Bruce E. Hetzler

Acute effects of alcohol on evoked potentials in visual cortex and superior colliculus of the rat

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.

Ketamine-induced locomotion in rats in an open-field.

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.

Dose effects of pentobarbital on evoked potentials in visual cortex and superior colliculus of the albino rat

Abstract This study examined the effects of pentobarbital on photic evoked potentials recorded from the primary visual cortex and superior colliculus of chronically implanted albino rats. Animals were given intraperitoneal injections of saline, and of 3, 6, 9, 18 and 40 mg pentobarbital/kg body weight on separate days. Evoked potentials were recorded at 5, 20, 40 and 60 min following injection. There were differential effects of pentobarbital on the amplitudes of individual visual cortex components. In general, the earliest components were augmented by pentobarbital, the late components were depressed, and the components in the middle of the waveform demonstrated biphasic effects. These middle components were increased in amplitude by one or more of the smaller doses, but were at or below control levels as a result of the 40 mg/kg dose. Increases in peak latency were also found in some components, beginning with the 6 mg/kg dose for the two earliest components, and beginning with the 18 mg/kg dose for the third component. In the superior colliculus, the peak amplitudes of two individual components of the early positive complex reacted in opposite directions to administration of pentobarbital. The first component was augmented, while the second was diminished (or even abolished by the 40 mg/kg dose). A later negative component demonstrated a biphasic effect, with increases at smaller doses and a return to control levels with the 40 mg/kg dose. Pentobarbital produced a reliable increase in latency for all three superior colliculus components, with the increase occurring at both the 18 and 40 mg/kg doses. A series of late oscillatory potentials recorded from the colliculus were increased in amplitude by pentobarbital.

Cholinergic role in alcohol's effects on evoked potentials in visual cortex of the albino rat

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 alcohols 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 ethanols augmentation of component P2 may result, at least in part, from alterations in cholinergic functions.

Characteristics of operant control of centrally evoked potentials in rats

Abstract Rats were trained to increase and/or decrease the amplitude of one component of visual cortex evoked potentials. The potentials were elicited by shock of the optic chiasm. Operant control was demonstrated with both fixed and random interstimulus intervals. However, animals were better able to decrease than increase the evoked component amplitude. Significant amplitude changes were seen only in the prespecified evoked component. Potentials recorded from the contralateral visual cortex tended to show changes related to those at the trained site. These data were discussed in relation to previous research involving the operant control of peripheral evoked potential components, and in relation to arousal hypotheses utilized in other feedback studies.

Operant conditioned potentials, centrally evoked at random intervals

Rats were operantly conditioned for both increasing and decreasing the amplitude of one component of both visual and somatic sensory evoked potentials. The potentials were recorded in visual cortex, somatic sensory cortex, or nucleus intercollicularis in the midbrain reticular formation. The visual cortical potentials were evoked by shocks to the optic chiasm. The somatic sensory cortical and subcortical potentials were evoked by shocks to the nucleus subcoeruleus of the pontine reticular formation. The evoking stimuli (shocks) were presented at random intervals. The results rule out trivial mediation of operant neural control and are discussed in these terms.

Operant-Controlled Evoked Responses: Discrimination of Conditioned and Normally Occurring Components

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.

Effects of Dizocilpine (MK-801) on Flash-Evoked Potentials, Body Temperature, and Locomotor Activity of Hooded Rats

The present study examined the effects of Dizocilpine (MK-801; a noncompetitive N-methyl-D-aspartate receptor antagonist) on flash-evoked potentials recorded from both the visual cortex (VC) and superior colliculus (SC) of chronically implanted hooded rats. The potentials were recorded at 5, 20, and 35 min following i.p. injections of saline, and of 0.1, 0.3, and 1.0 mg/kg MK-801 on separate days. The amplitude of VC component P1 was unaltered following drug treatment. N1 was increased in amplitude by the 0.1-, 0.3-, and 1.0-mg/kg doses, while two other negative peaks in the VC emerged, beginning with the 0.1-mg/kg dose, to complicate the waveform. One negative peak developed between N1 and P2, while the other effectively split peak P2 (forming P2A and P2B). P2A was depressed at all doses, while P2B was depressed at 0.1 mg/kg but augmented at the 1.0-mg/kg dose. N2 was elevated by the 0.3- and 1.0-mg/kg doses, while P3 was increased in amplitude by all doses. N3 was transiently enhanced by the 0.3-mg/kg dose. SC amplitudes were less affected, with P3 and N4 reduced in amplitude by the 0.3- and 1.0-mg/ kg doses. The latencies of most components in both structures were decreased, often with all doses, but generally at the later recording times. A second experiment demonstrated significant MK-801-induced hyperthermia at all of the above doses, although a higher dose of 3.0 mg/kg MK-801 caused hypothermia. The reduction in component latencies may, therefore, result at least in part from a drug-induced hyperthermia. A third experiment demonstrated MK-801-induced changes in locomotor activity in rats in an open field. The effects were both dose and time dependent. The 0.3-mg/kg dose of MK-801 produced significant increases in the number of line crossings from 20-60 min in comparison to the saline condition. Increases in the number of line crossings with the 1.0-mg/kg dose peaked at 15 min, and then gradually declined. It is unlikely, however, that these changes in movement can account for the effects of MK-801 on evoked potentials. In conclusion, the results show that blockade of the ion channel associated with the NMDA receptor produces profound changes in the activity of the neural pathways that are reflected in the middle components of the flash-evoked potential recorded from the VC.

Ketamine-induced modification of photic evoked potentials in the superior colliculus of hooded rats

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.

Effects of ketamine, naloxone, and physostigmine on flash evoked potentials in rat superior colliculus

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 ketamines 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.