Biomedical subjects

B E Hetzler

Publications and source records attributed to B E Hetzler.

At least 19 recordsLinked to original sources

PubMed2001

Effects of ethanol on flash-evoked potentials of rats: lack of antagonism by naltrexone.

The present study examined the effects of ethanol and naltrexone hydrochloride (a nonselective opiate receptor antagonist) on flash-evoked potentials recorded from both the visual cortex (VC) and the superior colliculus (SC) of chronically implanted hooded rats. There were four treatment conditions administered on separate days: Either saline or naltrexone (10 mg/kg; volume of 1.0 ml/kg) was given 10 min before either saline or ethanol (2.0 g/kg; 20% ethanol solution in a volume of 1.26 ml/100 g). Evoked potentials were recorded 15 min after the intraperitoneal injections were completed. Animals were tested at 23.1 degrees C room temperature. In the VC, ethanol significantly decreased the amplitude of components N1, P3, and N3, whereas it increased the amplitude of P2. Components P1 and N2 were unaffected by ethanol treatment. The SC components P3 and N4 were reduced in amplitude by ethanol, but component P1 was not altered. Latencies of all components in both structures were increased by ethanol. Naltrexone alone did not significantly affect the potentials, nor did naltrexone pretreatment significantly alter the effects of ethanol on the potentials. Naltrexone produced a modest hypothermia of about 0.25 degrees C, whereas ethanol resulted in hypothermia of about 1.0 degrees C. Ethanol, either alone or in combination with naltrexone, significantly reduced body movement during the evoked-potential recording sessions. The results indicate that endogenous opioid systems do not play a major role in the acute effects of ethanol on flash-evoked potentials recorded from primary areas of the visual system.

Animals↗

PubMed1999

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.

Animals↗

PubMed1997

THIP, a selective gamma-aminobutyric acid receptor agonist, alters flash-evoked potentials in rats.

This study examined the effects of the GABA(A) agonist THIP on flash-evoked potentials (FEPs) recorded from the primary visual cortex (VC) and superior colliculus (SC) of chronically implanted hooded rats. Animals were given I.P. injections of saline, and of 8, 16, and 24 mg THIP/kg body weight on separate days. Evoked potentials were recorded at 5, 20, and 35 min following injection. Animals were tested at a standard (22.5 degrees C) room temperature. Most significant effects were observed at the 20- and 35-min recording intervals for both the 16 and 24 mg/kg doses, with effects at the 24 mg/kg dose the most pronounced. VC P1 amplitude remained unchanged, while N1 was reduced to such an extent that it became positive, ultimately blending into the rising phase of a positive component appearing between N1 and P2. This positive component had a latency of about 6 ms longer than N1, and became larger in amplitude than P1 at the 24 mg/kg dose. P2 amplitude was drastically reduced, becoming negative. In contrast, components N2 and P3 were augmented, while the amplitude of N3 was unchanged. In the SC, P1 was augmented while P3 was reduced in amplitude. A biphasic (increase/decrease) effect was observed in the N4 complex. In both the VC and SC, latencies of most components were increased, with the late components in the VC increased to the greatest extent. A mild hypothermia was observed at 16 and 24 mg/kg. The results suggest that the GABA(A) receptor plays an important role in the elaboration of the middle (N1-P2) components of FEPs recorded from the rat VC, and that GABAergic mechanisms can influence other components in the VC and SC as well.

Animals↗

PubMed1993

Acute effects of ethanol on pattern reversal and flash-evoked potentials in rats and the relationship to body temperature.

The effects of acute ethanol treatment on flash and pattern reversal visual evoked potentials (FEPs and PREPs, respectively) were examined in three experiments using Long-Evans rats. The relationships of evoked potential parameters with blood ethanol concentration and body temperature were examined. In Experiment 1, rats were treated i.p. with vehicle or 0.5, 1.0 or 2.0 g ethanol/kg body weight, and tested 30 min later. The 2.0 g/kg group had prolonged latencies of PREP peaks, no changes in PREP peak-to-peak amplitudes, and lower body temperatures than saline-treated controls. The peak latency shifts were significantly correlated with both blood ethanol concentration and body temperature, and were of a magnitude to be expected from similar changes in body temperature alone. Experiment 2 measured both PREPs and paired-flash FEPs in rats 30 min after injection of either 0, 0.5 or 2.0 g/kg ethanol. PREP changes were found following treatment with the high dose which were similar to those of Experiment 1. Some FEP peak latencies were prolonged and peak-to-peak amplitudes were reduced by both doses of ethanol, despite the fact that body temperatures were reduced at only the high dose. At 2.0 g/kg ethanol, the FEP changes in latency, but not amplitude, were in accordance with what would be expected from body temperature changes alone. The third study attempted to investigate the role of reduced body temperature in producing the visual evoked potential changes by testing at room temperatures of 22 or 30 degrees C. Contrary to expectations, the rats receiving 2 g/kg ethanol were approx. 1 degree C cooler than controls at both room temperatures. Evoked potential latencies were greater in ethanol-treated rats than controls at both room temperatures. There were no significant effects of ethanol on FEP amplitudes. Overall, the effects of low doses of ethanol were independent of temperature changes, but the effects of higher doses of ethanol (2.0 g/kg) could not be distinguished from those produced by differences in body temperature alone.

Analysis of Variance↗

PubMed1989

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 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.

Animals↗

PubMed1988

Temperature-dependent changes in visual evoked potentials of rats.

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.

Animals↗

PubMed1987

Differential effects of ethanol on photic and acoustic evoked potentials in the reticular formation of rats.

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.

Animals↗

PubMed1985

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.

Animals↗

PubMed1984

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.

Animals↗

PubMed1984

Contribution of hypothermia to effects of chloral hydrate on flash evoked potentials of hooded rats.

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.

Animals↗

PubMed1983

Acute effects of alcohol on photic evoked potentials of rats: lateral geniculate nucleus and reticular formation.

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.

Animals↗

PubMed1982

Acute effects of alcohol on photic evoked potentials of albino rats: visual cortex and superior colliculus.

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.

Animals↗

PubMed1981

Infantile autism and the temporal lobe of the brain.

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.

Amnesia↗

PubMed1981

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.

Animals↗

PubMed1981