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Biomedical subjects

W Kostowski

Publications and source records attributed to W Kostowski.

At least 73 records · Page 4Linked to original sources
PubMed1988

Comparison of desipramine, amitriptyline, zimeldine and alaproclate in six animal models used to investigate antidepressant drugs.

In the present paper the acute actions primarily of the tricyclic antidepressants amitriptyline and desipramine, the atypical antidepressant zimeldine and the potential antidepressant alaproclate were evaluated in six models used for studying antidepressant agents. These included the forced swim test, a modified learned helplessness procedure, the clonidine hypothermia test, the social dominance test (using the interaction with clonidine), a differential-reinforcement-of-low-rates (DRL-72s) schedule and conditioned avoidance response. The results showed desipramine to be effective in all the tests employed. Zimeldine was effective in the learned helplessness, DRL-72s and domination tests, but also caused notable deficits in two-way active avoidance response. Alaproclate was effective in all the tests except the domination paradigm. Amitriptyline was effective in all tests employed. The results are discussed in relation to the possible mechanism of action of these compounds in the test models employed.

Alanine↗
PubMed1987

The effects of antidepressants and electroconvulsive shocks on the functioning of the mesolimbic dopaminergic system: a behavioral study.

The mesolimbic dopaminergic innervation is supposed to be involved in the mechanisms of central effects exerted by various classes of psychotropic drugs. Antidepressants have been found to interact with the brain dopaminergic system as well, although the precise central location of this interaction is unknown. Some data point to the mesolimbic dopaminergic system as a possible target for antidepressant action. The aim of the present experiment was to verify this hypothesis. It was found that a long-term treatment of rats with desipramine, citalopram or electroconvulsive shocks potentiated the dopaminergic mechanisms within the nucleus accumbens, as evidenced by an increase in or the appearance of behavioral effects (exploratory locomotion, an active behavior in the Porsolt test) following microinjections of dopaminergic agonists into this brain area. Similar results obtained with different methods of treatment for depression indicate that the effect of antidepressants and electroshocks on dopaminergic mechanisms within the nucleus accumbens may be linked directly to the mechanism of their antidepressant action.

Animals↗
PubMed1987

Norepinephrine-mediated suppression of apomorphine-induced aggression and locomotor activity in the rat amygdala.

The effect of injections of norepinephrine (NE)-depleting toxin DSP-4 into the central amygdala (AMY) on apomorphine-induced fighting (AIF) was studied. In addition, the influence of such treatment on related parameters such as spontaneous activity, pain sensitivity and changes in locomotion after (+)3-PPP or apomorphine (1 mg/kg SC each) were verified. Finally, injections of NE or phenylephrine into the AMY five min before AIF were performed. DSP-4 induced marked (-71%) and selective fall in NE within the AMY accompanied by significant increase in aggressive response to 5 mg/kg of apomorphine. DSP-4-treated animals were less active in the open field and more sensitive to pain in a hot plate test. They were also more responsive to locomotor-augmenting action of apomorphine. Significant suppression of AIF was seen after injections of NE and phenylephrine into the AMY. The results suggest that NE input to the AMY plays an inhibitory role in dopamine-related locomotion and aggressivity. Moreover, amygdalar NE appears to be involved in general activity and pain perception modulation.

Aggression↗
PubMed1987

Differential effects of chronic ethanol on apomorphine-induced locomotion, climbing and aggression in rats.

Male Wistar rats were tested for apomorphine-induced locomotion, climbing and aggression after 3 week's intragastric ethanol (EtOH) treatment, 5 g/kg as 20% solution daily. The ability of apomorphine (APO) to elicit rearing (1 mg/kg i.p.) and climbing (0.5 mg/kg i.p.) was significantly suppressed in EtOH withdrawn animals. General locomotor activity in response to 1 mg/kg of APO i.p. did not differ between control and EtOH-treated groups. Affective aggression was checked in pairs of low-aggressive rats, i.e. resistant to the aggression inducing action of 10 mg/kg APO. No symptoms of aggression appeared in control animals whereas EtOH administered rats responded with marked aggression to APO. The different effect of chronic EtOH on responsiveness to APO in three behavioral models is discussed in terms of varying involvement of dopaminergic systems and receptors in behavioral phenomena as well as their susceptibility to prolonged EtOH.

