Glutamate-dependent long-term presynaptic changes in corticostriatal excitability

García‐Muñoz, Marianela; Patino, P.; Masliah, Eliezer; Young, Stephen J.; Groves, Philip M.

doi:10.1016/0306-4522(96)00007-3

Cited by 17 publications

(7 citation statements)

References 88 publications

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“…This prevents cocaine-induced adaptations in VTA DA cell activity, and thereby prevents resultant downstream adaptations such as DA D1 receptor supersensitivity in the VTA. However, the mPFC also sends a substantial EAA projection directly to the NAc (Sesack and Pickel, 1992) and it is well established that corticostriatal projections are critical for synaptic plasticity exhibited by dorsal striatal and NAc neurons (Calabresi et al, 1992;Kombian and Malenka, 1994;Garcia-Munoz et al, 1996). Thus, it is conceivable that EAA projections to the NAc also play a critical role in sensitization-related changes in the excitability of NAc neurons, including DA D1 receptor supersensitivity.…”

Section: Role Of Nac Eaas In Cocaine Sensitizationmentioning

confidence: 95%

Both glutamate receptor antagonists and prefrontal cortex lesions prevent induction of cocaine sensitization and associated neuroadaptations

Berney

et al. 1999

Synapse

160

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Behavioral sensitization to psychomotor stimulants is accompanied by a number of alterations in the mesoaccumbens dopamine (DA) system, including DA autoreceptor subsensitivity in the ventral tegmental area (VTA) and DA D1 receptor supersensitivity in the nucleus accumbens (NAc). We investigated the role of excitatory amino acid (EAA) transmission in the induction of cocaine sensitization and these accompanying DA receptor alterations. To do so, we used three glutamate receptor antagonists, the noncompetitive NMDA receptor antagonist MK-801 (0.1 mg/kg), the competitive NMDA receptor antagonist CGS 19755 (10.0 mg/kg), and the AMPA receptor antagonist NBQX (12.5 mg/kg). Rats received daily double injections of either one of these antagonists or saline with either cocaine (15.0 mg/kg) or saline for 5 days. Cocaine sensitization was defined as an increase in horizontal locomotor activity in response to cocaine challenge (7.5 mg/kg) on the third day of withdrawal. All three antagonists prevented the induction of cocaine sensitization. Extracellular single cell recordings revealed that these antagonists also prevented the induction of DA autoreceptor subsensitivity in the VTA and DA D1 receptor supersensitivity in the NAc. To determine whether the relevant glutamate receptors were under regulation by medial prefrontal cortex (mPFC) EAA efferents, we next lesioned the mPFC bilaterally with ibotenic acid at least 7 days before repeated cocaine treatment began. These lesions also prevented the induction of cocaine sensitization and the associated neuroadaptations. Our findings indicate that glutamate transmission from mPFC to the mesoaccumbens DA system is critical for the induction of cocaine sensitization and its cellular correlates.

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Section: Role Of Nac Eaas In Cocaine Sensitizationmentioning

confidence: 95%

Both glutamate receptor antagonists and prefrontal cortex lesions prevent induction of cocaine sensitization and associated neuroadaptations

Berney

et al. 1999

Synapse

160

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“…Long-term potentiation (LTP) and long-term depression (LTD) are use-dependent forms of synaptic plasticity which may be relevant to basal ganglia-related learning and memory (Calabresi et al, 1996). In vitro and in vivo studies have shown that corticostriatal synapses can express both LTD and LTP (Calabresi et al, 1992;Charpier and Deniau, 1997;Garcia-Munoz et al, 1996;Lovinger et al, 1993;Wickens, et al, 1996). There is some disagreement, however, as to the preferred form of long-term plasticity expressed by these synapses.…”

