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Biomedical subjects

R L Hale

Publications and source records attributed to R L Hale.

33 records · Page 2Linked to original sources
PubMed1982

Factor analysis of the Quay-Peterson Behavior Problem Checklist across racially different exceptional children.

The factor structure of the Quay-Peterson Behavior Problem Checklist was investigated, across racial backgrounds of 358 American children, in order to determine its efficacy as an instrument in measuring personality dimensions in racially different exceptional children. Similarity across races was found on factors labeled in previous studies as conduct disorder, personality problem, and immaturity inadequacy. A fourth factor including items of laziness in school, irresponsibility, and dislike for school, was found to be race specific. This factor was interpreted as resistance by black exceptional students toward expectations within a white academic environment.

Affective Symptoms↗
PubMedDate not supplied

The effect of prenatal ethanol exposure on scentmarking in the C57BL/6J and C3H/He mouse strains.

In utero exposure to ethanol has been shown to alter sexually dimorphic behaviors in rats. However, it is not clear whether this phenomenon is robust in other species, such as the mouse, which is sensitive to ethanol-induced birth defects. Further, it is not known whether significant differences exist across murine strains. If similar to the classic teratogenic effects of ethanol, it would be expected that strain differences in sensitivity should be evident, with some strains demonstrating an alteration in sexually dimorphic behavior and other strains demonstrating little or no effect. As a first attempt to address these issues, we have examined two mouse strains widely used in prenatal alcohol research, the inbred C3H/He and C57BL/6J strains. Scentmarking was selected as the behavior of interest. It is robustly sexually dimorphic in the rat and mouse, with males marking more than females and preliminary reports have demonstrated that in utero ethanol exposure reduces this behavior in the male rat. In the mouse strains selected for study, pregnant females were provided with either a liquid diet consisting of 25% ethanol-derived calories or pair-fed an isocaloric liquid diet from gestation days 6-18. An additional control group was included which was fed laboratory chow ad lib throughout gestation. Male and female offspring of each strain were tested for scentmarking at 65-75 days of age. As expected, results showed that the effect of prenatal ethanol exposure on scentmarking varied with both strain and sex. In the C3H/He strain, scentmarking was reduced significantly in male ethanol-exposed offspring (i.e., the males were feminized).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Reduced sensitivity to the effects of clonidine on ethanol-stimulated locomotor activity in adult mouse offspring prenatally exposed to ethanol.

Prenatal exposure to ethanol (EtOH) alters developing catecholamine (CA) systems and acute sensitivity to the locomotor stimulant effects of EtOH. As an extension of previous work involving CA agents, this study addressed whether prenatal EtOH exposure influences central norepinephrine (NE) systems by examining the motoric effects of the direct alpha 2 adrenoreceptor agonist clonidine given alone and in combination with a low-dose stimulant challenge of EtOH. Standard lab chow or liquid diets containing either 25% EtOH-derived calories (EDC), or 0% EDC (pair-fed group) were given to pregnant C3H/He mice on gestation days 6-18. At 90 days of age, male offspring from each prenatal treatment group were monitored for 10 minutes in an open field following IP injections of clonidine (0, 0.0125, 0.025, or 0.05 mg/kg) and either EtOH (1.5 g/kg) or saline. In control offspring, clonidine suppressed locomotor activity and attenuated the stimulant response to EtOH in a dose-dependent fashion. In contrast, clonidine given alone did not suppress, but appeared to stimulate, activity in prenatal EtOH-exposed offspring. Furthermore, the ability of clonidine to attenuate the locomotor stimulant properties of EtOH was greatly reduced in prenatal EtOH-exposed animals. Taken together, these results indicate a shift to the right in the dose-response function for clonidine in prenatal EtOH-exposed offspring relative to control mice. Further, the results suggest that prenatal exposure to EtOH may result in long-lasting alterations in developing central NE systems, particularly presynaptic alpha 2 adrenoreceptor sensitivity.

Animals↗
PubMedDate not supplied

Prenatal ethanol exposure alters sensitivity to the effects of apomorphine given alone and in combination with ethanol on locomotor activity in adult male mouse offspring.

