Mechanisms of lateralized hyperactivity following focal brain injury in the rat.
Recent work in this lab which explores the differential behavioral and neurochemical changes following left versus right cerebral damage is reviewed and neural mechanisms which may account for this asymmetry are proposed. Damage to the right frontoparietal cortex in rats, caused by either ischemia or suction, produces hyperactivity for as long as a month after surgery. These lesions also produce decreases in norepinephrine (NE) levels in both ipsilateral and contralateral cortex and in the locus coeruleus. Similar lesions in the left cortex, however, do not produce these behavioral or biochemical changes. Similar lateralized responses have also been produced by intracortical injections of NE neurotoxins, by cortical island lesions, by destroying cortical efferents, and by producing lesions in the nucleus accumbens, which receives a cortical input. These lateralized responses suggest that the neural mechanisms that mediate this phenomenon include both cortical and subcortical components. It is proposed that the neuroanatomical asymmetry is in either accumbal efferents or their postsynaptic connections.
D000818:Animals; D002561:Cerebrovascular Disorders / Q000503:physiopathology*; D004292:Dominance, Cerebral / Q000502:physiology*; D004298:Dopamine / Q000502:physiology; D005625:Frontal Lobe / Q000098:blood supply; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009434:Neural Pathways / Q000503:physiopathology; D009638:Norepinephrine / Q000502:physiology; D010296:Parietal Lobe / Q000098:blood supply; D051381:Rats; D011919:Rats, Inbred Strains; D009435:Synaptic Transmission
D004298:Dopamine; D009638:Norepinephrine