Operant photic evoked potential control, unmediated by selective orientation.
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Biomedical subjects
Publications and source records attributed to B E Hetzler.
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Rats were rewarded for signaling large and small sensory evoked components with appropriate bar presses. Most rats operantly generated large components and correctly signaled only these. Two rats correctly signaled successful and unsuccessful attempts to generate large waves. One rat discriminated component amplitudes without operantly attempting to generate specific wave types.
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Two experiments were conducted to determine the effects of hypothermia and pentobarbital anesthesia, alone and in combination, on the brain-stem auditory evoked responses (BAERs) of rats. In experiment I, unanesthetized rats were cooled to colonic temperatures 0.5 and 1.0 degrees C below normal. In experiment II, 2 groups of rats were cooled and tested at 37.5, 36.0, 34.5 and 31.5 degrees C. One group was anesthetized during testing and the other group was awake. The rat BAER was sensitive to cooling of 1 degree C or less. Peak latencies were prolonged and peak-to-peak amplitudes were increased by hypothermia alone. The effect on amplitude may be related to the time course of temperature change or to stimulus level. Pentobarbital significantly affected both latencies and amplitudes over and above the effects of cooling. The specific effects of pentobarbital differed by BAER peak and by temperature. The findings point up the importance of the potential confound of anesthetic drugs in most of the evoked potential literature on hypothermia and, for the first time, quantify the complex interactions between pentobarbital and temperature which affect the BAER wave form.
Photic evoked potentials were recorded from the visual cortex of chronically implanted albino rats. Since photic evoked potential components are representations of neural pathways which are activated during photic stimulation, study of the effects of alcohol on these components may help to trace pathways which are affected by alcohol. In the present study, evoked potentials were recorded at 5, 20, and 40 min following IP injections of saline, ethanol (2.0 g/kg), physostigmine (0.6 mg/kg) or atropine (15.0 mg/kg) on separate days. Ethanol depressed the amplitudes of most evoked potential components in comparison to saline administration. Component P2, however, was increased in amplitude. Physostigmine briefly reduced the amplitude of most components, including P2. In contrast, atropine increased the amplitudes of components P1 and P2, while decreasing components N1, N2 and N3 for varying durations of time. Physostigmine pretreatment augmented the depressant effect of alcohol on the early components P1 and N1, while attenuating alcohol's influence on components P2 and P3. Pretreatment with atropine likewise further reduced the amplitudes of components P1 and N1, and produced a similar effect on component N3. Atropine, either alone or in combination with alcohol, produced approximately the same degree of enhancement of component P2. In comparison to saline values, all three agents produced reliable increases in peak latency for most of the components, with only N3 showing no effects. The amplitude data from this study suggest that ethanol's augmentation of component P2 may result, at least in part, from alterations in cholinergic functions.
Visual cortex flash evoked potentials (FEPs), pattern reversal evoked potentials (PREPs), and body temperature were measured in hooded rats following IP injections on separate days of saline, and of 15 and 30 mg pentobarbital/kg body weight. Two experiments were performed, differentiated by standard (23 degrees C) and warm (31 degrees C) room temperatures. The 30 mg/kg dose produced hypothermia of 2.6 degrees C in the standard environment, but not in the warm environment. Early components of FEPs were generally increased in amplitude by the 15 mg/kg dose, and decreased by the 30 mg/kg dose at 23 degrees C. At 31 degrees C, the 30 mg/kg dose did not decrease early component amplitude, suggesting that hypothermia can potentiate some effects of pentobarbital. Amplitudes of late FEP components were depressed at both ambient temperatures. The main PREP components N1P1 and P1N3 were increased in amplitude by the 15 mg/kg dose, but returned to near baseline levels at 30 mg/kg, at both temperatures. PREP component N2P2 was reduced in amplitude by the 30 mg/kg dose only at 23 degrees C. Treatment with 30 mg/kg pentobarbital increased FEP and PREP latencies at both ambient temperatures, but the magnitudes of the increases at 31 degrees C were typically less than half those observed at 23 degrees C. These results indicate that hypothermia contributes to some pentobarbital-induced changes in both FEPs and PREPs, but that pentobarbital also produces effects independent of hypothermia.
Sulfolane (tetrahydrothiophene-1, 1-dioxide) is a commercially important solvent. This report describes the consequences of acute exposure to sulfolane upon the visual system, as measured using flash evoked potentials (FEPs) and pattern reversal evoked potentials (PREPs). A single injection of either 1/2 or 1/4, but not 1/8 the IP LD50 (1600 mg/kg) produced significant changes in both FEPs and PREPs which were apparent within 1 hour and lasted longer than 6 hours. Amplitudes of FEP peaks to the first of a pair of stimuli were generally increased compared to control, an effect which was not temperature-dependent. In addition, sulfolane produced an ambient temperature- and dose-dependent hypothermia. Sulfolane increased latencies of FEP and PREP peaks, but attenuating hypothermia eliminated the effect of sulfolane on latencies.