Biomedical subjects
W Kostowski
Publications and source records attributed to W Kostowski.
[Neuroleptic drugs].
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[Antidepressive agents].
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A study of the effects of clonidine on the EEG in rats treated with single and multiple doses of antidepressants.
The influence of repeated and single administrations of desipramine, amitryptiline, and mianserin on the EEG effects of clonidine has been investigated in rats implanted with chronic cortical electrodes. Clonidine induced a dose-dependent EEG synchronization in control animals. Signs of behavioral depression occurred after administration of moderate (0.1 mg/kg) and higher (0.2 mg/kg) doses of clonidine. Single doses of desipramine and amitryptiline attenuated the clonidine effect, while mianserine potentiated clonidine-induced synchronization. Antidepressants given once daily for 14 days completely (desipramine and amitryptiline) or partially (mianserin) reduced the effect of clonidine. Antidepressants alone produced only a slight effect on cortical EEG pattern.
Brain serotonergic neurons: their role in a form of dominance-subordination behavior in rats.
The present study evaluated the possible role of brain serotonergic neurons in dominant-subordinate (D-S) behavior in Wistar male rats competing for water. Treatment of D rat with drugs that stimulate serotonergic neurons of receptors (tryptophan, 5-hydroxytryptophan, quipazine, femoxetine) resulted in D-S reversal. A similar effect was observed when the S animal was treated with drugs that blocked serotonin synthesis (p-chlorophenylalanine) or receptors (metergoline). The D-S relationship was unchanged when serotonergic drugs were given to the S subject (tryptophan or quipazine) or when D animal received p-chlorophenylalanine. None of the drugs tested influence the water intake and the general activity of rats. Rats with lesioned midbrain raphe nuclei were always dominant when paired with sham lesioned counterparts. Our results indicate that one form of dominance behavior can be inversely related to the activity of brain 5-HT system.
Activity of desipramine, fluoxetine and nomifensine on spontaneous and p-CPA-induced muricidal aggression.
Antidepressant drugs reportedly counteract mouse-killing activity by rats. There is evidence that antidepressant derivatives exert their anti-muricidal activity through both noradrenergic and serotonergic neurons. The experiments were performed in two types of muricidal aggression with three antidepressants characterized by different neurochemical activity. No major differences in the antimuricidal efficacy of the drug-employed were found, even though spontaneous muricidal animals resulted on the whole less sensitive to antidepressants than p-CPA-induced muricidal rats. In these last animals nomifensine proved to be more potent than desipramine and fluoxetine.
Studies on brain noradrenergic neurons in animal model for antidepressive activity.
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Chlordiazepoxide antagonizes locus coeruleus-mediated suppression of muricidal aggression.
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[Neurotransmitters and neuropeptides].
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[Role of membrane receptors in the pathogenesis of diseases in and/drug action].
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[Melanostatin (MIF-1): central action and clinical use].
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Antagonism of behavioural depression produced by clonidine in the Mongolian gerbil: a potential screening test for antidepressant drugs.
The effects of various antidepressant drugs and some other therapeutic agents on the depression of locomotion and exploratory activity induced by clonidine (0.1 mg/kg IP) were investigated in the Mongolian gerbil (Meriones unquiculatus). In parallel experiments, the effect of yohimbine on clonidine-induced sedation was observed. The following behavioral components were analysed: ambulation, rearing and novel object investigation. Yohimbine antagonized the effects of clonidine in a dose-dependent manner. All antidepressants similarly antagonized the effect of clonidine on ambulation but they differed to a greater extent in their potency in counteracting the clonidine action on exploration, particularly the novel object investigation. On the other hand diazepam and neuroleptic agents such as pimozide and flupentixol failed to antagonize the clonidine effects. The antagonism of clonidine-induced behavioral depression might be used in the selection of antidepressants.
Differential clonidine effects on EEG following lesions of the dorsal and median raphe nuclei in rats.
