Fig. 2.

Characterization of synaptic function in hippocampal slices. A, Representative population spike response in the CA1 pyramidal cell region in a hippocampal slice from an NPY^−/− mouse. Schaffer collaterals were stimulated at 4 × threshold (T) for generation of a population spike. B, Representative population spike response in the GC region in a hippocampal slice from an NPY^−/− mouse. The perforant path was stimulated at 4 × threshold for generation of a population spike. Stimulation protocols elicited typical paired-pulse facilitation of the second population spike response at both Schaffer collateral–CA1 (A) and perforant path–GC synapses (B). Stimulus artifacts are clipped in bothtraces. C, Input–output curves of population spike responses recorded in the CA1 pyramidal cell region (st. pyramidale) to stimulation of the Schaffer collaterals. Threshold for stimulation was defined for each slice as the minimum current required to elicit a detectable population spike (PS); the x-axis shows stimulus intensity in terms of threshold multiples. Responses are normalized with respect to maximumPS amplitude to allow averaging of responses from all slices from NPY-deficient animals (closed diamonds;n = 15) and all slices from littermate wild-type animals (open diamonds; n = 15). The values represent the mean ± SEM. D, Input–output curves of population spike responses recorded in the dentate GC body layer to stimulation of the perforant path. E, Plot of paired-pulse facilitation (amplitude of PS response to second stimulus divided by amplitude of population spike response to first stimulus) in the CA1 pyramidal cell region for hippocampal slices from NPY-deficient (closed diamonds;n = 11) and littermate wild-type control (open diamonds; n = 12) mice; stimulus intensity was at 4× threshold. F, Plot of paired-pulse facilitation in the GC region of hippocampal slices from NPY-deficient and littermate wild-type control mice.