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Biomedical subjects

J Z Nowak

Publications and source records attributed to J Z Nowak.

At least 91 records · Page 5Linked to original sources
PubMed1986

Effect of electroconvulsive shock (ECS) treatment on the histaminergic system in rat brain: biochemical and behavioural studies.

The effects of electroconvulsive shock (ECS) on brain histamine (HI) levels, 1-histidine decarboxylase (HD) and HI-methyltransferase (HMT) activities, and H2-receptor--mediated hypothermia were studied in rats. Single (x1) and repeated (x10, once daily) ECS had practically no effect on both HI levels and HMT activities in the rat hypothalamus, cerebral cortex and rest of the brain. ECS x10 significantly increased HI accumulation. ECS x1 (only after 24 h) and ECS x10 resulted in marked elevation of the brain HD activity; the most pronounced effect was observed in the cerebral cortex. Repeated, but not single, ECS reduced the hypothermic action of various centrally given histamine H2-receptor agonists (HI, 4-methylHI, dimaprit and impromidine). It is suggested that prolonged treatment with ECS activates the central histaminergic system in the rat. The histaminergic neurons in the cerebral cortex seem to be especially affected by repeated ECS.

Animals↗
PubMed1986

Tritoqualine and some aspects of histamine metabolism.

The influence of in vivo tritoqualine (Inhibostamin) given to mice as a single dose (100 mg/kg) or subchronically (40 mg/kg daily for 5 days) has been examined on 1. histamine release from peritoneal mast cells, 2. histamine level in some tissues, and 3. intestinal diamine oxidase activity. The effects of tritoqualine and alpha-hydrazinohistidine injected into eggs on the 16th, 17th or 18th day of chick embryo age on hatching time, histamine level and diamine oxidase (DAO) activity in brood's tissues were also examined. After a single administration of tritoqualine there was a drop of histamine level in brain, a similar tendency being observed in kidney and lung, and an opposite effect in intestine. With the latter coincides the reduced intestinal DAO. Subchronical treatment changes pattern of anti-IgE induced histamine release from mast cells, slightly reduces histamine content in brain, kidney and lung, and transiently increases intestinal DAO. Neither tritoqualine nor alpha-hydrazinohistidine influenced time of hatching. Both drugs differ in respect to direction and intensity of changes they evoke in histamine content and DAO activity in examined organs.

Amine Oxidase (Copper-Containing)↗
PubMed1985

Rapid desensitization of presynaptic dopamine autoreceptors during exposure to exogenous dopamine.

When nomifensine is employed to inhibit neuronal uptake, exposure to dopamine (DA) (0.1-0.3 microM) or apomorphine (0.01-0.1 microM) inhibited, in a concentration-dependent manner, the electrically evoked release of [3H]dopamine from slices of the rabbit caudate nucleus. Apomorphine inhibited transmitter release independently of the time of exposure to the drug (6-32 min). On the other hand, the inhibitory effect of exogenous dopamine occurred only if a short period (4-12 min) of exposure was employed. In studies on the electrically evoked release of [3H]acetylcholine in slices of the rabbit caudate nucleus there was no evidence for desensitization to apomorphine or exogenous dopamine at the level of the dopamine receptors that inhibit [3H]acetylcholine release. These results indicate that the dopamine autoreceptors modulating [3H]dopamine release in the caudate nucleus become subsensitive after a few minutes of exposure to exogenous dopamine. This effect does not occur at the level of the dopamine receptors which inhibit the release of [3H]acetylcholine.

Acetylcholine↗
PubMed1985

Histamine in the rabbit eye: distribution, synthesis, catabolism, and changes by light stimulation.

Histamine (HI) is present in all studied ocular (retina, choroid, optic nerve) and brain structures of the albino rabbit. HI levels in neural eye elements (retina and optic nerve) are relatively low, i.e. 70-140 ng/g tissue, and comparable with those found in the brain; a typical vascular tissue, i.e. choroid, contained approximately 10 times more HI. Histadine decarboxylase (HD) activity was found only in brain tissue, while histamine-methyltransferase (HMT) activity was present in all the eye and brain structures. Light stimulation produced changes in HI content only in the retina (decrease) and in the optic nerve (increase).

Animals↗
PubMed1985

Alteration of histamine metabolism in the rat brain under influence of various antidepressive treatments.

Effects of acute and prolonged (14 days, twice daily) treatments with various antidepressants: tricyclic (AMI, DMI, DOX, IMI), atypical (IPR, CIT), MAO-inhibitors (NIA, PARG), as well as ECS (X 1 or X 10) on histamine (HI) levels, histidine decarboxylase (HD) and histamine-methyltransferase (HMT) activities in particular brain structures of the rat were investigated. Acute treatment with all the tested drugs had no effect on the studied histaminergic parameters. Prolonged treatment with tricyclic drugs (except DMI) decreased HI level in the cerebral cortex; AMI and IMI increased HD activity. Atypical drugs changed neither HI levels nor HD activities. MAO-inhibitors showed no consistent effects on both histaminergic parameters. ECS X 10 (once daily) increased significantly HD activity in the cerebral cortex at 1 and 24 h. None of the antidepressant treatments affected HMT activity. It is concluded that various antidepressant treatments did not uniformly affect the histaminergic system in the rat brain. The observed changes varied depending on the kind of treatment and the brain structure analysed.

