Prestimulus effects on startle magnitude: Sensory or motor?

Abstract

Startle may be inhibited when the startling event is preceded by a stimulus; this is called prepulse inhibition (PPI) when the prestimulus is weak and nonstartling (s) and paired pulse inhibition when the prestimulus elicits startle (S1). The authors examined the relationship of these measures across species and tested whether paired pulse inhibition--like PPI--is independent of the startling effects of the prestimulus. PPI (s-S1 configuration) and paired pulse inhibition (S1-S2 configuration) were elicited in 1 test, using similar stimulus parameters in rats and humans. The amount of PPI and paired pulse inhibition was significantly correlated within subjects in both rats and humans. Paired pulse inhibition was not diminished when the startling effects of S1 were eliminated by a weak prepulse (s-S1-S2 configuration), nor was it enhanced when these prepulse effects were eliminated by the dopamine agonist apomorphine (in rats). Despite apparent differences in the inhibitory processes mediating PPI and paired pulse inhibition, both are independent of the motoric response to the prestimulus.

Neural network model of prepulse inhibition.

“…In this section we present verification that the model is able to describe, without any changes, other experimental results (Blumenthal, 1995;Swerdlow et al, 2002).…”

“…Startle magnitude in rats when two paired startle pulses (S1-S2) are presented at different intervals, when the paired pulses are preceded by a prepulse (s-S1-S2), and when one pulse is preceded by a prepulse (s-S1). Top: Data from Swerdlow et al (2002, Figure 3a). From Swerdlow, N., Shoemaker, J., Stephany, N., Wasserman, L., Ro, H., & Geyer, M. (2002).…”

Effects of amantadine and bromocriptine on startle and sensorimotor gating: parametric studies and cross-species comparisons

“…This finding suggests a divergence in the neural substrates regulating these two forms of prestimulus effects. Whether such a divergence applies to other measures of sensorimotor or sensory gating, e.g., paired-pulse inhibition (Peak 1939;Smith and Lees 1989) or suppression of P50 event-related potentials ("P50 gating") (Freedman et al 1996), is a question that can be answered using paradigms that simultaneously assess multiple measures of gating (Light and Braff 2001;Swerdlow et al 2002b). Most generally, however, this finding supports the notion that, despite structural similarities in stimulus delivery or response acquisition, measures of "gating" cannot be assumed to be assessing features of a common, unified brain inhibitory process.…”

Dendritic distributions of dopamine D1 receptors in the rat nucleus accumbens are synergistically affected by startle-evoking auditory stimulation and apomorphine

“…The changes in D1R distributions in rats receiving AS are most likely due to the high intensity AS (120 dB pulse), and not the low intensity prepulses, since prepulses themselves do not elicit motor responses (Hoffman and Searle, 1965;Swerdlow et al, 2002). Furthermore, high intensity pulses, when presented alone, produce a significant decrease in extracellular dopamine levels in the Acb, but this change is inhibited when a prepulse precedes the pulse (Humby et al, 1996).…”

“…Furthermore, they specifically identify the dendrites and spines in the Acb shell as the major neuronal compartments in which D1R distributions are most dynamically affected by sensory activation subject to dopamine modulation. There is no animal model for a complex psychiatric illness such as schizophrenia, but apomorphine-induced PPI disruption in rats provides a model of sensorimotor gating deficits seen in schizophrenia patients (Geyer et al, 2001;van den Buuse et al, 2005). The apomorphine-and AS-evoked redistribution of D1R in the Acb may significantly change striatal outputs affecting cortical activities that contribute to the sensorimotor gating deficit (Steiner and Kitai, 2000).…”