ABSTRACT

The development of lead stimulus modification of startle is characterized by increasing inhibitory and decreasing facilitatory modification during the childhood years. Inhibitory lead stimulus modification of startle is particularly weak during a stage of neurophysiological development that involves increased reactivity to stimuli at both cortical and subcortical levels. This neurophysiological stage, occurring during the preschool years, coincides with the Piagetian stage of preoperational behavior. Lead stimulus modification of startle matures during a period of cortical remodeling and other structural brain changes in association with other neurophysiological changes suggestive of the maturation of both cortical and subcortical inhibitory processes. This neurophysiological stage, occurring during the grade-school years, coincides with the Piagetian stage of concrete operations.

In contrast to lead stimulus modification of startle, mature rates of habituation of startle are already achieved during the preschool years. P300 responses to startling stimuli in school-age children show mature lead stimulus modification and habituation, as does the startle response itself. Attentional and affective modification of startle is different in children than in adults, but the direction of differences is inconsistent and requires further study. Autonomic, myogenic, and electroencephalography activity accompanying startle habituation in children do not habituate; heart rate increases as startle habituates, suggesting a state of arousal accompanying startle habituation. These relationships have not been studied in adults.

ABSTRACT

Studies of the neural basis of short lead interval startle modification have been one extension of the anatomical and behavioral “mapping” of the “primary startle circuit.” The neural substrates of prepulse inhibition (PPI) – an operational measure of sensorimotor gating – are studied partly because several neuropsychiatric disorders are characterized both by deficits in PPI and by clinical evidence of impaired inhibition of cognitive, sensory, or motor information. Brain regions implicated in the pathophysiology of these disorders – limbic cortex, ventral striatum, pallidum, and pontine tegmentum – critically regulate PPI. The neurochemistry of PPI includes neurotransmitters that subserve this circuitry, particularly dopamine, glutamate, serotonin, acetylcholine, and gamma-amino-butyric acid; specific neuropeptides also appear to regulate PPL These neural substrates have been studied via traditional neuropharmacological techniques in laboratory rats, via studies of PPI in specific patient populations, and via developmental and genetic manipulations. Collectively, these studies may identify perturbations of brain function in this circuitry that lead to deficits in PPI – such as those observed in schizophrenia and other disorders – and, conversely, what interventions might act at each level of the circuitry to enhance or restore normal levels of sensorimotor gating.

ABSTRACT

This chapter describes the neural pathways involved in the acoustic startle reflex itself and those involved in modification of startle by fear and stress. In the rat, the primary acoustic startle pathway probably involves three synapses onto (1) cochlear root neurons, (2) neurons in the nucleus reticularis pontis caudalis, and (3) motoneurons in the facial motor nucleus (pinna reflex) or spinal cord (whole body startle). The excitatory amino acid glutamate may well mediate startle at each of the three central synapses along the acoustic startle pathway. Startle can be potentiated by eliciting the reflex in the presence of a cue that has previously been paired with shock. This effect is blocked by chemical lesions or chemical inactivation of the amygdala. Very high levels of fear may fail to lead to increased startle because of activation of a brain area (the periacqueductal gray) which produces active escape behavior incompatible with startle. Startle also can be increased by sustained exposure to bright light or intraventricular administration of the stress peptide corticotropin-releasing hormone. These effects depend on a brain area called the bed nucleus of the stria terminalis. These results suggest that different brain areas may be involved in short-term increases in startle, akin to stimulus-specific fear, versus longer-lasting increases in startle, akin to anxiety.

ABSTRACT

Although affective modification of the startle reflex is a robust phenomenon, it does not occur universally. Research is reviewed suggesting that affective startle modification varies systematically in relation to affective trait dispositions and clinical diagnosis of anxiety, mood, and schizophrenia spectrum disorders. Evidence supports a reliable association between high trait fearfulness and enhanced startle modification by affective valence. Findings for other affective individual differences are thus far only suggestive. Despite the fact that much interest in startle stems from reports of exaggerated startle in posttraumatic stress disorder (PTSD), the precise pattern of startle reactivity and modification in this disorder remains uncertain. Nevertheless, recent studies of affective startle modification in PTSD, as well as in schizophrenia and depression, have yielded provocative results that may ultimately inform our understanding of these disorders. The review emphasizes the need to use a range of affect manipulations and modification paradigms, more powerful research designs, and more appropriate statistical comparisons in future research in this area.

