Effects of dopamine depletion on the morphology of medium spiny neurons in the shell and core of the rat nucleus accumbens

Abstract

Nucleus accumbens receives a dense dopaminergic innervation which is important in regulating motivated states of behavior such as goal- directed actions, stimulus-reward associations and reinforcement of addictive substances. The shell and core territories of this nucleus each receive functionally and morphologically distinct dopaminergic inputs and lesions of the ascending pathways totally deprive the core but not the shell of dopaminergic fibers. Medium spiny neurons are the principal targets of dopaminergic terminals. The present study explored whether the loss of dopamine inputs can affect these neurons and whether cells in the shell and core would be equally susceptible to such a loss. Intracellular injection in fixed slices and neuronal reconstruction were used to analyze the dendritic trees of 62 neurons in the shell and core of animals that received a unilateral, chronic 6- hydroxydopamine lesion of the medial forebrain bundle. In the dopamine- depleted core, dendrites are significantly shorter (16% decrease) than in the intact core and in both the dopamine-depleted core and lateral shell, dendrites are less spiny than in respective control regions. Dopamine loss in the medial shell is associated with significantly more tortuous dendrites that are lower in spine density. However, the number of spines is not reduced which may mean that the increase recorded for segment length, although insignificant in tests, could be responsible for the change in spine density. These data suggest that the loss of dopamine can affect accumbal neuronal morphology and, moreover, can affect neuronal structures differentially in the shell and core.

Dendritic distributions of dopamine D1 receptors in the rat nucleus accumbens are synergistically affected by startle-evoking auditory stimulation and apomorphine

“…This possibility is supported by studies showing that Acb medium spiny neurons are structurally plastic. Dopamine depletion, psychostimulants and dyskinesia are all known to alter spine density and dendritic branching in Acb dendrites (Meredith et al, 1995;Robinson and Kolb, 1999;Meredith et al, 2000). In our study, however, less than one hour elapsed between AS and processing of brain tissue, and most reported changes in dendritic architecture occur after chronic manipulations.…”

A neuroinductive biomaterial based on dopamine

“…In contrast, the filopodium density was lower for analogous neurites on PCY (1.38 Ϯ 0.707 filopodia per 10-m neurite). Low dopamine levels are known to cause a reduction of dendritic spine density in dopaminoceptive neurons (37). The higher filopodium density on PCD indicated that the catecholamine functional groups could induce unique responses in differentiated PC12 cells.…”

Cocaine-induced proliferation of dendritic spines in nucleus accumbens is dependent on the activity of cyclin-dependent kinase-5

“…Thus, changes in Cdk5 activity within nerve terminals of NAc could alter neurotransmitter release that, in turn, could change spine density. Dendritic spines are highly responsive to fluctuations in dopaminergic and glutamatergic transmission (Meredith et al, 1995;Segal and Andersen, 2000;Robinson et al, 2001). Postsynaptically, Cdk5 can modulate D1/cAMP/PKA/DARPP-32 intracellular signaling and regulate NMDA receptor function (Bibb et al, 1999a,b;Li et al, 2001).…”