Aggression↗
PubMed1987

Chronic treatment with antidepressant drugs and ECT differentially modifies the hypothermic action of clonidine and guanfacine.

The hypothermia inducing action of clonidine and guanfacine was abolished by yohimbine and idazoxan pretreatment which suggests an alpha 2-adrenoceptor involvement in this effect. The effects of acute and chronic treatment with the antidepressant drugs desipramine (DMI), amitriptyline (AMI), maprotiline (MAP), mianserin (MIAN), iprindol (IPR), alaproclate (ALA) and electroconvulsive treatment (ECT) on the hypothermic action of the alpha 2-adrenoceptor agonists clonidine and guanfacine were studied. Acute administration of MIAN potentiated clonidine induced hypothermia whereas acute MIAN, IPR and ALA potentiated guanfacine induced hypothermia. Repetitive DMI, AMI and MAP treatment attenuated clonidine-induced hypothermia whereas guanfacine-induced hypothermia was potentiated by chronic treatment with DMI, AMI, MAP and MIAN, ECT applied without anaesthesia attenuated both clonidine and guanfacine hypothermia, however, under ethyl ether anaesthesia ECT was effective only towards guanfacine hypothermia. This discrepancy is discussed in terms of the relative selectivity of the agonists used, the reliability of agonist studies for indexing receptor function, and possible pharmacokinetic interaction.

Animals↗
PubMed1986

Effect of chronic administration of alprazolam and adinazolam on clonidine- or apomorphine-induced aggression in laboratory rodents.

The activity of chronic (3 weeks) treatment with the triazolobenzodiazepines, alprazolam and adinazolam, on clonidine- and apomorphine-induced aggression were studied. Adinazolam, like desipramine, potentiated aggression induced by clonidine while diazepam and alprazolam completely abolished it. In the apomorphine-induced aggression, adinazolam suppressed both aggressivity and stereotypy, while diazepam slightly potentiated it. Alprazolam did not modify the effect of aggression induced by apomorphine. On the whole, while adinazolam seemed to develop an activity closer to that of a classical antidepressant like desipramine, alprazolam appeared to be more similar to the benzodiazepines on clonidine-induced aggression in mice. Compared to desipramine and diazepam, adinazolam left these two effects induced by apomorphine almost unchanged. The experiments performed showed differences between the profiles of action of the two triazolobenzodiazepines studied.

Aggression↗
PubMed1986

Suppression of ethanol tolerance and dependence in rats treated with DSP-4, a noradrenergic neurotoxin.

The formation of tolerance to the hypothermic effect of ethanol was inhibited in rats after intraperitoneal injection of the neurotoxin DSP-4 50 mg/kg. The neurotoxin also significantly suppressed the ethanol withdrawal syndrome; hyperlocomotion, audiogenic seizures and spasticity. These behavioural changes were accompanied by a 52% decrease of the brain norepinephrine (NE) content, with no alterations in the dopamine or serotonin levels. The results indicate that intact NE neurons are necessary for the development of tolerance to ethanol-induced hypothermia and are involved in the expression of the ethanol withdrawal syndrome.

Alcoholism↗
PubMed1985

Modification of behavioral response to intra-hippocampal injections of noradrenaline and adrenoceptor agonists by chronic treatment with desipramine and citalopram: functional aspects of adaptive receptor changes.

