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Biomedical subjects

M Hauptmann

Publications and source records attributed to M Hauptmann.

At least 37 records · Page 2Linked to original sources

Rotational behavior produced by unilateral ventral noradrenergic bundle lesions: evidence for a noradrenergic-dopaminergic interaction in the brain.

In this study the effect of unilateral electrocoagulation of the ventral noradrenergic bundle (VB) on rotational behavior produced by dopaminergic agonists was investigated. Unilateral lesions to the VB produced a decrease in the concentration of noradrenaline but not dopamine, serotonin or 5-hydroxyindoleacetic acid (5-HIAA) in the ipsilateral part of the forebrain. These lesions produced also strong and dose-dependent preference for ipsilateral rotation after systemic injection of apomorphine or amphetamine. The results are discussed in terms of possible interaction between noradrenergic and dopaminergic systems and it is proposed that the VB plays a regulatory role in the function of brain nigro-striatal dopaminergic system.

Amphetamine↗

Effect of 6-hydroxydopamine-induced lesions of A10 dopaminergic neurons on aggressive behavior in rats.

The present study evaluated the effects of microinjections of 6-hydroxydopamine into the ventral mesencephalic tegmental area (nucleus A10) on aggressive behavior in rats. This treatment resulted in a reduction in foot-shock-induced fighting but failed to influence muricide (mouse-killing) behavior in chronically isolated rats. The general activity of animals tested in the open field was significantly increased two weeks after lesions. These behavioral changes were accompanied by a significant depletion of forebrain dopamine, with no difference between lesioned and sham-lesioned rats in norepinephrine and 5-hydroxyindole acetic acid levels.

Aggression↗

Lesion of serotonergic neurons antagonizes clonidine induced suppression of avoidance behavior and locomotor activity in rats.

The effects of clonidine on avoidance acquisition and locomotor activity were studied in male Wistar rats with 5,6-dihydroxytryptamine (5,6-DHT) lesions of the median raphe nucleus. Lesioned animals showed marked depletion in forebrain serotonin and 5-hydroxyindole acetic acid concentrations. clonidine (0.2 mg/kg IP in a single daily dose for 6 consecutive days) inhibited avoidance acquisition and reduced locomotor activity in unlesioned rats. In 5,6-DHT rats clonidine failed to produce depressive effect. The resistance of raphe-lesioned rats to clonidine is discussed on the basis of possible interaction between noradrenergic and serotonergic brain systems.

5,6-Dihydroxytryptamine↗

Studies on the effect of lesions of the ventral noradrenergic tract on the antinociceptive action of morphine.

In rats, lesions were placed in the ventral tegmental noradrenergic tract (VT). In some animals lesions also involved the dorsal tegmental noradrenergic tract (DT). Morphine (Mf) analgesia was examined by the tail compression method 8-9 days after lesions. VT lesions produced no changes in Mf activity, while lesions involving VT + DT produced a partial attenuation of the antinoceptive action of Mf. These results suggest that the ascending NA fibres forming the VT are not essential for the antinoceptive effect of Mf.

Analgesics↗

Effects of lesions in the ventral noradrenergic bundle on behavior and response to psychotropic drugs in rats.

Bilateral lesions of the ventral noradrenergic bundle (VB) decreased concentration of noradrenaline within the mesendiencephalon but not in the cortex. Lesioned rats showed increased activity measured in the open field test. Cataloptogenic effects of chlorpromazine and haloperidol were almost completely abolished in VB-lesioned animals. The stereotypy induced by both--amphetamine and apomorphine was, however, unchanged. It is supposed that lesions of the VB lead to increased activity in dopaminergic neurons in the brain.

Amphetamine↗

Behavioral effects of neuroleptics, apomorphine and amphetamine after bilateral lesion of the locus coeruleus in rats.

Bilateral lesions of the locus coeruleus (LC) markedly increased susceptibility to the cateleptogenic effects of neuroleptics. The apomorphine-induced stereotypy was enhanced in rats with lesioned LC whilst amphetamine stereotypy was only slightly increased. No changes in locomotor activity have been observed in LC-lesioned rats treated with apomorphine and amphetamine. This data indicates that lesions of the LC produce decreased activity of dopaminergic brain neurons as well as supersensitivity of dopaminergic receptors.

Animals↗

Lesions of midbrain raphe and ethanol narcosis in rats.

