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L R Hegstrand

Publications and source records attributed to L R Hegstrand.

33 records · Page 2Linked to original sources
PubMed1981

Cyclic nucleotides and aggressive behavior.

Cyclic nucleotides, particularly cyclic AMP, have been implicated as second messengers in neuronal activity. Attempts to demonstrate an association between endogenous cAMP or cGMP levels and rodent aggressive behavior have been only partially successful. Low levels of cAMP in rodent brain appear associated with lower levels of affective aggression. Consistent with this possible relationship is our finding that the infusion of dibutyryl cAMP into rodent cerebroventricles decreases aggressive behavior. The infusion of dibutyryl cyclic GMP, conversely, facilitates shock-induced fighting in the rat.

Aggression↗
PubMed1980

Dietary tryptophan modulation and aggressive behavior in mice.

The effects of a tryptophan-free diet on isolation-induced fighting and predatory cricket killing in mice were examined. The results demonstrated that consumption of a tryptophan-free diet for 18-20 days decreased both the number of fighters and duration of isolation-induced fighting; increased the number of cricket-killing mice and decreased the latencies to attack and the latencies to kill crickets; reduced brain serotonin 27%; increased water intake 38%; and decreased body weight 27% without affecting food intake. To determine if these effects were due specifically to the lack of dietary tryptophan, other groups of mice were fed a 5% tryptophan load in the standard chow; a 0.15% tryptophan supplement in the tryptophan-free diet; or a 3 grams/day restricted chow diet. The lack of tryptophan in the diet produced the marked inhibition in isolation-induced fighting, the reduction in brain serotonin, and the large decrease in body weight. The other non-specific effects appeared to be related to general factors such as dietary need for the cricket killing or diet composition (other than the lack of tryptophan) for the water intake.

Aggression↗
PubMed1980

Effects of dietary supplements and a tryptophan-free diet on aggressive behavior in rats.

The effects of dietary excesses of tryptophan, histidine, tyrosine or choline and of a tryptophan-free diet were examined on shock-induced fighting, muricide and jump-flinch thresholds. Following the tryptophan-free diet, shock-induced fighting and pain sensitivity were specifically increased. The increased incidence of muricide was not specific to the lack of tryptophan in the diet. Groups of rats which were pair fed chow or had 0.15% L-tryptophan added to the tryptophan-free diet increased muricide as well. Brain 5-HT levels were 41% depleted following the tryptophan-free diet and reduced 13% with the 0.15% tryptophan supplement. In addition body weights were reduced in the three groups compared to control. None of the excess diets affected shock-induced fighting, muricide and jump-flinch thresholds. Body weights were decreased in the excess tryptophan, histidine, tyrosine and choline groups. These data indicate that the expression of different forms of aggression appears to be influenced by a tryptophan deficiency in the diet, but not by excesses of tryptophan, tyrosine, histidine and choline.

Aggression↗
PubMed1980

Elevation of beta-adrenergic receptor density in human lymphocytes after propranolol administration.

Abrupt withdrawal after the chronic administration of propranolol has resulted in clinical syndromes that suggest adrenergic hypersensitivity. The effect of propranolol administration and withdrawal on beta-adrenergic receptors was studied in human lymphocyte membranes. Receptor density was quantitated by direct binding assays with the radioligand [125I]iodohydroxybenzylpindolol. Administration of propranolol (160 mg/d) for 8 d resulted in trough plasma levels of approximately 35 ng/ml. By day 5 of propranolol administration the density of beta-adrenergic receptors had increased 43 +/- 4% (P less than 0.01) above pretreatment levels. Abrupt withdrawal of propranolol was followed by the disappearance of propranolol from the plasma within 24 h. The density of beta-adrenergic receptors did not return to pretreatment level for several days. Physiologic supersensitivity of beta-adrenergic receptor-mediated responses was suggested by the appearance of significant increases in the orthostatic change in heart rate (P less than 0.05) and the orthostatic change in the heart rate-systolic blood pressure product (P less than 0.01) during the first 48 h after propranolol withdrawal. These data show that propranolol administration leads to an increase in the density of beta-adrenergic receptors in human tissue. The results are consistent with the hypothesis that some of the untoward effects observed after abrupt discontinuation of propranolol are caused by beta-receptor-mediated adrenergic hypersensitivity.

Adrenergic beta-Agonists↗
PubMed1975

Evidence for involvement of protein kinase in the activation by adenosine 3':5'-monophosphate of brain tyrosine 3-monooxygenase.

Addition of adenosine 3':5'-monophosphate (cAMP) to high speed supernatant preparations obtained from rat brain caused a 3- to 4-fold increase in tyrosine 3-monooxygenase (tyrosine hydroxylase) activity. The tyrosine 3-monooxygenase remained in an activated state upon removal of the cAMP by passing the enzyme through a Sephadex G-25 column. Substances which inhibit cAMP-dependent protein kinase, namely, EDTA, ADP, and adenosine, and protein kinase modulator, each antagonized the activation of tyrosine 3-monooxygenase produced by cAMP. Furthermore, addition of partially purified brain cAMP-dependent protein kinase caused a several-fold increase in tyrosin 3-monooxygenase activity. The activation of tyrosine 3-monooxygenase by added cAMP and protein kinase required the presence of ATP and Mg-2+. These data suggests that the cAMP activation of tyrosine 3-monooxygenase may be mediated by a cAMP-dependent protein kinase.

Adenosine↗
PubMedDate not supplied

Effect of total parenteral nutrition on histamine in the rat brain and other tissues.

The effects of a constant infusion of total parenteral nutrition on the histamine content of the hypothalamus was studied in adult male rats. Histamine content of the stomach, kidney, liver, and heart was also determined. The relationship between tissue histamine levels and duration of the infusion was examined. Rats receiving intravenous infusions of total parenteral nutrition had significantly higher (p less than 0.001) histamine levels in the hypothalamus than did orally-fed control rats. No difference was observed in the histamine level in the remainder of the brain. Animals receiving parenterally infused nutrient solutions had a higher histamine content in the kidneys but lower histamine levels in the stomach than did the control rats. No changes in the histamine content of liver or heart were observed. It appears that increases in histamine levels in the kidney and hypothalamus of rats given total parenteral nutrition persist up to 5 days and 9 days, respectively. The mechanisms responsible for and the consequences of the alterations of histamine content of these tissues remain to be established.

Animals↗