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Previous research has suggested that the Wistar-Kyoto Hyperactive (WKHA) rat strain may model some of the behavioral features associated with attention-deficit/hyperactivity disorder (ADHD). We have shown that, in cerebellar-dependent eyeblink conditioning, male WKHAs emit eyeblink CRs with shortened onset latencies. To further characterize the shortened CR onset latencies seen in male WKHA rats, we examined 750-ms delay conditioning with either a tone conditional stimulus (CS) or a light CS, we extended acquisition training, and we included Wistar rats as an additional, outbred control strain. Our results indicated that WKHAs learned more quickly and showed a shortened CR onset latency to a tone CS compared to both Wistar-Kyoto Hypertensive (WKHT) and Wistars. WKHAs and Wistars show a lengthening of CR onset latency over conditioning with a tone CS and an increasing confinement of CRs to the later part of the tone CS (inhibition of delay). WKHAs learned more quickly to a light CS only in comparison to WKHTs, and showed a shortened CR onset latency only in comparison to Wistars. Wistars showed an increasing confinement of CRs to the late part of the light CS over conditioning. We used unbiased stereology to estimate the number of Purkinje and granule cells in the cerebellar cortex of the three strains. Our results indicated that WKHAs have more granule cells than Wistars and WKHTs and more Purkinje cells than Wistars. Results are discussed in terms of CS processing and cerebellar cortical contributions to EBC.

Gerbils show a postischemic increase in locomotor activity that correlates to the extent of neuron loss in the hippocampal CA1 subfield. It has been suggested that this hyperactivity is predictive of neuron loss in the CA1. In this study the correlation between postischemic hyperactivity and neuron loss in several hippocampal subfields was investigated, and the theory that the hyperactivity is due to a reduced ability for spatial navigation was evaluated. Significant correlations were found between hyperactivity and neuron loss in several hippocampal subfields; the correlation was stronger for the CA3 than for the CA1 subfield, suggesting that postischemic hyperactivity can be used as a predictor of neuron loss in the CA3 rather than in the CA1. From observations of the pattern of hyperactivity within the test arenas and during the test period, this study challenges the spatial mapping theory of postischemic hyperactivity.