Persistent Alterations in Dendrites, Spines, and Dynorphinergic Synapses in the Nucleus Accumbens Shell of Rats with Neuroleptic-Induced Dyskinesias

摘要: Chronic treatment of humans or experimental animals with classical neuroleptic drugs can lead to abnormal, tardive movements that persist long after the are withdrawn. A role in these neuroleptic-induced dyskinesias may be played by a structural change shell nucleus accumbens where opioid peptide dynorphin is upregulated treated rats show vacuous chewing (VCMs). The normally contains dense plexus dynorphinergic fibers especially its caudomedial part. After 27 weeks haloperidol administration and 18 withdrawal, immunoreactive labeling this intensified when compared vehicle treatment. In addition, medium spiny neurons here significant increase spine density, dendritic branching, numbers terminal segments. VCM-positive animals, surface area reduced, dynorphin-positive terminals contact more spines form asymmetrical specializations than do those without syndrome (VCM-negative vehicle-treated groups). Persistent, oral could therefore caused incontrovertible alterations, involving remodeling sprouting, synaptic connectivity accumbal shell.