Section: Introductionmentioning

confidence: 99%

“…There is some disagreement, however, as to the preferred form of long-term plasticity expressed by these synapses. Depending on the preparation and tetanus parameters, LTP and/or LTD can be expressed at cor-ticostriatal synapses (Calabresi et al, 1992;Charpier and Deniau, 1997;Dunia and Walsh, 1993;Garcia-Munoz et al, 1996;Wickens, et al, 1996). Experimentally, corticostriatal LTD is induced by 100 Hz stimulation, which lies in contrast to the low-frequency requirement (1-5 Hz) for inducing LTD at excitatory synapses in the hippocampus and cortex (Christie et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Functional state of corticostriatal synapses determines their expression of short- and long-term plasticity

Akopian

Musleh

Smith

et al. 2000

Synapse

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Relationships between presynaptic function and short‐ and long‐term plasticity were investigated at adult corticostriatal synapses. Wide variability was observed in the expression of short‐ and long‐term synaptic plasticity. Intracellular records from 47 cells produced 17 examples of LTD (<90% of control), 10 examples of no long‐term change (between 90–110% of control), and 20 examples of LTP (>110% of control). Similar variation existed in paired‐pulse and posttetanic plasticities. The variability expressed in all three forms of plasticity appears to be related, based on correlations found between the paired‐pulse ratio (PPR) and tetanus‐induced short‐ (3 min posttetanus) and long‐term plasticities (16–20 min posttetanus). These data suggest that tetanus‐induced changes in synaptic strength are related to the intrinsic, preconditioned behavior of synapses. Every cell showing paired‐pulse depression also expressed LTD in response to high‐frequency activation of its afferents. Those synapses showing paired‐pulse potentiation tended to express LTP, although exceptions did exist. Similar relationships were found in a parallel analysis of population spikes. PPR also changed in association with the expression of posttetanic and long‐term depression. Greater paired‐pulse potentiation was observed in medial intracellular recordings, but no medial to lateral differences were seen in posttetanic plasticities. Field recordings also showed a medial bias toward paired‐pulse and posttetanic potentiation, but not in long‐term plasticity. Block of postsynaptic L‐type Ca2+ channels with nifedipine eliminated LTD expression, but overall no differences were found between nifedipine and control cells. Synapse 38:271–280, 2000. © 2000 Wiley‐Liss, Inc.

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“…NMDA activation causes striatal neurons to dephosphorylate and thereby to inactivate the protein phosphatase inhibitor DARRP-32 (Halpain et al, 1990), an important regulator of dopaminergic neurotransmission , whose activity may be necessary for the potentiation of NMDA receptors by protein kinase A (Blank et al, 1997). NMDA receptors participate in the regulation of striatal synaptic plasticity, through processes such as long-term potentiation of synaptic strength (Calabresi et al, 1992;Walsh and Dunia, 1993;Garcia-Munoz et al, 1996). Striatal lesioning with the NMDA agonist quinolinic acid mimics Huntington's disease (Beal et al, 1986(Beal et al, , 1991DiFiglia, 1990;Roberts et al, 1993;Figueredo-Cardenas et al, 1994), a hereditary neurodegenerative disorder that primarily affects striatal projection neurons and spares interneurons (Ferrante et al, 1987a,b;Reiner et al, 1988;Harrington and Kowall, 1991;Albin et al, 1992;Augood et al, 1996).…”

mentioning

confidence: 99%

Localization of alternatively spliced NMDAR1 glutamate receptor isoforms in rat striatal neurons

et al. 1999

J. Comp. Neurol.

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Glutamate-dependent long-term presynaptic changes in corticostriatal excitability

Cited by 17 publications

References 88 publications

Both glutamate receptor antagonists and prefrontal cortex lesions prevent induction of cocaine sensitization and associated neuroadaptations

Both glutamate receptor antagonists and prefrontal cortex lesions prevent induction of cocaine sensitization and associated neuroadaptations

Functional state of corticostriatal synapses determines their expression of short- and long-term plasticity

Localization of alternatively spliced NMDAR1 glutamate receptor isoforms in rat striatal neurons

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