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Biomedical subjects

J Brick

Publications and source records attributed to J Brick.

At least 37 records · Page 2Linked to original sources
PubMed1986

The effect of menstrual cycle on blood alcohol levels and behavior.

To determine whether the behavioral effects of alcohol were altered by menstrual cycle phase, 10 women between the ages of 21 and 24 who reported regular menstrual cycles of 28-31 days participated in three experimental sessions, the dates of which coincided with the flow, midcycle and premenstrual phases of their cycles. In each session, the effects of alcohol (.65 g/kg) were measured on memory for words, standing steadiness, coding vigilance and blood alcohol level (BAL). The following measures were obtained in each of three testing rounds: baseline, the ascending limb of the BAL curve and the descending limb of the BAL curve. Peak BALs of 83 +/- 2 mg/d1 were obtained. On coding vigilance, the subjects were observed to perform better during the flow phase of their cycle than they did in either the midcycle or premenstrual phase. No significant phase by alcohol effects were obtained, however. These results suggest that neither the pharmacokinetics of alcohol nor certain behaviors affected by alcohol were affected by menstrual cycle phase. These results are generally consistent with previous research, and they question the logic of excluding women subjects from studies on the effects of alcohol on behavior, at least for the variables used in this study.

Adult↗
PubMed1984

Role of noradrenergic neurons in ethanol-induced elevation of free fatty acids and corticosterone.

The effects of ethanol (2 or 3 g/kg) on plasma corticosterone and free fatty acids were examined in rats with bilateral electrolytic lesions of locus coeruleus or pretreated with the noradrenergic neurotoxin DSP 4 (50 mg/kg). Both lesions and DSP 4 significantly attenuated ethanol induced elevation of free fatty acids. No changes in basal levels of free fatty acids or corticosterone were observed nor did either treatment alter the elevating effect of ethanol on corticosterone. The results indicate that ethanol alters plasma free fatty acids through mechanisms involving noradrenergic neurons in the central nervous system.

Animals↗
PubMed1984

Raphe lesions modify ethanol's effects on plasma corticosterone and NEFA.

Male rats received dorsal or median raphe electrolytic lesions or sham operations. Ten days later subjects received 3.0 g/kg ethanol or saline and were decapitated 30 minutes later. Both dorsal and median raphe lesions significantly increased corticosterone and non-esterified fatty acid levels. Ethanol significantly increased corticosterone and non-esterified fatty acid levels in rats with dorsal or median raphe lesions. Dorsal raphe lesions significantly attenuated the elevating effect of ethanol on corticosterone. These results confirm, in part, previous pharmacological studies and suggest the effects of ethanol on corticosterone, but not non-esterified fatty acid, involve serotonergic neurons.

Animals↗
PubMed1984

A simple cannula for intraventricular drug administration in rodents.

We describe a new cannula for the intraventricular administration of drugs which is easily and rapidly constructed, is inexpensive and has significant advantages over other cannulas of similar type. The structure of the cannula includes a guiding funnel which greatly facilitates insertion of the injection needle. The cannula also has a locking cap/stylet which is rat-tamper-resistant.

Animals↗
PubMed1983

Effect of ethanol on surface body temperature as measured by infrared radiation detection.

A prominent effect of ethanol is on rectal body temperature. The use of a rectal probe to measure temperature can be stressful to the subject, especially when used repeatedly. We now present data on the hypothermic effect of ethanol (0.5, 1.0, 3.0, 3.5, or 4.0 g/kg) on surface body temperature in rats as detected by infrared radiation. Ethanol produced significant decreases in nasal temperature that were significantly correlated with changes in rectal temperature. Ethanol (3.5 g/kg) also produced a significant reversal in nasal hypothermia 15 min postinjection that was detected only with the infrared method. This new method is very rapid, accurate, requires minimal handling and may, therefore, be less stressful than rectal measurement to the subject.

Animals↗
PubMed1983

Tolerance and cross-tolerance to morphine and ethanol in mice selectively bred for differential sensitivity to ethanol.

Ethanol-sensitive long-sleep mice showed greater sensitivity to ethanol-induced hypothermia whereas the less sensitive short-sleep mice showed greater sensitivity to morphine-induced hypothermia. The short-sleep mice, but not the long-sleep mice, displayed a degree of cross-tolerance to the hypothermic effects of ethanol following repeated exposure to morphine.

Animals↗
PubMed1982

Ethanol-stress interaction: biochemical findings.

Previous research suggested that low doses of ethanol (ETOH) may have a protective effect against stress: We now report confirmation and extension of that preliminary study. Male Sprague-Dawley rats were injected with 0.50 g/kg ETOH (10% w/v) or an equivalent volume of saline and randomly assigned to one of four groups in Experiments I and II (saline-stress, saline-nonstress, ethanol-stress, ethanol-nonstress). In Experiment III, only two groups were tested (ethanol-stress, saline-stress). The stressors consisted of 30 trials (intertrial interval 60 s) of a 2-s duration 0.40 mA foot shock (Experiment I), 90 min restrain stress at 21 degrees C (Experiment II) or 10 min tail-pinch (Experiment III). In Experiments I and II, plasma nonesterified fatty acids (NEFA) were significantly increased in the saline-stress groups compared to the saline-nonstress or ethanol-nonstress groups. In contrast, subjects treated with ETOH and stress had significantly lower levels of plasma NEFA than saline-stress subjects in Experiments I and III. Plasma corticosterone was significantly elevated in response to stress. Subjects in the ethanol-stress groups had significantly lower levels of plasma corticosterone than subjects in the saline-stress group (Experiments I and II). These results suggest that ETOH has some protective effect against stress-induced increases in plasma corticosterone and NEFA. Furthermore, this finding may be generalized to several different types of stressors.

