Abstract
To explore the functional consequences of cannabinoid withdrawal in the rat mesolimbic dopamine system, we investigated the anatomical morphology of the mesencephalic, presumed dopaminergic, neurons and their main post-synaptic target in the Nucleus Accumbens. We found that TH-positive neurons shrink and Golgi-stained medium spiny neurons loose dendritic spines in withdrawal rats after chronic cannabinoids administration. Similar results were observed after administration of the cannabinoid antagonist rimonabant to drug-naïve rats supporting a role for endocannabinoids in neurogenesis, axonal growth and synaptogenesis. This evidence supports the tenet that withdrawal from addictive compounds alters functioning of the mesolimbic system. The data add to a growing body of work which indicates a hypodopaminergic state as a distinctive feature of the “addicted brain”.
Highlights
Clinical reports described that chronic consumers of even low daily doses of cannabis derivatives, experience upon cessation of drug administration, overt abstinence signs [1, 2]
Post hoc analysis revealed that cell bodies in the Ventral Tegmental area (VTA) exhibited smaller somata under both THC withdrawals
The present study shows that withdrawal from a regimen of chronic cannabinoid administration profoundly affects the morphological characteristics of TH-positive neurons of the rat VTA and dendritic spine density of MSN in the NAcc shell
Summary
Clinical reports described that chronic consumers of even low daily doses of cannabis derivatives, experience upon cessation of drug administration, overt abstinence signs [1, 2]. The morphological analysis of neurons [10, 11] has recently seen a widespread increase of the studies concerning consequences of long-term administration of drugs [12,13,14,15] These measures are likely to reflect plasticity of active synapses and, synaptic remodelling as a consequence of experience and/or drug-exposure [12]. In this regard, addiction has been conceptualized as one example of experience-dependent plasticity whereby experience (i.e. long-term exposure to addictive drugs) may affect behavioural, cognitive and psychological functions in a long lasting way [12, 16]
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