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Christopher L. Stitt

Bio: Christopher L. Stitt is an academic researcher from Bryn Mawr College. The author has contributed to research in topics: Stimulus (physiology) & Startle response. The author has an hindex of 16, co-authored 19 publications receiving 1098 citations.

Papers
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Journal ArticleDOI
TL;DR: Data support the proposition that the lateral tegmental area is involved in the inhibition of the rat's acoustic startle response and cross-modal in that the group with lesions of the lateral Tegmental Area showed decreased inhibition to both acoustic and visual prestimuli.

95 citations

Journal ArticleDOI
TL;DR: The overall configuration of the results suggests that a pathway including the reticulospinal tract and the bulbopontine reticular nuclei could be the major mediator of startle.
Abstract: A series of seven experiments related amplitude and latency of the pigeon's startle response, elicited by an intense visual stimulus, to antecedent auditory and visual events in the sensory environment. The data indicated that (a) within broad limits the amplitude of the reflex is a positive function of the intensity of the sensory background prevailing at the time of startle elicitation, (b) a change in the sensory environment occurring 15-2,000 msec prior to the startle-eliciting stimulus inhibits the amplitude of the response, and (c) a change in the sensory environment less than 10 msec prior to the startle-eliciting stimulus reduces the latency of the response. These findings are consistent with previous research on acoustic elicited startle in the rat. The overall configuration of the results suggests that a pathway including the reticulospinal tract and the bulbopontine reticular nuclei could be the major mediator of startle. In these terms, latency-reduction effects would occur because of partial activation of this pathway, amplitude inhibition would occur because of cerebellar influence, and amplitude facilitation would reflect cerebral or striatal influences.

51 citations


Cited by
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Journal ArticleDOI
TL;DR: In this article, it was shown that downward comparison is a process evoked by negative affect, and that there is considerable evidence for self-enhancing comparison processes, which is involved in several areas of social-psycho logical research.
Abstract: The literature of social psychology contains a number of phenomena that appear to be paradoxical. For example, persons who face a threatening experience prefer to affiliate with threatened others rather than with nonthreatened others (Schachter, 1959), and persons in groups in which reward is equally distributed are less satisfied compared with persons in groups that include one particularly unfortunate member (Brickman, 1975). The purpose of this article is to show that these phenomena are best construed as social comparison processes and that various phenomena derive from one basic process termed downward comparison; the essence of this process is that persons can enhance their own subjective well-being by comparing themselves with a less fortunate other. In this article I show that downward comparison is a process evoked by negative affect, that there is considerable evidence for self-enhancing comparison processes, and that downward comparison effects are involved in several areas of social-psycho logical research.

2,430 citations

Journal ArticleDOI
TL;DR: A review of the literature on prepulse inhibition (PPI) in humans can be found in this article, where a relatively weak sensory event (the prepulse) is presented 30-500 ms before a strong startle-inducing stimulus, and reduces the magnitude of the startle response.
Abstract: Rationale: Since the mid-1970s, cross-species translational studies of prepulse inhibition (PPI) have increased at an astounding pace as the value of this neurobiologically informative measure has been optimized. PPI occurs when a relatively weak sensory event (the prepulse) is presented 30–500 ms before a strong startle-inducing stimulus, and reduces the magnitude of the startle response. In humans, PPI occurs in a robust, predictable manner when the prepulse and startling stimuli occur in either the same or different modalities (acoustic, visual, or cutaneous). Objective: This review covers three areas of interest in human PPI studies. First, we review the normal influences on PPI related to the underlying construct of sensori- (prepulse) motor (startle reflex) gating. Second, we review PPI studies in psychopathological disorders that form a family of gating disorders. Third, we review the relatively limited but interesting and rapidly expanding literature on pharmacological influences on PPI in humans. Methods: All studies identified by a computerized literature search that addressed the three topics of this review were compiled and evaluated. The principal studies were summarized in appropriate tables. Results: The major influences on PPI as a measure of sensorimotor gating can be grouped into 11 domains. Most of these domains are similar across species, supporting the value of PPI studies in translational comparisons across species. The most prominent literature describing deficits in PPI in psychiatrically defined groups features schizophrenia-spectrum patients and their clinically unaffected relatives. These findings support the use of PPI as an endophenotype in genetic studies. Additional groups of psychopathologically disordered patients with neuropathology involving cortico-striato-pallido-pontine circuits exhibit poor gating of motor, sensory, or cognitive information and corresponding PPI deficits. These groups include patients with obsessive compulsive disorder, Tourette's syndrome, blepharospasm, temporal lobe epilepsy with psychosis, enuresis, and perhaps post-traumatic stress disorder (PTSD). Several pharmacological manipulations have been examined for their effects on PPI in healthy human subjects. In some cases, the alterations in PPI produced by these drugs in animals correspond to similar effects in humans. Specifically, dopamine agonists disrupt and nicotine increases PPI in at least some human studies. With some other compounds, however, the effects seen in humans appear to differ from those reported in animals. For example, the PPI-increasing effects of the glutamate antagonist ketamine and the serotonin releaser MDMA in humans are opposite to the PPI-disruptive effects of these compounds in rodents. Conclusions: Considerable evidence supports a high degree of homology between measures of PPI in rodents and humans, consistent with the use of PPI as a cross-species measure of sensorimotor gating. Multiple investigations of PPI using a variety of methods and parameters confirm that deficits in PPI are evident in schizophrenia-spectrum patients and in certain other disorders in which gating mechanisms are disturbed. In contrast to the extensive literature on clinical populations, much more work is required to clarify the degree of correspondence between pharmacological effects on PPI in healthy humans and those reported in animals.

1,649 citations

Journal ArticleDOI
TL;DR: Mise au point sur les explications de certains biais lies aux recherches sur la formation des impressions, and presentation d'un modele fonde sur des indices de categorisation du stimulus for rendre compte de tels Biais as mentioned in this paper.
Abstract: Mise au point sur les explications de certains biais lies aux recherches sur la formation des impressions, et presentation d'un modele fonde sur des indices de categorisation du stimulus pour rendre compte de tels biais

1,419 citations

Journal ArticleDOI
TL;DR: The neuronal basis underlying the mediation of the AsR, as well as the neuronal and neurochemical substrates of different phenomena of enhancement and attenuation of the ASR are described to elucidate the biological background of these forms of behavioral plasticity.

1,244 citations