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Biomedical subjects

R A Mueller

Publications and source records attributed to R A Mueller.

At least 145 records · Page 8Linked to original sources
PubMed1979

Dopaminergic interaction with the respiratory control system in the rat.

Apomorphine given to rats lightly anesthetized with halothane produces a dose dependent increase in respiratory frequency and minute ventilation. Although basal arterial CO2 tensions were not significantly altered by apomorphine, the mechanical response to exogenous CO2 exposure was greatly increased in rats given apomorphine. Haloperidol returned the apomorphine-stimulated respiratory pattern to control values. It is concluded that dopamine neurons may have important interactions with respiratory control.

Animals↗
PubMed1979

Change in brain guanosine 3',5'-monophosphate (cGMP) content by thyrotropin-releasing hormone.

Thyrotropin-releasing hormone (TRH) causes a significant increase in rat cerebellar guanosine 3',5'-monophosphate (cGMP) content after parenteral administration. A smaller but still significant increase in cGMP was also observed in brain stem, whereas no significant changes were observed in cGMP in other gross brain regions or in adenosine 3',5'-monophosphate in any brain region. TRH also caused a similar increase in cerebellar cGMP content in hypophysectomized rats indicating that the increase is independent of an intact pituitary. The time course of cGMP elevation in the cerebellum after administration of 10 mg/kg of TRH i.v. showed a peak at 2.5 to 5.0 min followed by a less rapid decrease. The time course of TRH immunoreactivity in the same cerebellar homogenates roughly paralleled these changes. Only those TRH analogs which were previously shown to antagonize pentobarbital sleeping time in mice caused an elevation in cGMP content in the cerebellum. TRH also caused a significant increase in cerebellar cGMP in rats pretreated with phenobarbital and chlordiazepoxide. The TRH-induced increase in cerebellar cGMP was not affected by cerebellar climbing fiber lesions caused by 3-acetylpyridine nor blocked by haloperidol, suggesting that TRH acts by mechanisms different from harmaline or apomorphine in raising cerebellar cGMP.

Animals↗
PubMed1979

Role of monoamine neural systems in L-dihydroxyphenylalanine-stimulated activity.

The potentiation of the stimulatory response to L-dihydroxyphenylalanine (L-dopa) in 6-hydroxydopamine-treated rats given a peripheral decarboxylase inhibitor occurred only after treatments that destroyed dopamine-containing fibers, Destruction of serotonin- or norepinephrine-containing fibers did not potentiate the action of L-dopa. Furthermore, other data indicated thatL-dopa-induced activity could not be attributed to release of serotonin or to the formation of norepinephrine. That the L-dopa must be converted to catecholamines was demonstrated by antagonism of the activity responses to L-dopa with inhibition of decarboxylases in brain. After destruction of serotonin-containing fibers with 5,7-dihydroxytryptamine, L-dopa-induced activity in 6-hydroxydopamine-treated rats was significantly reduced, as was the accumulation of dopamine formed from L-dopa. These latter data provide direct evidence that serotonergic fibers contribute to the accumulation of dopamine in brain after L-dopa administration to 6-hydroxydopamine-treated rats.

5,7-Dihydroxytryptamine↗
PubMed1978

Behavioral and prolactin responses to 5-hydroxytryptophan in rats treated during development with 5,7-dihydroxytryptamine.

The serotonin precursor, 5-hydroxytryptophan (5-HTP), can induce a behavioral syndrome characterized by rigidity, splayed feet, tremor, head weaving, salivation and forepaw treading. This response to 5-HTP was markedly potentiated in adult rats treated intracisternally with 5,7-dihydroxytryptamine (5,7-DHT) during development. Prevention of the 5,7-DHT-induced reduction of brain norepinephrine with pargyline or desipramine did not diminish the potentiation of 5-HTP, suggesting that noradrenergic fibers are not contributing to the altered 5-HTP response. It was also found that treatments with 5,7-DHT potentiated the release of prolactin and the disruption of responding in a fixed-ratio operant task induced by 5-HTP. Other experiments indicated that 5,7-DHT treatments potentiated 5-HTP without affecting the action of L-dihydroxyphenylalanine. In addition, administration of the decarboxylase inhibitor, R0-4-4602, at a dose that inhibits enzyme activity in brain, blocked the 5-HTP-induced behavioral syndrome in 5,7-DHT-treated rats, indicating that 5-HTP must be converted to serotonin for 5-HTP to alter behavior. Thus, the present studies indicate that destruction of serotonergic fibers during development can produce permanent changes in central serotonergic mechanisms.

5,7-Dihydroxytryptamine↗
PubMed1978

Lead exposure during infancy permanently increases lithium-induced polydipsia.

Lead (200 milligrams per kilogram) was administered daily by intubation to Long-Evans rats on days 3 through 30 of life. Thirty to 180 days after cessation of lead administration, the lead-treated rats were consistently more polydipsic after lithium administration (2 millimoles per kilogram per day) than were pair-treated controls. Lithium increased the plasma renin activity equally in both the lead treated and the control groups. These data are evidence that there may be permanent neural changes induced by postnatal exposure to lead that are manifested by pharmacological challenge with lithium.

Animals↗
PubMed1978

Evaluation of the effects of nerve growth factor and anti-nerve growth factor on the development of central catecholamine-containing neurons.

Intracisternal NGF or anti-NGF has been found to produce no long-term major alterations in central norepinephrine (NE) or dopamine levels when administered to neonatal rats. While NGF and anti-NGF were found to produce significant changes in brain NE content within one week of treatment, changes in central NE were no longer detectable at 30 days of age. Modification of the growth response of the central adrenergic neurons following 6-OHDA treatment was also not affected by NGF or anti-NGF when evaluated 3 weeks after treatment. However, centrally administered anti-NGF did induce a loss of peripheral NE terminals, which was attributed to leakage of the anti-NGF from the central injection site.

Adrenergic Fibers↗
PubMed1978

Biochemical and behavioral alterations in developing rats treated with 5,7-dihydroxytryptamine.

Intracisternal administration of 5,7-dihydroxytryptamine (5,7-DHT) to immature rats produced a marked reduction of brain norepinephrine and serotonin. Accompanying these reductions of brain amines were a decrease in body weight and alterations in behavior. After treatment with 5,7-DHT at 3 days of age, locomotor activity was significantly elevated at 14 days of age, but was reduced at 28 days of age. 5,7-DHT alone also induced a significant deficit in acquisition of the shuttle-box avoidance response and blocked body movements observed after decapitation. Treatment with either pargyline or desipramine before injection of 5,7-DHT eliminated the effect of 5,7-DHT on noradrenergic fibers while enhancing the effects of 5,7-DHT on brain serotonergic fibers. These treatments also minimized the deficits of 5,7-DHT on growth and on acquisition of the avoidance response and reversed the blockade of decapitation convulsions. However, animals pretreated with pargyline or desipramine before they received 5,7-DHT still demonstrated hyperactivity at 14 days of age equivalent to that observed in neonates that received only 5,7-DHT. Furthermore, a behavioral syndrome induced by 30 mg/kg of 5-hydroxytryptamine was markedly potentiated by all of the 5,7-DHT treatments which suggest that serotonin receptors were supersensitive.

5,7-Dihydroxytryptamine↗