The effects of clonidine on EEG activity and gross behavior were studied in rats with electrolytic lesions of the median (MR) and dorsal (DR) raphe nuclei. Lesioned animals showed significant depletion in forebrain serotonin concentrations. Clonidine (0.1 mg/kg and 0.2 mg/kg IP) produced synchronization in cortical EEG pattern and markedly increased alpha and theta activities in unlesioned animals. Clonidine treatment resulted also in a sedative response. In MR lesioned rats clonidine effect upon EEG was significantly reduced and, additionally, sedative response was not seen. On the other hand clonidine effect on EEG was markedly increased in rats with lesioned DR. These results are discussed on the basis of possible interaction between serotonergic and noradrenergic neurons in the brain.
Interaction between noradrenergic and serotonergic brain systems as evidenced by behavioral and biochemical effects of microinjections of adrenergic agonists and antagonists into the median raphe nucleus.
The effects of microinjections of adrenergic receptors agonists and antagonists into the median raphe nucleus (MR) on behavior and serotonin (5HT) metabolism was examined in rats. Administration of adrenergic alpha 1 and alpha 2 receptor agonists (noradrenaline, phenylephrine, clonidine) produced behavioral excitation in the open field test and a tendency to decrease the forebrain 5-hydroxyindolo-acetic acid (5HIAA) concentration. Opposite effects were seen after microinjection of adrenergic alpha receptor antagonists (phenoxybenzamine, phentolamine but not yohimbine). A significant negative correlation was found between the effects on locomotor activity and 5HIAA levels in these rats. No effect was present after injection of beta receptor agonist salbutamol or antagonist propranolol. It is suggested that noradrenaline released from noradrenergic terminals in the MR tonically inhibits the activity of 5HT neurons thus producing symptoms of 5HT deficiency and that this action of noradrenaline is probably limited to the effects on alpha 1 but not alpha 2 nor beta adrenoceptors in this brain region.
Aggressive behaviour and the central serotonergic systems.
A brief critical review of serotonin involvement in two classes of aggressive behaviour, i.e. affective and predatory aggression, is presented. Special emphasis is put on the differentiation between the role played in aggression by the two ascending serotonergic systems, the mesolimbic and the mesostriatal. It is concluded that only serotonergic neurons from the dorsal raphe nucleus forming the mesostriatal system play an inhibitory role in both classes of aggression. The mesolimbic system does not seem to be directly involved in an aggression modulation. The data suggesting that the dorsal raphe may mediate its inhibitory influence through the medial amygdala is presented and discussed. Finally some attention is given to the problem of serotonin metabolism variability (biorhythm) and its implications in behavioural studies.
Behavioral studies in spontaneously hypertensive rats.
In the present study we examined some behavioral patterns in spontaneously hypertensive (SHR) male rats as compared with Wistar (W) rats. The following methods were employed: open field test, two-way active avoidance, passive avoidance, shock-induced fighting, shock-induced suppression of drinking (conflict test), and dominant-subordinate behavior in rats competing for water. Spontaneously hypertensive rats showed higher level of locomotor activity, lower emotionality, lower anxiety level, increased acquisition of avoidance tasks, and enhanced dominance behavior. In addition, hypertensive rats were less aggressive in shock-induced fighting test. It is concluded, that spontaneously hypertensive rats seem to be hyperactive in terms of locomotor activity while their emotionality appears to be paradoxically reduced.
[Beta adrenergic receptors].
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The involvement of brain serotonin in the clonidine-induced hypothermia in rats.
The effects of manipulation with brain serotonergic (5HT) activity on clonidine-induced hypothermia in rats were investigated. Lesion to the median raphe nucleus as well as p-chlorophenylalanine pretreatment significantly potentiated the temperature decrease after 0.2 mg/kg of clonidine. Pretreatment with a 5HT releasing agent--fenfluramine, or a 5HT receptor agonist--m-chlorophenylpiperazine (mCPP) antagonized the effect of clonidine. Additionally, both fenfluramine and mCPP given alone produced an elevation in body temperature. These results are discussed in terms of an involvement of the 5HT neuronal system in clonidine hypothermia, and the dissociation of the role of 5HT system in clonidine-induced behavioral and vegetative effects is suggested.