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L R Troncone

Publications and source records attributed to L R Troncone.

7 recordsLinked to original sources

Effects of selective adrenoceptor agonists and antagonists on aggressive behavior elicited by apomorphine, DL-dopa and fusaric acid in REM-sleep-deprived rats.

REM sleep deprivation (REMSD) results in behavioral changes such as the appearance of affective aggression induced by apomorphine (APO) and other dopaminergic agents. REMSD modifies dopamine-mediated behavior as well as the adrenergic receptor sensitivity. This paper evaluates the interaction between these two neurotransmission systems through changes in APO-, DL-DOPA- and fusaric acid (FA)-induced aggressive behavior in REMSD rats pretreated with phentolamine, propranolol, metaraminol, prazosin, clonidine, yohimbine, isoproterenol, butoxamine and maprotiline. Only isoproterenol reduced FA-induced aggressiveness. No specific changes in aggressiveness were noticed with other treatments and not even inhibitors of norepinephrine transmission induced aggressive behavior. It is concluded that norepinephrine had a slight inhibitory action on aggressiveness elicited by dopaminomimetic agents in REMSD rats. Beta-adrenoceptors could be responsible for this effect since only beta-selective drugs reduced aggression. As REMSD reduces beta-adrenoceptor sensitivity, only minor changes in aggressiveness could be observed. It was noted that the three drugs used to induce aggressive behavior elicited different patterns of aggression.

Aggression

Effects of chronic haloperidol on stress-induced oral behaviour in rats.

Rats received daily injections of haloperidol (HAL, 5 mg/kg SC, or IP) or tartaric acid vehicle for 14-21 days. Four to six days after discontinuation of the daily injections, rats were given a single 5-min tail pinch (TP) test. HAL-treated rats showed significantly shorter latencies to display oral behaviours (OB: licking, gnawing, or drinking) compared to controls in five separate replications. Food consumption per se was not consistently affected. Shorter OB latencies were significantly correlated both with increased striatal 3H-spiperone binding and with apomorphine stereotypy scores. In a final experiment, this effect of HAL on OB latencies was blocked by a systemic injection of naloxone (2 mg/kg IP) prior to the TP test. Naloxone did not affect OB latency in control rats, suggesting the possibility of endogenous opiate involvement in the chronic HAL effects. The overall results suggest that OB latencies following mildly activating stimulation may provide a useful behavioural assay for neuroleptic-induced oral abnormalities as well as a functional index of striatal dopamine D-2 receptor sensitivity.

Animals

Reversal of the increase in apomorphine-induced stereotypy and aggression in REM sleep deprived rats by dopamine agonist pretreatments.

REM sleep deprivation (REMSD) induces augmented responses to dopaminergic agonists. Prolonged administration of neuroleptics induces a similar state, probably by the production of supersensitivity of dopaminergic receptors. Such a supersensitive state could be induced by REMSD as a result of impairment of dopamine neurotransmission. In order to test this hypothesis, bromocriptine, nomifensine, amphetamine, L-dopa, imipramine and electroconvulsive shock (ECS) were administered to rats during REMSD, and aggressive and stereotyped behaviors were measured. Amphetamine and L-dopa pretreatment attenuated the increases in apomorphine-induced stereotypy and aggression in REMSD rats, but ECS selectively reduced apomorphine-induced aggression. The other drugs tested were ineffective on both behavioral tests. Such a selective action may reflect different effects of ECS on different dopaminergic systems such as those involved with stereotypy and aggression. The results suggest that REMSD induces an increase in dopaminergic sensitivity which may be reversed by pretreatment with some dopaminergic agonists.

Aggression

Does REM sleep deprivation induce subsensitivity of presynaptic dopamine or postsynaptic acetylcholine receptors in the rat brain?

Yawning behavior was used to evaluate the sensitivity of presynaptic dopamine receptors and postsynaptic acetylcholine receptors of normal and REM sleep-deprived (REMSD) rats. The results show a lowering of the dose-response curve obtained with apomorphine and pilocarpine, as well as a shift to the right in the curve obtained with physostigmine. These results suggest that REMSD induces subsensitization of presynaptic dopamine receptors and/or postsynaptic acetylcholine receptors with different characteristics related to the mechanism of action of the cholinomimetic agent employed.

Animals

REM sleep deprivation induces a decrease in norepinephrine-stimulated 3H-cyclic AMP accumulation in slices from rat brain.

Beta adrenergic sites in rat brain are reduced after repeated treatment with antidepressant drugs, with REM sleep deprivation (REMSd) having the same effect. This paper reports the effects of REMSd in the production of 3H-cyclic AMP in frontal cortical slices by NE challenge. Data presented in this paper report a marked decrease in 3H-cyclic AMP synthesis after REMSd, which is in accordance with previous results showing adrenergic receptor down-regulation following REMSd. Results are discussed in view of possible interaction with dopaminergic systems and depression management.

Adenylyl Cyclases

Modifications on dopaminergic and cholinergic systems induced by the water tank technique: analysis through yawning behavior.

Animals deprived of REM sleep by the water tank technique show an important decrease in frequency of yawning, induced by dopaminergic (apomorphine in low doses) and cholinergic (physostigmine and pilocarpine) agonists, if they are tested immediately after the 96 hr of deprivation. In order to understand the mechanisms underlying the effects of REM sleep deprivation on dopaminergic and cholinergic systems, we decided to test the animals after a recovery period of 24 hr. It was observed that apomorphine-induced yawning was still significantly reduced, whereas pilocarpine-induced yawning had returned to normal. The findings suggest that REM sleep deprivation alters dopaminergic and cholinergic systems in different ways: it seems that the interference on the dopaminergic system is prior and stronger than on the cholinergic system, thus its recovery demands more time.

Animals