Prepulse inhibition
The reduction of the amplitude of startle reflects the ability of the nervous system to temporarily adapt to a strong sensory stimulus when a preceding weaker signal is given to warn the organism.
Although the extent of the adaptation affects numerous systems, the most comfortable to measure are the muscular reactions, which are normally diminished as a result of the nervous inhibition.
Deficits of prepulse inhibition manifest in the inability to filter out the unnecessary information; they have been linked to abnormalities of sensorimotor gating.
Such deficits are noted in patients with conditions like schizophrenia and Alzheimer's disease, and in people under the influence of drugs, surgical manipulations, or mutations.
Pulse-alone results are compared to prepulse-plus-pulse, and the percentage of the reduction in the startle reflex represents prepulse inhibition.
By this step, artifacts from eye movements and muscle activity independent of blink responses are removed.
To avoid aliasing artifacts the sampling rate of the signal should be at least 1024 Hz which is larger than twice the upper bound of the bandpass filter (twice the Nyquist frequency).
[6] The magnitude of PPI is often significant, reaching as much as 65% in healthy subjects, with maximum inhibition is typically observed at 120 ms interval.
[15] However a thousandth prepulse also induces inhibition; the phenomenon is highly robust [16] Response and reaction are affected by interval duration and attention.
In one study, normal college students were instructed to attend to one of the kind of prepulses, high- or low-pitched, and ignore the other.
His many papers on the reflex and its modification laid the groundwork for the widespread use of prepulse inhibition today in studies of schizophrenia and other disorders.
[27] Dopamine, which plays a major role in schizophrenia, had been shown to regulate sensorimotor gating in rodent models.
[34][35] Contrary to the predictions, nicotine receptor alpha7 subunit knockout mice do not show disruptions in PPI.
[36] Murine models are widely used to test hypotheses linking genetic components of various diseases with sensorimotor gating.
[38] Schizophrenia-like PPI disruption techniques in rodents have been classified in one review[39] into four models: Diverse chemical compounds are tested on animals with such deficits.
A review of the genetic underpinnings of prepulse inhibition can be found in a meta-analysis conducted by Quednow et al.
[40] Additionally an updated summary of both preclinical and clinical findings with PPI can be found in a recent comprehensive review.
