PubMed2004
The human P1/P50 midlatency auditory evoked potential and the auditory startle response (SR) have been used for investigating sensory gating and sensorimotor modulation which is impaired in various psychiatric diseases. In the present study, we demonstrated that auditory stimulation was capable of eliciting excitation of flexor and extensor neurograms from the hindlimb nerves in the paralyzed decerebrate cat, a phenomenon which corresponds to a "fictive" startle response (FSR). Previous studies have shown that the SR consists of distinct excitatory components, "early" and "late", separated by an inhibitory phase. However, in the FSR, unlike the SR in the intact preparation, the "late" excitatory phase never occurred. Recordings from the pedunculopontine nucleus (PPN) simultaneously with the FSR revealed the presence of an auditory evoked potential at a 20-25 ms latency, presumably the depth-recorded equivalent of the vertex-recorded wave A, which has been shown to be the feline equivalent of the human P1 potential. The depth-recorded wave A appeared to share neurological substrates with the excitatory phase of the FSR, since both responses were facilitated in a similar manner by increasing stimulus duration. We previously reported that, in the intact rat, the vertex-recorded P13 potential, the putative rodent equivalent of the human P1 potential, is generated, at least in part, by outputs of the PPN, and that the P13 potential shares neurological substrates with the "early" excitatory phase of the SR. Taken together, the results of the present study indicate that, along with the SR and the P13 potential in the intact rat, the FSR and the depth-recorded wave A in the paralyzed cat may be unique animal models for further examining, in the absence of neural structures rostral to the precollicular decerebration, the cellular basis of startle behavior.