R. I. Chaplin

Bio: R. I. Chaplin is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Stimulus (physiology) & Electrophysiology. The author has an hindex of 3, co-authored 3 publications receiving 126 citations.

Long latency event related potentials in rats: The effects of changes in stimulus parameters and neurochemical lesions

Abstract: Animal models of event related potentials (ERPs) have recently been developed in order to gain further understanding of the psychobiological variables which may underlie these brain potentials. In the present study, unanaesthetized rats were utilized in order to evaluate the effects on rat ERP morphology of changes in the auditory stimulus parameters used to elicit these potentials such as tone probability and intensity. In addition, the consequences of reductions in norepinephrine (NE) produced by six-hydroxydopamine (6-OHDA) lesions to the area of the dorsal noradrenergic bundle in ERP wave forms were evaluated. Forty, experimentally naive, male rats chronically implanted with electrodes were used in this study. The results of these studies showed that in all electrode sites (frontal cortex, ventral thalamus, dorsal hippocampus, locus coeruleus) a series of large amplitude potentials in the 10–200 msec latency range could be recorded, some of which were sensitive to changes in the auditory stimulus parameters such as probability and tone intensity. Late positive potentials in the 300–400 msec range could be identified in recordings from the dorsal hippocampus and were found to be sensitive to probability independent of tone intensity. Dorsal noradrenergic bundle lesions were also found to produce significant changes in these rat ERP components. Lesioned animals were found to have increases in amplitude to the early negative potentials (in the 50–100 msec range) in response to frequent tones in cortical leads and decreases in the amplitude of the late positive potentials (in the 300–400 msec range) recorded in hippocampal leads in response to infrequent tones. These findings are consistent with a role for NE in the forebrain in the processing of novel or “selective” stimuli.

Decision making, the P3, and the locus coeruleus-norepinephrine system.

Abstract: Psychologists and neuroscientists have had a long-standing interest in the P3, a prominent component of the event-related brain potential. This review aims to integrate knowledge regarding the neural basis of the P3 and to elucidate its functional role in information processing. The authors review evidence suggesting that the P3 reflects phasic activity of the neuromodulatory locus coeruleus-norepinephrine (LC-NE) system. They discuss the P3 literature in the light of empirical findings and a recent theory regarding the information-processing function of the LC-NE phasic response. The theoretical framework emerging from this research synthesis suggests that the P3 reflects the response of the LC-NE system to the outcome of internal decision-making processes and the consequent effects of noradrenergic potentiation of information processing.

The Role of Glutamatergic Neurotransmission in the Pathophysiology of Alcoholism

Abstract: Recent evidence suggests that ethanol abuse produces its diverse effects on the brain to a substantial degree by disrupting the function of the major excitatory neurotransmitter, glutamate. Ethanol, at concentrations associated with behavioral effects in humans, inhibits the N-methyl-d-aspartate (NMDA) receptor, which mediates the post-synaptic excitatory effects of glutamate. Tolerance to ethanol results in up-regulation of the NMDA receptor so that abrupt withdrawal produces a hyperexcitable state that leads to seizures, delerium tremens, and excitotoxic neuronal death. Ethanol's inhibition of the NMDA receptor in the fetal brain likely contributes to the CNS manifestations of fetal alcohol syndrome. Therapeutic strategies aimed at correcting glutamatergic dysregulation in alcoholism need to be explored.

Glucocorticoids are critical regulators of dendritic spine development and plasticity in vivo

Abstract: Glucocorticoids are a family of hormones that coordinate diverse physiological processes in responding to stress. Prolonged glucocorticoid exposure over weeks has been linked to dendritic atrophy and spine loss in fixed tissue studies of adult brains, but it is unclear how glucocorticoids may affect the dynamic processes of dendritic spine formation and elimination in vivo. Furthermore, relatively few studies have examined the effects of stress and glucocorticoids on spines during the postnatal and adolescent period, which is characterized by rapid synaptogenesis followed by protracted synaptic pruning. To determine whether and to what extent glucocorticoids regulate dendritic spine development and plasticity, we used transcranial two-photon microscopy to track the formation and elimination of dendritic spines in vivo after treatment with glucocorticoids in developing and adult mice. Corticosterone, the principal murine glucocorticoid, had potent dose-dependent effects on dendritic spine dynamics, increasing spine turnover within several hours in the developing barrel cortex. The adult barrel cortex exhibited diminished baseline spine turnover rates, but these rates were also enhanced by corticosterone. Similar changes occurred in multiple cortical areas, suggesting a generalized effect. However, reducing endogenous glucocorticoid activity by dexamethasone suppression or corticosteroid receptor antagonists caused a substantial reduction in spine turnover rates, and the former was reversed by corticosterone replacement. Notably, we found that chronic glucocorticoid excess led to an abnormal loss of stable spines that were established early in life. Together, these findings establish a critical role for glucocorticoids in the development and maintenance of dendritic spines in the living cortex.

The role of the locus coeruleus in mediating the attentional blink: a neurocomputational theory.

Abstract: The attentional blink refers to the transient impairment in perceiving the 2nd of 2 targets presented in close temporal proximity. In this article, the authors propose a neurobiological mechanism for this effect. The authors extend a recently developed computational model of the potentiating influence of the locus coeruleus–norepinephrine system on information processing and hypothesize that a refractoriness in the function of this system may account for the attentional blink. The model accurately simulates the time course of the attentional blink, including Lag 1 sparing. The theory also offers an account of the close relationship of the attentional blink to the electrophysiological P3 component. The authors report results from two behavioral experiments that support a critical prediction of their theory regarding the time course of Lag 1 sparing. Finally, the relationship between the authors’ neurocomputational theory and existing cognitive theories of the attentional blink is discussed.