Unilateral temporal lobectomy to treat seizure disorders in humans often results in cognitive impairment after the surgery. To determine the potential utility of a rodent model of unilaterally induced cognitive deficits, the present experiment evaluated spatial cognition in adult rats after either left or right hemisphere lesioning of temporal neocortex and underlying hippocampal regions. Evaluation of performance in the eight arm radial maze revealed that both lesioned groups committed more reference memory errors than did nonoperated controls. Working memory errors did not differ statistically between groups. The production of a spatial learning deficit by unilateral damage suggests that this rodent model could serve to test potential improvements in interventional strategies aimed at attenuating cognitive effects of the surgical treatment.
Pathological changes in the hippocampal formation have been noted in schizophrenic patients and manipulation of neurochemical functions within the limbic system has been shown to yield behavioral changes consistent with schizophrenia. The present study evaluated the impact of kainic acid induced hippocampal cellular damage and manipulation of NMDA receptor function (agonism and antagonism) on common behavioral markers of schizophrenia (habituation and prepulse inhibition of the acoustic startle response in rats). Cellular damage significantly impaired habituation and NMDA antagonism disrupted prepulse inhibition. Damage induced impairment of habituation is consistent with effects on latent inhibition (which is also unaffected by NMDA antagonism) while the antagonist disruption of prepulse inhibition is consistent with effects on associative plasticity. The current findings provide further support for a diverse neurobiological substrate of schizophrenic symptoms suggesting that pharmacologic intervention may need to be multifaceted and could involve competing mechanisms. Cognitive impairments may reflect diminished NMDA receptor function whereas positive symptoms may reflect heightened engagement of anatomically disturbed cellular elements.
Corticosteroids appear to be involved in a variety of cognitive processes. The present research examined their role during extinction of an appetitive instrumental response in rats. In the first experiment, a high negative correlation was documented between the magnitude of the corticosterone level evoked by removal of reinforcement and the number of behavioral responses given during the session. In the second experiment, administration of exogenous corticosterone decreased the number of behavioral responses occurring during the extinction session; dexamethasone had no significant effect. It would appear possible that the behavioral effects reflect corticosterone mediated changes in neuronal activity within brain structures contributing to learning and memory processes. Thus, in appetitive instrumental conditioning, corticosterone levels are elevated by a removal of reinforcement (extinction) and may contribute to the suppression or decay of the previously reinforced behavioral response.A relation between stress-related hormones and associative learning has long been noted. Elevated levels of ACTH and/or corticosterone have been linked to facilitated acquisition of learned responses in shuttlebox avoidance
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