Amine Oxidase (Copper-Containing)↗
PubMed1984

Distribution and localization of histamine in bovine and rabbit eye.

Histamine (HI) is present in various structures of the bovine and rabbit eye (retina, choroid, sclera) and in the optic nerve of both species. The amine levels in particular structures of either cow or rabbit are highly differentiated, as well as profile of HI distribution which differs markedly between both species, except only the retina structure (HI levels were between 70-80 ng per g tissue). In the bovine retina HI is stored in non mast cell compartment, while in the optic nerve at least 50% of the amine is of mast cell origin. Approximately 90% of the retinal HI was recovered in the P1 subcellular fraction. HI in the bovine retina is metabolized by methylation. The data are discussed in terms of a possible physiological role of HI in the retina.

Animals↗
PubMed1983

Interaction between mianserin, an antidepressant drug, and central H1- and H2-histamine-receptors: in vitro and in vivo studies and radioreceptor assay.

Mianserin bimodally inhibited the stimulation of cyclic AMP accumulation mediated by histamine H1- and H2-receptors in slices from guinea-pig hippocampus with Ki values of 0.003 and 4 microM, respectively. Various treatments with mianserin were undertaken to determine whether the drug significantly interacted with cerebral histamine receptors in vivo in such a way that the response of the slice preparation could be modified. In hippocampal slices from animals treated with mianserin, the H2-receptor-mediated effect was estimated by constructing concentration-response curves to impromidine, a highly selective agonist, and that mediated by H1-receptors was measured by use of 0.5 mM 2-thiazolylethylamine (a predominantly H1-receptor agonist) in the presence of a maximal concentration of impromidine. After an acute treatment (10 mg/kg), the response mediated by H1-receptors was abolished whereas the response to impromidine in increasing concentrations was unchanged. After 1 week of drug administration (10 mg/kg twice daily), a 44% reduction in the response to 2-thiazolylethylamine was observed with no change in the response mediated by H2-receptors. When a dose of mianserin equivalent to a clinical dose (1 mg/kg, twice daily) was administered for 21 days, a partial but not significant decrease of the responsiveness to the H1-receptor agonist was accompanied by a significant increase of the maximal response to impromidine. Plasma levels of mianserin were estimated by a sensitive radioreceptor assay based upon inhibition of [3H]mepyramine binding. A good correlation was found between the concentration of mianserin in plasma and the tentative estimation of an equivalent concentration of mianserin in slices.

Animals↗
PubMed1983

Changes in sensitivity of release modulating dopamine autoreceptors after chronic treatment with haloperidol.

The release of recently taken up [3H]dopamine ([3H]DA) elicited by electrical stimulation (3 Hz, 2 min, 16 mA) from slices of the rabbit caudate nucleus is inhibited by apomorphine (0.01-0.1 microM) in a concentration-dependent manner. This action is mediated through the activation of presynaptic inhibitory DA autoreceptors. The inhibition of [3H]DA release by apomorphine (0.1 microM) was antagonized 2 hr, but not 24 hr after the single administration of haloperidol (1 mg/kg s.c.). After 2 days of withdrawal after 28 days of chronic treatment with haloperidol (1 mg/kg s.c.) once daily, apomorphine (0.01-0.1 microM) was more effective in inhibiting [3H]DA release elicited by electrical stimulation when compared with rabbits injected chronically with either the vehicle for haloperidol or with saline. In superfused slices of the rabbit caudate nucleus, exposure to S-sulpiride (0.1 and 1 microM) increased in a concentration-dependent manner the release of [3H] DA elicited by electrical stimulation. After 28 days of chronic treatment with haloperidol, the facilitation of [3H]DA release by S-sulpiride was significantly reduced when compared with the controls. The inhibition of central noradrenergic transmission by DA receptor agonists was studied in hypothalamic slices prelabeled with [3H]norepinephrine ([3H-NE]). Apomorphine (0.01-1 microM) inhibited the electrically evoked (5 Hz, 2 min, 26 mA) release of [3H]NE from hypothalamic slices of untreated rabbits. The sensitivity to the inhibitory effect of apomorphine on [3H]NE overflow remained unaffected after 2 days of withdrawal following 28 days of chronic treatment with haloperidol. In summary, our results indicate that chronic haloperidol administration induces changes in sensitivity of the DA autoreceptors regulating dopaminergic neurotransmission but does not affect the sensitivity of DA receptors modulating NE release in the central nervous system. These results suggest that the DA autoreceptors that regulate dopaminergic neurotransmission may play a physiological role in the modulation of transmitter release and consequently are susceptible to the development of changes in sensitivity after chronic receptor blockade. The possible implication of changes in sensitivity of the DA autoreceptor during the treatment of schizophrenia with neuroleptics is discussed.

Animals↗