the reinforcer that is predicted by a stimulus and the actual reinforcer is also required 3±6 . This discrepancy can be characterized as a`prediction error' 7 . Presentations of surprising or unpredicted reinforcers generate positive prediction errors, and thereby support learning, whereas omissions of predicted reinforcers generate negative prediction errors and lead to reduction or extinction of learned behaviour. Expected reinforcers do not generate prediction errors and therefore fail to support further learning even when the stimulus is consistently paired with the reinforcer. Modelling studies have shown that neuronal messages encoding prediction errors can act as explicit teaching signals for modifying the synaptic connections that underlie associative learning 8±17 .Current research suggests that one of the principal reward systems of the brain involves dopamine neurons 18±21 . Both psychopharmacological manipulations and lesions of the dopamine system impair reward-driven behaviour of animals 18,21 , and drugs of abuse, which provide strong arti®cial rewards, act via dopamine neurons 19,20 . Neurobiological investigations of associative learning have shown that dopamine neurons respond phasically to rewards in a manner compatible with the coding of prediction errors 22±28 , whereas slower dopamine changes are involved in a larger spectrum of motivating events 18,28,29 . Dopamine neurons show short-latency, phasic activations when rewards occur unpredictably, they are not modulated by fully predicted rewards and show phasically reduced activity when predicted rewards are omitted. During initial learning, when rewards occur unpredictably, dopamine neurons are activated by rewards. They gradually lose the response as the reward becomes increasingly predicted 24,25,27 . The co...

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Unilateral Dopamine Denervation Blocks Corticostriatal LTP

Cited by 192 publications

References 41 publications

Chronic Haloperidol Promotes Corticostriatal Long-Term Potentiation by Targeting Dopamine D2L Receptors

Chronic Haloperidol Promotes Corticostriatal Long-Term Potentiation by Targeting Dopamine D2L Receptors

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

Dopamine responses comply with basic assumptions of formal learning theory

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