ABSTRACT

Disorders of the inhibitory control of attention have long been noted in schizophrenia spectrum patients. Operational, behavioral techniques were first applied to the construct of impaired sensory filtering in schizophrenia in the 1970s. Braff et al. (1978) noted Frances Graham's (1975) observation of short lead interval inhibition in normal subjects, and hypothesized, then demonstrated, that schizophrenia patients have diminished short lead interval inhibition reflecting impaired gating. Although originally thought to reflect an automatic, preattentive sensorimotor gating function, Dawson et al. (1993) demonstrated that short lead interval inhibition is modulated by attention and may represent a state-independent vulnerability marker for schizophrenia. The findings of impaired short lead interval inhibition in schizotypal subjects (Cadenhead et al., 1993), in conjunction with confirmation of a theoretical link between impaired short lead interval inhibition and thought disorder in schizophrenia patients (Perry & Braff, 1994), added further support to the notion that impaired short lead interval inhibition reflects a trait-linked deficit in sensorimotor gating in schizophrenia spectrum individuals. The neural basis of sensorimotor gating deficits in rats is now better understood, allowing the study of proposed brain abnormalities in schizophrenia patients in animal models. Future directions in application of short lead interval inhibition techniques to schizophrenia spectrum research will continue to include parallel animal model research in conjunction with studies of medication effects, gross and specific psychopathology, gender, laterality, family studies, and attentional manipulation in schizophrenia spectrum populations.

ABSTRACT

Startle modification refers to a set of reliable and ubiquitous phenomena. Specifically, the startle modification phenomena include the inhibition and facilitation of the startle reflex by nonstartling stimuli that accompany or precede the startle-eliciting stimulus. This chapter introduces these phenomena through historical examples drawn from both the human and nonhuman animal literature. Both the inhibition and the facilitation of the startle reflex are illustrated. The standard terms used throughout this book – “startle stimulus,” “lead stimulus,” and “lead interval” – are defined by reference to these prototypical examples. Potential implications of startle modification phenomena are identified for cognitive science, neuroscience, and clinical science, with special emphasis on integrative implications. Finally, the book is outlined with reference to each of the subsequent chapters.

ABSTRACT

Neuroscientists such as Kandel (1978) and Thompson (1986) have exploited the behavioral and neuranatomical simplicity of reflexes in their development of reductionistically approachable model systems of learning and memory. It is argued in this chapter that the field of attention and performance would similarly benefit from the development of a simple model system based on startle and related reflexes. Representative studies are reviewed with respect to the three attentional subsystems distinguished by Posner and Petersen (1990) – the orienting, alerting, and executive networks. To integrate data from reflexology into the broader field of cognitive neuroscience, information processing models that incorporate a vertical architecture are recommended.

ABSTRACT

Startle modification at long lead intervals has been assessed during orienting to signal stimuli and during Pavlovian conditioning to investigate attentional and emotional processes in humans. The results obtained in studies of orienting are not consistent with the assertion that startle is inhibited if attentional resources are allocated to a modality that is different from the one in which the startle-eliciting stimulus is presented. Research in Pavlovian conditioning that focused on the effects of emotion on startle modification has replicated the fear-potentiated startle effect observed in nonhuman animals. Research in both realms provides strong evidence that attentional and emotional processes interact to affect startle.

ABSTRACT

In this chapter we review typical paradigms employed in investigations of startle modification at long lead intervals. We also summarize some of the basic phenomena associated with long lead interval startle modification. Such phenomena include the facilitation or inhibition of startle magnitude as a function of lead stimulus intensity and duration, cardiac deceleration, the modalities of the lead stimulus and the startle probe, whether participants are instructed to attend to or ignore the lead stimulus, and the emotional valence and arousal of the lead stimulus. Both relevant animal and human studies are reviewed, some of which have appeared previously only in doctoral dissertations. In addition, we discuss some of the conceptual issues that have driven much of this research, highlighting particular controversies that have received more attention, such as whether the relationship between lead stimulus intensity and startle amplitude is actually an inverted-U function, and what are the relative contributions of attentional and emotional processes in long lead startle modification.