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We have previously demonstrated that exposing rats to cold (5°C)for 3-4 weeks potentiates the increase in extracellularnorepinephrine (NE) in the medial prefrontal cortex produced by acute tail shock. In the present study, we used microdialysis to determine the duration of cold exposure required to produce this sensitization and explored the mechanism of the phenomenon. Tail shock elicited a twofold greater increase in extracellular NE in the medial prefrontal cortex of rats exposed to cold for 2 weeks than in naive control rats or in rats exposed to cold for 1 week and tested either immediately or after a 2-week delay. Local infusion of 10 pM D-amphetamine or 30 mM Kĩncreased extracellular NE in the medial prefrontal cortex (.-~350and 190%, respectively) comparably in control rats and rats exposed to cold for 3 weeks. In contrast, intraventricular administration of 3.0 pg of corticotropin-releasing hormone increased extracellular NE in the medial prefrontal cortex by 65% in rats exposed to cold for 2 weeks, but only 35% in control rats. These results indicate that an enhanced responsiveness of noradrenergic neurons to acute tail shock (1) requires -~2weeks of cold exposure to develop and (2) may be mediated by a change at the level of the noradrenergic cell bodies rather than the nerve terminals.

Pyrithiamine-induced thiamine deficiency (PTD) in rats is used to model the etiology, diencephalic neuropathology, and memory deficits of Korsakoff's amnesia. We assessed the performance of rats exposed to PTD on a test of object recognition--nonrecurring-items delayed nonmatching-to-sample (DNMS). PTD produced thalamic lesions similar to those of Korsakoff's amnesics and similar to those previously observed in PTD rats. PTD rats required more trials to master DNMS at a 4-s retention delay than did controls, and after they had done so, they performed more poorly than controls at delays of 15, 30, 60, and 120 s. DNMS deficits were also observed in PTD rats that received training prior to PTD treatment. These findings support the validity of the PTD rat model of Korsakoff's disease by demonstrating that PTD rats display object-recognition deficits that are similar to those reported in Korsakoff amnesics.

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