Serotonin -- depleting lesions involving nucleus raphe medianus markedly prolonged ethanol-induced sleep in rats. Lesioned animals showed increased general activity and decreased serotonin and 5-hydroxy-indoleacetic acid concentrations in the forebrain.

Animals↗

Brain serotonin and epileptic seizures in mice: a pharmacological and biochemical study.

5-Hydroxytryptophan (5-HTP) reduced the intensity of both audiogenic and pentylenetrazol seizures. p-Chlorophenylalanine reduced audiogenic seizure (AGS) susceptibility but failed to change the pentylenetetrazol seizure (PTS). Drugs blocking brain serotonin (5-HT) receptors suppressed AGS but caused no clear effects upon PTS. Pentylenetetraziol-induced shock increased brain 5-hydroxyindoleacetic acid (5hiaa) concentrations and decreased 5-HT levels. Single audiogenic shock decreased the acumulation of 5-HT and 5-HIAA in the brains of mice pretreated with 5-HTP. On the other hand PTS increased the accumulation of 5-HT and 5-HIAA in the brains of mice pretreated with 5-HTP. It is suggested that AGS decrease brain 5-HT turnover whilst PTS cause an opposite effect.

5-Hydroxytryptophan↗

[Blood MAO/DBH index and the results of the treatment of endogenous depression].

In the group of 115 endogenous depression patients 84 responded to tricyclic antidepressant medication and 31 remained drug-resistance. The changes of platelet MAO activity and serum DBH activity in the latter group were found. Among drug-resistant patients, 40% showed low MAO/DBH index (.6) and in 36% the index was within the medium range (.6-1.9). The low value of the index is predominantly connected with the increase of DBH and decrease of MAO activity, and it may become the potential predictive factor for the pharmacotherapy in endogenous depression. The results show the influence of the disturbances of catecholamines synthesis and degradation on the phenomenon of drug-resistance to tricyclic antidepressants.

Antidepressive Agents, Tricyclic↗

Are ascending noradrenergic and serotonergic pathways necessary for effects of electroconvulsive treatment? Clonidine hypothermia and forced swim study.

Are ascending noradrenergic and serotonergic pathways necessary for effects of electroconvulsive treatment? Clonidine hypothermia and forced swim study. W. DANYSZ , W. KOSTOWSKI, M. HAUPTMANN, A. BIDZINSKI. Pol. J. Pharmacol. Pharm., 1989, 41, 15-22. Influence of chemical lesions to the noradrenergic locus coeruleus (intracerebral 6-OHDA injection, systemic administration of DSP-4) and serotonergic raphe system (intracerebral 5,7-DHT) on some effects produced by electroconvulsive shock (ECS) was studied. Administration of ECS slightly but significantly attenuated clonidine (CLO)-induced hypothermia and reduced rats immobility in forced swim test. DSP-4 reduced ECS action on CLO hypothermia remaining without effect upon ECS action in the second test. Other lesions were ineffective in both tests. This finding is in contrast to results obtained previously in animals receiving desipramine. The possible difference between ECS and antidepressant drugs action is discussed.

Animals↗

On the role of noradrenergic neurotransmission in the action of desipramine and amitriptyline in animal models of depression.

Three weeks of treatment with desipramine (DMI) and amitriptyline (AMI) reduced the hypothermic action of clonidine in rats. Both electrolytic and 6-hydroxydopamine lesions of the locus coeruleus (LC) and administration of DSP-4 counteracted the reduction of clonidine hypothermia produced by antidepressants. Lesions of the LC and DSP-4 administration also antagonized the anti-immobility action of single doses of DMI but failed to modulate the action of AMI in the forced swim test. Chronic DMI action on the rat immobility was reduced by 6-hydroxydopamine lesions of the LC: other lesions (electrolytic, DSP-4) were ineffective. Electrical stimulation of the LC increased the rat activity in the forced swim paradigm, producing an effect similar to that of antidepressants. The anti-immobility effect of DMI as well as LC stimulation were antagonized by drugs blocking alpha-adrenoceptors (phenoxybenzamine, prazosin) but not by propranolol, a non-selective antagonist of beta-adrenoceptors. On the other hand, the anti-immobility action of AMI was unchanged by all adrenolytics used in that study. The results indicate that the LC system and alpha 1-adrenoceptors play an important role in the antidepressive action of DMI, but not AMI, in the forced swim test.

Amitriptyline↗