Abstract:
RATIONALE:Caveolin-1 (CAV1) is a structural protein critical for spatial organization of neuronal signaling molecules. Whether CAV1 is required for long-lasting neuronal plasticity remains unknown. OBJECTIVE AND METHODS:We sought to examine the effects of CAV1 knockout (KO) on functional plasticity and hypothesized that CAV1 deficiency would impact drug-induced long-term plasticity in the nucleus accumbens (NAc). We first examined cell morphology of NAc medium spiny neurons in a striatal/cortical co-culture system before moving in vivo to study effects of CAV1 KO on cocaine-induced plasticity. Whole-cell patch-clamp recordings were performed to determine effects of chronic cocaine (15 mg/kg) on medium spiny neuron excitability. To test for deficits in behavioral plasticity, we examined the effect of CAV1 KO on locomotor sensitization. RESULTS:Disruption of CAV1 expression leads to baseline differences in medium spiny neuron (MSN) structural morphology, such that MSNs derived from CAV1 KO animals have increased dendritic arborization when cultured with cortical neurons. The effect was dependent on phospholipase C and cell-type intrinsic loss of CAV1. Slice recordings of nucleus accumbens shell MSNs revealed that CAV1 deficiency produces a loss of neuronal plasticity. Specifically, cocaine-induced firing rate depression was absent in CAV1 KO animals, whereas baseline electrophysiological properties were similar. This was reflected by a loss of cocaine-mediated behavioral sensitization in CAV1 KO animals, with unaffected baseline locomotor responsiveness. CONCLUSIONS:This study highlights a critical role for nucleus accumbens CAV1 in plasticity related to the administration of drugs of abuse.
journal_name
Psychopharmacology (Berl)journal_title
Psychopharmacologyauthors
Eisinger KRT,Chapp AD,Swanson SP,Tam D,Lopresti NM,Larson EB,Thomas MJ,Lanier LM,Mermelstein PGdoi
10.1007/s00213-020-05564-2subject
Has Abstractpub_date
2020-09-01 00:00:00pages
2673-2684issue
9eissn
0033-3158issn
1432-2072pii
10.1007/s00213-020-05564-2journal_volume
237pub_type
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