Abnormal Synaptic Plasticity in the Striatum of Mice Lacking Dopamine D2 Receptors

Calabresi, Paolo; Saiardi, Adolfo; Pisani, Antonio; Baik, Ja Hyun; Centonze, Diego; Mercuri, Nicola Biagio; Bernardi, Giorgio; Borrelli, Emiliana

doi:10.1523/jneurosci.17-12-04536.1997

Cited by 257 publications

(228 citation statements)

References 66 publications

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“…The intrinsic and synaptic membrane properties of neurons recorded in vitro from D2 lacking striatal slices were similar to those recorded from wild-type mice and control rats, as previously reported (Calabresi et al 1997).…”

Section: Methodssupporting

confidence: 82%

“…As already reported (Calabresi et al 1997), the intrinsic and synaptic properties of striatal neurons recorded from these mice were indistinguishable from those of their wild-type counterparts and from rat striatal neurons (not shown). In these mice, however, both cocaine (30 M) (n ϭ 4; p Ͼ .05) and amphetamine (30 M) (n ϭ 4; p Ͼ .05) failed to affect striatal IPSCs ( Figures 6A and 6B), implying DA D2 receptors in the pharmacological action of these drugs within the striatum.…”

Section: Effects Of the Genetic Disruption Of Da D2 Receptors On Cocasupporting

confidence: 79%

“…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%

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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: Methodssupporting

confidence: 82%

Section: Effects Of the Genetic Disruption Of Da D2 Receptors On Cocasupporting

confidence: 79%

See 1 more Smart Citation

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

Centonze

Picconi

Baunez

et al. 2002

Neuropsychopharmacology

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“…Thus, a cannabinoid other than 2-AG may mediate LTD, and in particular anandamide could be a plausible candidate. This is suggested by the fact that, as already discussed, anandamide is selectively produced following dopaminergic D2 receptor activation in the striatum (Giuffrida et al, 1999) and that D2 receptors are indeed necessary for LTD induction (Calabresi et al, 1997). …”

Section: Endocannabinoids and Long-term Depression (Ltd)mentioning

confidence: 86%

Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

Diana

Marty

2004

British J Pharmacology

235

177

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Depolarization-induced suppression of inhibition (DSI) and depolarization-induced suppression of excitation (DSE) are two related forms of short-term synaptic plasticity of GABAergic and glutamatergic transmission, respectively. They are induced by calcium concentration increases in postsynaptic cells and are mediated by the release of a retrograde messenger, which reversibly inhibits afferent synapses via presynaptic mechanisms. We review here:(1) The evidence accumulated during the 1990s that has led to the conclusion that DSI/DSE rely on retrograde signaling. (2) The more recent research that has led to the identification of endocannabinoids as the retrograde messengers responsible for DSI/DSE. (3) The possible mechanisms by which presynaptic type 1 cannabinoid receptors reduce synaptic efficacy during DSI/DSE. (4) The possible modes of induction of DSI/DSE by physiological activity patterns, and the partially conflicting evaluations of the calcium concentration increases required for cannabinoid synthesis. (5) Finally, the relation between DSI/DSE and other forms of long-and short-term synaptic inhibition, which were more recently associated with the production of endocannabinoids by postsynaptic cells.We conclude that recent studies on DSI/DSE have uncovered a specific and original mode of action for endocannabinoids in the brain, and that they have opened new avenues to understand the role of retrograde signaling in central synapses.

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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. …”

mentioning

confidence: 99%

Dopamine responses comply with basic assumptions of formal learning theory

Waelti

Dickinson

Schultz

2001

Nature

941

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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Abnormal Synaptic Plasticity in the Striatum of Mice Lacking Dopamine D2 Receptors

Cited by 257 publications

References 66 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

Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

Dopamine responses comply with basic assumptions of formal learning theory

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