Facilitation of the acoustic startle reflex by ponto-geniculo-occipital waves: effects of PCPA

Abstract

The relationship between ponto-geniculo-occipital (PGO) waves and motor activity during waking and non-rapid eye movement (non-REM) sleep stages was studied in cats treated with the serotonin synthesis inhibitor p-chlorophenylalanine (PCPA). PGO waves appeared in waking after daily treatment with PCPA. The magnitude of the acoustic startle elicited in the absence of prior PGO waves was increased (by a mean of 555%) by the PCPA treatment as compared to that of the pre-drug level. When startle-eliciting stimuli were presented shortly after the occurrence of the PGO wave, the response amplitude was further enhanced as compared to that of the baseline startle. The effect was maximal 50 ms following the peak of the PGO wave (average 192% of the baseline level), with return to the baseline startle level within 200 ms. A similar effect could also be seen with waking eye-movement potentials (EMPs) in drug-naive animals. Over half of the spontaneous PGO waves were found to be preceded or followed by discrete head-body movements. After PCPA, the amplitude of auditory-evoked LGN PGO waves increased during quiet waking (QW) while those in non-REM and REM sleep states did not change. It was concluded that serotonergic systems produce a tonic suppression of startle response and PGO amplitude in waking. PGO spikes in waking are associated with a phasic facilitation of the sensorimotor mechanisms involved in startle.

Fig. 1.

A: spontaneously occurring PGO waves facilitated the subsequently elicited startle response. The facilitation was maximal at 50 ms following the peak of the PGO wave (* P < 0.05, N–K, compared to the control level). The baseline startle amplitude, with no immediate preceding PGO wave, was also increased (555%) by PCPA treatment as compared to the pre-drug level (■) (⁺⁺ P < 0.004, t-test). Note that the pre-drug baseline startle level is shown here as a percentage of the post-drug level. B: eye-movement potentials also tended to facilitate startle response, and the temporal relationship of facilitation was similar to that produced by PGO waves (* P < 0.05, Bonferroni t-test).

Fig. 2.

Spontaneously occurring PGO waves were often accompanied by discrete head-body movements resembling orienting reflexes and measurable by the accelerometer. This is the average of the PGO waves and the accelerometer output of head-body movements of a PCPA-treated cat over 300 randomly selected trials during QW and non-REM sleep states. Auditory stimuli were not presented in this experiment. The magnitude of head-body movements peaked right after the PGO wave, and the lead time of head-body movements over the PGO wave tended to be greater in waking than in non-REM sleep.

Fig. 3.

The amplitude of the auditory-evoked PGO wave was normally greatest in non-REM sleep and the transition to REM sleep, smaller during QW, and smallest during REM sleep and active waking. This relationship changed after PCPA treatment. A is the average of the auditory-evoked PGO responses of a cat before and after PCPA treatments. B compares the average evoked PGO spike amplitude over 3 cats before and after PCPA treatments. The evoked PGO amplitude during QW increased 63% over the pre-drug level (** P < 0.002, simple main effect ANOVA), while those in other states did not change significantly.