Animals↗
PubMed1982

A new method for the determination of blood ethanol levels in rodents.

A procedure is described for the estimation of ethanol in blood of rodents. The procedure is based on the same principle as the breath analyzer method used with human subjects. Using a specifically designed mask, samples of rebreathed air are collected under equilibrium conditions. These are injected directly into gas chromatograph for the quantitation of ethanol. We determined the conversion factor for calculating blood ethanol levels from those determined in breath to be 1:2857. The method was validated by comparing blood (from the jugular vein) and breath values obtained on the same animal after the administration of various doses of ethanol either intraperitoneally or intragastrically.

Animals↗
PubMed1982

Alcohol and morphine induced hypothermia in mice selected for sensitivity in ethanol.

We have used changes in body temperature as an index of responsiveness to alcohol and morphine in mice selectively bred for differential sensitivity to ethanol. In agreement with other laboratories, we found that mice which show longer duration of loss of righting reflex following hypnotic doses of ethanol (long sleep; LS) also showed greater loss in body temperature following subhypnotic doses of ethanol than did the less sensitive short sleep (SS) mice. This effect was dose dependent in both lines. In contrast, SS mice were more sensitive than LS mice to the hypothermic effects of morphine, although the difference was only evident 30 min after morphine administration. Naloxone attenuated morphine induced hypothermia in mice of both genotypes, but attenuated alcohol induced hypothermia only in SS mice. Thus, SS mice may be more sensitive to an opiate agonist and an antagonist, at least as indexed by changes in body temperature, and may prove to be a useful population for evaluating both alcohol-opiate interactions and genetic differences in opiate responsiveness.

Animals↗
PubMed1980

Chronic administration of haloperidol during development: behavioral and psychopharmacological effects.

Chronic haloperidol treatment during prenatal and postnatal development was found to induce long-term behavioral and psychopharmacological effects. Rats tested shortly after termination of the chronic treatment at weaning or as young adults were hyperactive in the open field and exhibited an attenuated behavioral response to amphetamine and an accentuated cataleptic response to later doses of haloperidol, when compared with control offspring of the same age. Tests at an intermediate interval (adolescence period) showed no significant difference from control offspring on any of these behavioral measures. Adult rats administered haloperidol chronically for the same duration were also hyperactive after termination of treatment. In contrast to the effects of haloperidol during development, these adults exhibited an accentuated behavioral response to amphetamine and an attenuated cataleptic response to a later dose of haloperidol. Compensatory mechanisms in response to chronic haloperidol treatment during development thus appear to be different from those in adulthood.

Animals↗
PubMed1979

Stress responses of rats with septal lesions.

Rats which had received septal lesions or underwent control surgery were exposed to stress in four experiments. We examined plasma corticosterone (Experiment 1), gastric ulceration (Experiment 2), motor activity (Experiment 3) and whole brain norepinephrine (Experiment 4) following 3 hours of prone-restraint-stress conditions at 21 degrees C or 5 degrees C. Rats with special lesions had higher steroids, less severe ulceration, greater motor activity and higher brain norepinephrine than controls following stress. Changes in hyperemotionality and differences in coping strategies are discussed.

Animals↗
PubMed1976

The startle response in rats: effect of ethanol.

The effects of acute and chronic ethanol intake on the startle response was examined in male rats. Ethanol given IP produced a dose-dependent decrease in the amplitude of the startle response measured 30 min later. With a dose of 1 g/kg, the effect was evident at 15 min and had recovered substantially by 60 min. The effect of ethanol on the startle response was potentiated by pretreatment of the animals with pimozide, haloperidol, and p-chlorophenylalanine but not by propranolol, phenoxybenzamine, alpha-methyltyrosine, or pargyline. After 3 weeks on an ethanol-containing diet, the startle response was greater than that shown by rats on the control iso-caloric, sucrose-containing diet. After ethanol withdrawal, the startle response was further increased, with a peak about 9 to 12 hr after discontinuation of ethanol; thereafter, the response declined. This time course of heightened startle response during ethanol withdrawal corresponds to the time course of the activation of noradrenergic neurons during withdrawal. It appears that dopaminergic and serotonergic neurons are involved in the mediation of the startle response in rats.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Monoamines and the effect of ethanol on corticosterone and non-esterified fatty acids.

The effect of locus coeruleus lesions, DSP-4 neurotoxin, intraventricular propranolol and dorsal or median raphe lesions on ethanol-induced elevations of corticosterone and NEFA were examined in rats. Locus coeruleus lesions, DSP-4 and propranolol attenuated ethanol-induced elevations of NEFA, but not corticosterone. Dorsal raphe lesions attenuated the action of ethanol on corticosterone but not NEFA. It is hypothesized that ethanol's action on NEFA levels is mediated by a central noradrenergic system, whereas, its action on corticosterone levels involves the central serotonergic system.

Animals↗