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- Title
Dopamine Restores Limbic Memory Loss, Dendritic Spine Structure, and NMDAR-Dependent LTD in the Nucleus Accumbens of Alcohol-Withdrawn Rats.
- Authors
Cannizzaro, Carla; Brancato, Anna; Talani, Giuseppe; Biggio, Giovanni; Sanna, Enrico; Mulas, Giovanna; Saturnino Spiga; De Luca, Maria Antonietta; Sanna, Angela; Marino, Rosa Anna Maria; Diana, Marco
- Abstract
Alcohol abuse leads to aberrant forms of emotionally salient memory, i.e., limbic memory, that promote escalated alcohol consumption and relapse. Accordingly, activity-dependent structural abnormalities are likely to contribute to synaptic dysfunctions that occur from suddenly ceasing chronic alcohol consumption. Here we show that alcohol-dependent male rats fail to perform an emotional-learning task during abstinence but recover their functioning by L-3,4-dihydroxyphenylalanin (i.-DOPA) administration during early withdrawal. l-DOPA also reverses the selective loss of dendritic "long thin" spines observed in medium spiny neurons of the nucleus accumbens (NAc) shell of alcohol-dependent rats during abstinence, as well as the reduction in tyrosine hydroxylase immunostaining and postsynaptic density-95-positive elements. Patchdamp experiments in NAc slices reveal that both in vivo systemic l-DOPA administration and in vitro exposure to dopamine can restore the loss of long-term depression (LTD) formation, counteract the reduction in NMDAR-mediated synaptic currents and rectify the altered NMDAR/AMPAR ratio observed in alcohol-withdrawn rats. Further, in vivo microdialysis experiments show that blunted dopaminergic signaling is revived after l-DOPA treatment during early withdrawal. These results suggest a key role of an efficient dopamine signaling for maintaining, and restore, neural trophism, NMDA-dependent LTD, and ultimately optimal learning.
- Publication
Journal of Neuroscience, 2019, Vol 39, Issue 5, p929
- ISSN
0270-6474
- Publication type
Article
- DOI
10.1523/JNEUROSCI.1377-18.2018