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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.

This study examined the contribution of hypothermia to the effects of chloral hydrate on the flash evoked potential (FEP) of hooded rats. Three experiments were performed, all employing intraperitoneal injections of saline, and of 75, 150 and 300 mg chloral hydrate/kg body weight. In the first experiment, body temperature was measured in a standard (23 degrees C) environment for 6 hr following injection. Rats were hypothermic following administration of the 150 and 300 mg/kg dosages for up to 1 and 2 hr, respectively. In the second experiment, FEPs were recorded from the visual cortex of chronically implanted rats 30 min after injection (22 degrees C environment). P1N1, N1P2 and P2N2 amplitudes and P1, N1, P2, N2 and P3 peak latencies were significantly increased by the 300 mg/kg dosage. Increased latencies were also noted for the primary components with the 150 mg/kg dosage. The final experiment replicated the second experiment, but at an ambient temperature of 30 degrees C, which prevented hypothermia. Amplitudes were unaffected by chloral hydrate. Significantly increased peak latencies were observed, even with the 75 mg/kg dose for some components. However, the magnitude of the latency increases of the primary components was less than half of that found with a standard environment. These results indicate that depending upon ambient temperature, hypothermia may contribute to chloral hydrate-induced alterations in FEPs.

Studies are reviewed that support the hypothesis that infantile autism results from a neuropathology of the temporal lobes of the brain. First, there are parallels between symptoms noted in autism and those found in the Kluver-Bucy and amnesic syndromes. Second, there is a similarity between developmental dysphasia and autism. Third, the formation of cross-modal associations may be deficient in autistic children, a symptom resembling aspects of Geschwind's disconnection syndromes. Finally, a large number of organic factors have been associated with the development of autism, some of these having specific implications for temporal lobe involvement. It is concluded that the main autistic symptoms are most consistent with a neurological model involving bilateral dysfunction of the temporal lobes. Individual differences in the extent of bilateral involvement and/or other coexistent neuropathologies could contribute to the heterogeneity of the autistic population.

This study examined the effects of ethanol on photic evoked potentials recorded from the dorsal lateral geniculate nucleus (LGN) and midbrain reticular formation (MRF) of chronically implanted albino rats. Animals were given intraperitoneal injections of saline, or of 0.5, 1.0, 1.5 or 2.5 g ethanol/kg body weight on separate days. Evoked potentials were recorded at 5, 20, 40 and 60 min following injection. An early positive component recorded from each structure was depressed in amplitude by only the 2.5 g/kg alcohol dose, while the succeeding negative component was depressed by both the 1.5 and 2.5 g/kg doses. Latencies of both early components in each structure were increased by the 1.5 and 2.5 g/kg alcohol doses. Alcohol doses of 1.0-2.5 g/kg depressed the amplitude of a later positive component in the LGN (latency of 78 msec), but latency was not altered. In contrast, a late positive component in the MRF (latency of 150 msec) was both decreased in amplitude and increased in latency by only the 2.5 g/kg dose. These results on subcortical structures are discussed in relation to alcohol's effects on cortical evoked potentials.

This study examined the effects of alcohol on visually evoked potentials recorded from the primary visual cortex (VC) and superior colliculus (SC) of chronically implanted rats. Animals were given intraperitoneal injections of saline, and of 0.15, 0.5, 1.0 and 1.5 g ethanol/kg body weight on separate days. Evoked potentials were recorded at 5, 20, 40, and 60 min following injection. There were differential effects of both alcohol and habituation on the early versus late VC components. The amplitudes of the late components decreased over time and were also depressed by both the 1.0 and 1.5g/kg doses of alcohol. Amplitudes of the early components increased over time and were unaffected by the 1.0g/kg alcohol dose. The 1.5g/kg dose depressed the early negative component but augmented the early positive component. In contrast to the amplitudes, the latencies of both early components were increased at both the l.0 and 1.5g/kg doses. However, the latency of the late positive component was increased at only the 1.5 g/kg dose, while the latency of the late negative component was unaffected by any alcohol dose. In the SC, the peak amplitude of the early positive complex was unaffected by either habituation or alcohol. However, both the amplitude and latency of a later negative component (latency of 52 msec) were affected by alcohol. The 1.0 and 1.5g/kg doses decreased peak amplitude, while the latency was increased at the highest dose. These effects of alcohol on the SC component were in directions opposite to those resulting from habituation.