The present study investigated the effects of acute and of chronic treatment with desipramine (DI) and citalopram (CT) on the alterations in rat behavior in the open field and in the forced swim tests produced by intra-hippocampal microinjections of noradrenaline (NA) and adrenoceptor agonists. Chronic but not acute treatment with DI potentiated the stimulatory effects of NA on the rats' behavior in the open field test and in the forced swim test as well as revealed the excitatory effect of microinjections of phenylephrine at a dose producing insignificant changes when given alone. The depressive effects of clonidine in the open field test were antagonized by acute DI administration and reversed by chronic DI. No characteristic changes in the isoproterenol-induced increase in rat locomotion were observed following chronic DI since the antagonistic interaction was found after both acute and chronic DI pretreatment. Chronic though not acute administration of CT produced effects in the forced swim test similar to those of DI, i.e. excitatory effects of phenylephrine and clonidine on behavior. The data indicate a potentiation of excitatory processes in the brain limbic structure, probably mediated via alpha 1-adrenoceptors.

Adaptation, Biological↗
PubMed1985

A stimulatory effect of intraaccumbens injections of noradrenaline on the behavior of rats in the forced swim test.

Intraaccumbens injections of catecholamines noradrenaline and dopamine, though not of serotonin, stimulated locomotion by rats in an open field, 10-15 min later. Similar effects were observed 5 min after microinjection of apomorphine whereas clonidine only attenuated locomotor activity. On the other hand, intraaccumbens administration of phenylephrine, isoproterenol and quipazine, in doses similar to an effective dose of noradrenaline, did not alter rat open field behavior. The escape-directed activity of rats in the forced swim test (FST) was stimulated 5 min after local administration of noradrenaline, phenylephrine, isoproterenol or apomorphine only. No effects in the FST were observed 15 min after noradrenaline injection or after intracaudate noradrenaline administration. The stimulatory effects of intraaccumbens noradrenaline injection in the FST were antagonized by the local pretreatment of rats with phentolamine, though not with propranolol. Accordingly, it is possible to conclude that both catecholamines, but not serotonin, play complex and probably distinct roles within the nucleus accumbens in the stimulation of activity by rats in the FST and the open field test.

Analysis of Variance↗
PubMed1985

Some behavioral effects of microinjections of noradrenaline and serotonin into the amygdaloid body of the rat brain.

The effects of microinjections of noradrenaline (NA) and serotonin (5HT) into the basomedial part of the amygdaloid body (BM AB) on various forms of behavior were studied in rats. NA as well as 5HT administered to the BM AB had dose-related and general inhibitory influence on the rats' behavior in the open field test. The reactivity of rats to pain (tail compression) was attenuated by 5HT injections. The effect of NA in this test was less clear, though some inhibitory tendency was also present. Pretrial injections of NA (40 micrograms) and 5HT (40 micrograms) significantly impaired the retention of a passive avoidance reaction. NA injections also produced some disinhibitory effects on shock-suppressed drinking in the conflict test. The effects of intra-amygdalar administration of NA and 5HT on open field behavior were potentiated by pretreatment of rats with nialamide, a monoaminooxidase inhibitor. The results are discussed in terms of an involvement of the amydalar NA and 5HT in the regulation of animal behavior.

Amygdala↗
PubMed1985

Aggressive behavior inhibition by serotonin and quipazine injected into the amygdala in the rat.

The effects on aggressive behavior, open-field activity, and pain threshold of bilateral microinjections of serotonin (20 micrograms) and quipazine (20 micrograms), the direct serotonergic receptor agonist, into the cortico-medial amygdala were investigated in Wistar rats. Both drugs significantly prolonged the attack latency in isolated killer rats (predatory aggression model), and suppressed the incidence of aggressive postures/attacks in shock-induced fighting test (affective aggression). The only difference in the open-field behavior was the lower number of central square entries in drug-treated compared to saline-injected rats. None of the substances produced any significant change in jump threshold. It is concluded that stimulation of serotonin receptors within the amygdala produces inhibition of affective and muricidal behavior in isolated rats. The effect does not seem to be dependent on changes in general activity and pain sensitivity.

Aggression↗