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Hypothalamic concentrations of epinephrine and norepinephrine were determined in rats following 6-hydroxydopamine lesions of the locus coeruleus and subcoeruleus system and following sham-operation. These concentrations were correlated with pituitary ACTH content. While the lesion procedure did not have a major effect on hypothalamic monoamine levels, we were able to demonstrate a strong negative correlation between hypothalamic epinephrine and pituitary ACTH content independent of the experimental condition. Only a weak negative correlation was observed for hypothalamic norepinephrine and pituitary ACTH. Our recent and previous data suggest a tonic and phasic inhibition of ACTH release by hypothalamic monoamines.

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Unilateral nigrostriatal lesions in rats that almost totally depleted striatal dopamine had no effect on striatal levels of dopamine's precursor, tyrosine, nor on those of leucine. Since prolonged electrical stimulation of the slices markedly depletes them of tyrosine (1,2) we conclude that tyrosine can be mobilized from non-dopaminergic striatal cells to augment dopamine release.

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Acute, uncontrollable stress increases norepinephrine (NE) turnover in the rat's brain (depleting NE) and diminishes the animal's subsequent tendency to explore a novel environment. Pre-treatment with tyrosine can reverse these adverse effects of stress, presumably by preventing the depletion of NE in the hypothalamus. Numerous studies suggest that NE inhibits the release of adrenocorticotropic hormone (ACTH) by suppressing corticotropic releasing factor (CRF) secretion in the hypothalamus. In the present study, we found that pre-treatment with supplemental tyrosine not only prevented the behavioral depression and hypothalamic NE depletion observed after an acute stress, but also suppressed the rise in plasma corticosterone. These results support a role for brain NE in stress-induced corticosterone secretion and demonstrate that supplemental tyrosine can protect against several adverse consequences of such stress.

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Exposure of rats to an acute, uncontrollable stressor can increase brain norepinephrine (NE) turnover and decrease locomotor and exploratory behavior. We examined the ability of exogenous tyrosine, NE's amino acid precursor, to protect rats from developing these neurochemical and behavioral changes when stressed. Animals pretreated with saline or tyrosine (200 mg/kg, i.p.) were subjected to tail shock (15 v, 2 mA, 5 sec/30 sec) or to no shock during a 60-min period. Exposure to shock depleted NE and increased its turnover [as indicated by altered NE and 3-methoxy-4-hydroxy-phenylene-glycol sulfate levels (MHPG-SO4)] within the locus coeruleus, the hippocampus and the hypothalamus. Behavioral deficits were observed using measures of locomotion, standing on hind legs, and hole-poking in an open-field apparatus. Animals given tyrosine before shock displayed neither shock-induced NE depletion nor the deficits in locomotion and hole-poking; brain MHPG-SO4 levels tended to be greater than after shock alone. These observations suggest that the stress caused NE to be released from some neurons more rapidly than it could be restored by synthesis or reuptake, thereby impairing noradrenergic transmission and NE-dependent exploratory behaviors. Tyrosine administration presumably enhanced the transmitter's synthesis in stressed animals, thereby preventing both the neurochemical and the behavioral deficits.

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Acute, uncontrollable stress increases norepinephrine (NE) turnover in the rat's brain (thereby depleting NE) and diminishes the animal's subsequent tendency to explore a novel environment. We determined whether supplemental dietary tyrosine could prevent some of these changes. Rats given a control diet or diets enriched with tyrosine or tyrosine plus valine were exposed to tail-shock stress or to no stress over a 60-min period. Exposure to the stress caused an increase in NE turnover, decreasing NE and increasing 3-methoxy-4-hydroxy-phenylethylene glycol sulfate (MHPG-SO4) concentrations within the locus coeruleus, hypothalamus and hippocampus. No changes were detected in serotonin (5-HT) levels or turnover. Behavioral deficits following the stress were observed using measures of locomotion and of exploration in a novel open-field environment: stressed animals displayed much less spontaneous motor activity, hole-poking or frequency of standing on their hind legs than control animals. Animals receiving the tyrosine-enriched diet displayed neither the stress-induced depletion of NE nor the behavioral depression. These preventive effects of tyrosine were abolished by co-administration of valine, a large neutral amino acid that competes with tyrosine for transport across the blood-brain barrier. Since tyrosine alone, in animals not subjected to stress, did not change NE turnover nor the behaviors studied, our observations affirm that catecholaminergic neurons respond to the precursor amino acid only when they are physiologically active. Supplementary tyrosine may be useful therapeutically in people exposed chronically to stress.

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Three strains of mice were tested on an 8-arm radial maze, an index of hippocampus-dependent spatial memory. Levels of performance differed between strains with C57Br/cj greater than Balb/cj greater than C57Bl/6j. Lesions of the fimbria/fornix disrupted performance in the C57Br and Balb strains: the C57Bl mice never performed better than chance before or after surgery. Choline acetyltransferase activity in hippocampus was not correlated with radial maze performance. These findings suggest a possible genetic contribution towards radial maze behavior.

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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.

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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.

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