Photic evoked potentials were recorded from the primary visual cortex (VC) and superior colliculus (SC) of chronically implanted rats. Animals were given intraperitoneal injections of saline, 1.5 and 2.5 g ethyl alcohol/kg body weight on separate days. Evoked potentials were recorded at 5, 20, 40 and 60 min following injection. The amplitudes of all of the VC components except P2 (latency of 52 msec) were depressed to some extent by both doses of alcohol. In contrast, the amplitude of component P2 was increased by both alcohol doses. In the SC, the peak amplitudes of two individual components of the early positive complex were diminished by both doses of alcohol, as was a later negative component. A series of late oscillatory potentials recorded from the SC were minimally depressed by the 1.5 g/kg dose of alcohol, but showed a more prolonged depressant effect at the higher dose. Both doses of alcohol produced reliable increases in peak latency for the primary components in the VC and SC.

The effects of ketamine on photic evoked potentials, recorded from the superior colliculus, were determined in hooded rats. Animals were given intraperitoneal injections of saline, or of 1, 10, 50 or 100 mg ketamine/kg body weight on separate days. Evoked potentials were recorded at 5, 20, 40 and 60 min following injection. Individual components in an early positive complex were augmented by the 100 mg/kg dose. Following administration of the 50 and 100 mg/kg doses, a positive spike (latency of 53 msec) emerged from the middle of a negative wave. A second positive spike (latency of 65 msec) also became prominent at these doses. Late oscillatory potentials were slightly augmented by the 100 mg/kg dose of ketamine. The relationship between these effects of ketamine on photic evoked potentials, and the postanaesthetic psychological manifestations of ketamine, is yet to be determined.

Flash and click evoked potentials were recorded from the same electrode in the midbrain reticular formation of hooded rats. Animals were given i.p. injections of saline, 0.25, 0.5, 1.0 or 2.0 g ethanol/kg body wt. on separate days. The click data demonstrated both a biphasic effect of ethanol and an enhanced sensitivity relative to the flash data. It is suggested that differing evoking stimuli may sample the activity of functionally different populations of neurons within the reticular formation.

The effects of alterations in body temperature on flash and pattern reversal evoked potentials (FEPs and PREPs) were examined in hooded rats whose thermoregulatory capacity was compromised with lesions of the preoptic/anterior hypothalamic area and/or cold restraint. Body temperature, measured with a rectal thermometer, was manipulated via exposure to different ambient temperatures. To describe the data, a model was used in which both linear and quadratic relationships could be estimated. PREP amplitudes were not significantly influenced by body temperature over the range of 27-42 degrees C, although in one experiment FEP amplitudes did show a linear decline as temperatures fell below approximately 30 degrees C. Both FEP and PREP latencies were strongly influenced by temperature and became progressively longer as body temperature was lowered. The non-linear component affecting latencies became more prominent as body temperature decreased. These data demonstrate the temperature dependence of FEP and PREP latencies independent of anesthetic or other drugs.

Flash evoked potentials were recorded from the superior colliculus of chronically implanted hooded rats at 5 and 20 min following IP injections of saline, ketamine (75 mg/kg), naloxone (10 mg/kg), or physostigmine (0.4 mg/kg) on separate days. Components in an early positive complex were unaffected by ketamine and naloxone, but were reduced in amplitude by physostigmine. A positive spike emerged from the middle of a later negative wave following ketamine administration, but the amplitude of the negative wave was unaltered by naloxone or physostigmine. A succeeding positive component was enhanced by both ketamine and physostigmine. Physostigmine produced the most consistent alterations in latency, with most components increasing in latency. Naloxone pretreatment did not alter ketamine's influence on evoked potential amplitudes. Pretreatment with physostigmine briefly decreased the amplitude of the ketamine-induced positive spike, augmented the amplitude of the succeeding positive component, and also increased most peak latencies. Ketamine, naloxone and physostigmine all produced approximately equivalent hypothermia. Physostigmine, but not naloxone, pretreatment augmented the ketamine-induced hypothermia. The body temperature data suggest that some of the observed latency alterations are secondary to hypothermia. The amplitude data indicate that ketamine and physostigmine produce a combination of similar, distinct, and antagonistic effects on evoked potentials.

The effects of ketamine on locomotion in an open-field were determined in hooded rats. Animals were given intraperitoneal injections of saline, or of 1, 10, 50 or 100 mg ketamine/kg body weight on separate days. Open-field behavior was examined for 60 min following injection. The 50 mg/kg dose of ketamine produced an increase in locomotion which peaked approximately 30 min after injection. A cataleptic immobility produced by the 100 mg/kg dose was followed by postanesthetic locomotion. The ketamine-induced locomotion consisted largely of ambulation about the perimeter of the field and was accompanied by ataxia, but included relatively little tight circling (rotation) during the peak of activity. Comparisons with the results of past research suggests that test-chamber design influences the type of locomotion induced by ketamine.

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.

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.

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.