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Biomedical subjects

R L Isaacson

Publications and source records attributed to R L Isaacson.

At least 73 records · Page 4Linked to original sources
PubMed1982

Time course of certain behavioral changes after hippocampal damage and their alteration by dopaminergic intervention into nucleus accumbens.

Independent groups of rats with hippocampal, neocortical, or sham lesions were observed 7, 14, or 28 days after surgery in an open field-hole board apparatus and in a smaller circular apparatus. In the circular apparatus, animals were observed after unilateral injection of the dopamine agonist, 3,4-dihydroxyphenylamino-2-imidazoline (DPI) or saline into nucleus accumbens. Behavioral changes in locomotion, exploration and grooming measured in the open field were consistent with those found previously after hippocampal damage, with each behavioral anomaly demonstrating a specific pattern of change after surgery. In general, the injection of DPI into nucleus accumbens produced greater behavioral change in animals with hippocampal damage than in animals with either neocortical or sham lesions. The drug-induced changes in the hippocampally lesioned rats made their behavior more like that of control animals. These results suggest that destruction of the hippocampus may induce alterations in dopaminergic mechanisms in nucleus accumbens which can be modified by appropriate pharmacologic intervention.

Animals↗
PubMed1981

Behavioral and temperature changes induced by clonidine in the developing rat.

Changes in core body temperature and the behavioral activation produced by clonidine were measured in 10-day-old rats at 3 different ambient temperatures (25, 30 and 36 degrees C). Behavioral activation after clonidine is comprised of head raising and rotational movements of the limbs which result in locomotion in open areas and wall climbing if the animal is confronted by a vertical surface. Clonidine enhanced locomotion and wall climbing at all environmental temperatures, but a drug-induced hypothermia was found only in the 25 and 30 degrees C testing conditions. This suggests that the clonidine-induced motor changes are not secondary to a fall in body temperature. In a second experiment the open field responses to clonidine at 25 degrees C were observed in 10-day-old rats pretreated with phentolamine (2 and 15 mg/kg), phenoxybenzamine (2 and 15 mg/kg) or naloxone (0.2 and 2 mg/kg). Phentolamine pretreatment at 15 mg/kg reduced locomotion, wall climbing and attenuated the reduction in core temperature. Phenoxybenzamine at 15 mg/kg only affected the clonidine-induced change in temperature. Thus, it is likely that these behavioral and temperature changes are adrenergically mediated and that the clonidine-induced locomotion and temperature effects may be due to different alpha-adrenergic receptors.

Animals↗
PubMed1981

Changes in dopamine and DOPAC following systemic administration of apomorphine and 3,4-dihydroxyphenylamino-2-imidazoline (DPI) in rats.

Rats were injected systemically with either saline, apomorphine, or one of four doses of DPI (3,4-dihydroxyphenylamino-2-imidazoline) and the levels of dopamine and DOPAC determined in the nucleus accumbens and the caudate regions. DPI reduced dopamine and DOPAC levels in the nucleus accumbens, while apomorphine did not. On the other hand, apomorphine reduced the levels of dopamine and DOPAC in the caudate but not the nucleus accumbens. DPI largely was without effect in the caudate. The results are discussed in terms of possible specificity of the two dopamine agonists in the two forebrain regions.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1981

Hippocampal involvement in the pharmacologic induction of withdrawal-like behaviors.

Kainic acid is an analog of glutamate. The CA3-4 field of the hippocampus is extremely sensitive to its toxic properties. Intracerebroventricular injection of of nontoxic doses of kainic acid in rats produces behaviors similar to morphine withdrawal. Lesion of CA3-4 abolishes this response to kainic acid. Destruction of CA3-4 blocks the ability of Met-enkephalin, ketocyclazocine, and 5-hydroxytryptophan, but not sodium valproate or ice water to induce withdrawal-like behaviors. The actions of kainic acid, endorphins, and ketocyclazocine are blocked by naloxone and enhanced by opiate agonists. Sodium valproate, ice water, and withdrawal itself are released by naloxone and blocked by opiate agonists. Similar discriminations by CA3-4 lesions and challenge by naloxone and morphine may indicate that two neural circuits exist through which withdrawal-like behaviors are evoked. The hippocampal circuit is not directly involved in dependence, but may modulate withdrawal. Withdrawal-like behaviors are observed in rats in situations where behavior is blocked. These withdrawal-like behaviors are reminiscent of verbal reports of anxiety. In particular, wet-dog shakes in these situations may be analogous to shuddering. In humans, monosodium glutamate intolerance is associated with shuddering.

Animals↗
PubMed1979

Intracerebral adrenocorticotropic hormone mediates novelty-induced grooming in the rat.

Intact male rats exhibited more grooming in unfamiliar testing chambers than in their home cages. Hypophysectomized rats showed a much reduced increase in grooming in these testing chambers. Intraventricular injections of antiserum to adrenocorticotropic hormone to intact rats decreased the grooming usually observed in the novel situation, whereas a similar injection of control serum did not produce this effect. Peripheral injections of the antiserum did not affect grooming. Since intraventricularly injected adrenocorticotropic hormone induces excessive grooming, these results suggest that the increased grooming observed in the novel environment may be at least partly due to the release of this hormone directly into the cerebral ventricular system.

Adrenocorticotropic Hormone↗
PubMed1979

Stretching and yawning: a role of glutamate.

Systemic injection of GDEE (glutamate diethyl ester), an antagonist of glutamate and aspartate receptors, induces stretching and yawning in rats. This was not accompanied by excessive grooming. Coupled with previous work these findings give evidence that a glutamatergic mechanism is involved in stretching and yawning.

Animals↗
PubMed1978

The influence of brain damage on locomotor behavior of mice selectively bred for high or low activity in the open field.

Locomotor activity was measured in mice with lesions restricted to the neocortex, in animals with hippocampal damage, and in sham-operated control mice of the selectively bred high and low open-field activity lines developed by J. C. DeFries. Postoperatively, the high-activity animals with hippocampal lesions showed reduced activity relative to those with only neocortical damage, and their postoperative activity levels were uncorrelated with those obtained preoperatively. Testing the animals under reduced illumination enhanced locomotor activity, with the greatest increase demonstrated by high-activity mice with hippocampal damage. While increases in activity under low illumination did occur in the low-activity line, no significant group differences were observed. Amphetamine did not affect locomotor behavior of the high-activity control animals, whereas doses of 1.0 and 10.0 mg/kg reduced the activity of the low-activity mice. High-activity mice with hippocampal damage evidenced a significant increase in locomotor behavior after the 10.0 mg/kg dose. These results emphasize that the behavioral effects of brain lesions and pharmacological manipulations cannot be adequately assessed without regard to genotype of the animals under investigation.

Amphetamine↗