Previous studies have indicated that prenatal ethanol (EtOH) exposure alters developing catecholamine (CA) systems and acute sensitivity to the locomotor stimulant effects of EtOH. The purpose of this study was to examine whether prenatal EtOH exposure influences the effects of the direct dopamine (DA) agonist apomorphine given alone as well as in combination with a low-dose stimulant challenge of EtOH. Standard lab chow or liquid diets containing either 25% EtOH-derived calories (EDC), or 0% EDC were given to pregnant C3H/He mice on gestation days 6-18. At 90 days of age, male offspring from each prenatal treatment group were monitored for 10 min in an open field following IP injections of apomorphine (0, 0.15, 0.3, 0.6, or 1.2 mg/kg) and either EtOH (1.5 g/kg) or saline. EtOH alone increased activity by 120-143% in all three groups of offspring. In control offspring, apomorphine dose-dependently decreased activity up to 74%-78% and blocked the stimulant effect of EtOH at all doses tested. However, in prenatal EtOH-exposed offspring, higher doses of apomorphine were significantly less effective in reducing both baseline and EtOH-stimulated activity compared to control mice. This effect is most likely not due to differences in pharmacokinetics, because blood EtOH concentrations were similar across apomorphine doses and prenatal treatment conditions. As such, these results support the hypothesis that prenatal exposure to EtOH alters acute sensitivity to the locomotor stimulant effects of EtOH, particularly under conditions in which CA systems mediating those effects are additionally challenged. In addition, the results suggest that prenatal EtOH exposure results in a long-lasting perturbation of central DA receptor sensitivity.

Animals↗
PubMedDate not supplied

Exacerbation of ethanol withdrawal seizures in mice with a history of multiple withdrawal experience.

Repeated ethanol withdrawal experience has been shown to result in an exacerbation of future withdrawal episodes. This sensitization of the withdrawal response has been hypothesized to represent a "kindling" phenomenon. We previously demonstrated that mice exposed to ethanol vapor for a total of 48 h exhibited more severe withdrawal seizures if the exposure was divided into three 16 h intoxication/8 h abstinence cycles than if the 48 h of exposure occurred in a single bout. The present study was designed to further characterize this model of ethanol withdrawal "kindling" and determine whether such a "kindled" response may be evident when withdrawal testing is conducted after an additional bout of intoxication that is the same for all groups. Adult C3H mice were chronically exposed to ethanol vapor in inhalation chambers for 40 h prior to withdrawal testing. Prior to this 40 h intoxication period, one group (Multiple Withdrawal; MW) received three cycles of 16 h ethanol vapor separated by 8 h abstinence; a second group (Single Withdrawal; SW) did not receive any ethanol exposure prior to the 40 h test cycle; a third group (Continuous Exposure; CE) received the same total ethanol exposure as the MW group (48 hr), but without interruption: and a control group (C) did not receive any ethanol treatment throughout the experiment. Blood ethanol levels following the 40 h bout of ethanol intoxication were 100-140 mg/dl for all ethanol-exposed groups. The severity of handling-induced convulsions during withdrawal was significantly greater in the MW group compared to CE and SW groups. These results suggest that differences in the severity of ethanol withdrawal seizures due to differences in prior withdrawal experience can be demonstrated even when later ethanol exposure patterns are equated. As such, the results provide further support for the "kindling" hypothesis of ethanol withdrawal.

Alcoholic Intoxication↗
PubMedDate not supplied

A methodological study of the Shipley Institute of Living Scale in alcoholics and non-alcoholics: reliability, discriminating items and alternate forms.

In Study 1, 430 sober male alcoholics and 98 nonalcoholics completed the Shipley Institute of Living-Vocabulary (SILS-V) and Abstraction (SILS-A) under the standard instructions. Alcoholics performed significantly more poorly than the nonalcoholics on SILS-A. High test-retest reliability of the SILS with a 2-week interval between testings was obtained. Item analysis of the 20-item SILS-A revealed that only items 4-14 discriminated alcoholics and controls, six items required reversal of a cognitive set (reversal) and five did not (nonreversal items). Exploratory factor analyses confirmed essentially the same division of items. In Study 2, two 10-item forms of SILS-A equated for difficulty level and reversal-nonreversal cognitive demands were administered to 186 male and female college students. Results indicate the two forms are equivalent in difficulty, demonstrate no gender differences and correlate significantly with cumulative college grade point averages.

Journal Article↗