Time‐dependent changes in dopamine agonist‐induced striatal fos immunoreactivity are related to sensory neglect and its recovery after unilateral prefkontal cortex injury

Abstract

This study examined interactions between the corticostriatal glutamatergic system and the nigrostriatal dopaminergic system via immunocytochemical examination of dopamine (DA) agonist induction of the striatal immediate early gene product Fos following cortical injury. After unilateral aspiration of the medial agranular cortex (AGm) region of prefrontal cortex, rats were tested for orientation to visual, tactile, and auditory stimuli. Fos immunoreactivity induced by d-amphetamine (5 mg/kg) or apomorphine (5 mg/kg) was quantified in dorsolateral and ventrolateral regions of caudate-putamen (CPu) in rats still demonstrating sensory neglect (5 days postsurgery) and in rats recovered from sensory neglect produced by AGm ablation (29+ days postsurgery). The pattern of immunoreactivity of rats still demonstrating neglect differed from that of unlesioned rats or recovered AGm-ablated rats. In rats demonstrating sensory neglect, d-amphetamine or apomorphine induction of Fos in the ipsilateral CPu was reduced by about 40% compared to the contralateral CPu or to comparable readings in unlesioned controls. These asymmetries were restricted to dorsolateral CPu, the region receiving the densest input from AGm. In contrast, recovered AGm-ablated rats had DA agonist-induced striatal Fos immunoreactivity that was symmetrical between the two hemispheres and comparable to control values. These findings indicate that adaptations involving the striatal medium spiny neuron, a site of convergence of cortical glutamatergic and nigral dopaminergic afferents, may contribute to recovery from behavioral deficits resulting from neocortical injury.

Amphetamine‐evoked gene expression in striatopallidal neurons: regulation by corticostriatal afferents and the ERK/MAPK signaling cascade

“…Transection of corticostriatal projections reduced amphetamine‐evoked c‐ fos expression in denervated regions of the striatum, consistent with previous reports (Cenci and Bjorklund 1993, 1994; Vargo and Marshall 1995, 1996). The present study extends these findings by demonstrating that the transection specifically altered the ability of amphetamine to engage striatopallidal (Enk+) neurons, leaving the number of amphetamine‐evoked c‐ fos + striatonigral (Enk−) neurons unchanged.…”

Dysregulation of gene induction in corticostriatal circuits after repeated methylphenidate treatment in adolescent rats: differential effects on zif 268 and homer 1a

“…Excitatory cortical output drives psychostimulant‐induced IEG expression in the striatum (Cenci & Björklund, 1993; Vargo & Marshall, 1995; Ferguson & Robinson, 2004) in interaction with striatal dopamine receptor stimulation (Yano et al ., 2006; see e.g. Hyman et al ., 1996, for review).…”

Secondary Motor Cortex: Where ‘Sensory’ Meets ‘Motor’ in the Rodent Frontal Cortex

“…the sudden loss of cortical inputs [39]. In support of diaschisis, lesion of M2 is accompanied by changes in activity-dependent gene expression in the striatum, which correlate with the amount of head turning to sensory cues [40]. Moreover, animals recover faster from M2 lesion if they are subjected to visual deprivation at the same time [41].…”