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L Jaworska

Publications and source records attributed to L Jaworska.

At least 19 recordsLinked to original sources
PubMed1995

Repeated morphine administration down-regulates glucocorticoid, but not mineralocorticoid, receptors in the rat hippocampus.

Activation of the hypothalamic-pituitary-adrenal axis (HPA) is known to be an important component of a neuroendocrine response to opiates. Since this axis is under inhibitory control of hippocampal corticosteroid receptors, the present study has been designed to determine the effects of single (20 mg/kg IP) and repeated (from 20 to 100 mg/kg/day, IP, twice a day for 10 days) morphine administration on binding parameters of these receptors. Glucocorticoid (GR) and mineralocorticoid (MR) receptors were examined by an in vitro [3H]-corticosterone binding in the cytosol from the rat hippocampus, using the selective GR agonist RU 28362 to discriminate between MR and GR. Repeated, but not single, treatment with morphine significantly (by approximately 22%) reduced the density of GR at 2 h and tended to decrease it at 72 h after the last drug injection. The density of MR was unchanged at those time points. No changes in dissociation constants of either type of the receptors were found following single or repeated morphine administration. The plasma corticosterone level was significantly increased 1 h after acute and chronic administration of morphine (382 and 527%, respectively). These results indicate that repeated morphine administration downregulates GR receptors, which may impair the feedback control mechanism of the HPA activity.

Animals↗
PubMed1994

Repeated amphetamine evokes biphasic alterations in the tyrosine hydroxylase mRNA level in the rat adrenal medulla: an in situ hybridization study.

In the present study we estimated the effects of single and repeated administration of d-amphetamine (5 mg/kg, i.p., twice a day for 14 days) on tyrosine hydroxylase (TH) mRNA levels in the rat adrenal medulla. In situ hybridization experiments, conducted using a [35S]d-ATP-labelled deoxyoligonucleotide probe and a densitometric analysis of autoradiograms, showed that repeated d-amphetamine moderately increased the TH mRNA level (by ca. 24%) in the adrenal medulla at 2 h after the last injection. In contrast, after 48 h the TH mRNA level was decreased (by ca. 21%). No significant changes in the TH mRNA level in the adrenal medulla were found following single administration of d-amphetamine. These results suggest that repeated d-amphetamine administration leads to biphasic changes in the adrenal TH biosynthesis, which may reflect an adaptive response to chronic drug treatment.

Adrenal Medulla↗
PubMed1994

The effect of repeated amphetamine administration on the proopiomelanocortin mRNA level in the rat pituitary: an in situ hybridization study.

The effect of single and repeated administration of amphetamine (5 mg/kg i.p., twice daily, 14 days) on the proopiomelanocortin (POMC) mRNA level was investigated in the rat pituitary. In situ hybridization histochemistry, using a 35S-d-ATP-labelled deoxyoligonucleotide probe and densitometric analysis of autoradiograms, showed that repeated administration of amphetamine moderately increased the POMC mRNA level (by approximately 16%) in the anterior and the intermediate lobes of the pituitary at 72, but not 2, hr after the last injection. Adrenalectomy (48 h after the last drug injection) increased the POMC mRNA level only in the anterior lobe of repeated saline- and amphetamine-treated rats by 59 and 67%, respectively. No significant changes in POMC mRNA level in either lobe were found following single administration of amphetamine. These results suggest that repeated amphetamine administration leads to a delayed and moderate increase in POMC biosynthesis in the rat pituitary. On the other hand, the responsiveness of the POMC pituitary system to adrenalectomy was not significantly altered in rats treated repeatedly with amphetamine.

Adrenalectomy↗
PubMed1993

The effect of repeated combined treatment with nifedipine and antidepressant drugs or electroconvulsive shock on the hippocampal corticosteroid receptors in rats.

The effect of nifedipine, a calcium channel antagonist, on changes in the density of glucocorticoid (GR) and/or mineralocorticoid receptors (MR), induced by long-term treatment with antidepressant drugs (imipramine and amitriptyline) or electroconvulsive shock (ECS) was investigated in the rat hippocampus. Long-term treatment with imipramine or amitriptyline significantly increased the density of GR, while chronic ECS significantly elevated the density of both GR and MR. Nifedipine administered repeatedly had no effect on the basal GR and MR levels, however when the rats were pretreated with nifedipine, the antidepressant drugs and ECS were unable to increase the density of GR, or GR and MR, respectively. These results indicate that, unlike in other models, nifedipine blocks the effects of antidepressant drugs and ECS on GR and/or MR. They also show, that antidepressant drugs and ECS differ in their effect on the density of GR and MR.

Amitriptyline↗
PubMed1993

The role of dopamine receptors in the release of thyrotropin-releasing hormone from the rat striatum and nucleus accumbens: an in vitro study.

In the present study we examined the influence of dopamine (DA) stimulants: amphetamine (an agent releasing DA), apomorphine (a non-selective agonist of DA receptors), quinpirole (a selective agonist of D2 receptors) and SKF-38393 (a selective agonist of D1 receptors) on the in vitro release of thyrotropin-releasing hormone (TRH) from the rat striatal slices and nucleus accumbens fragments. It was shown that amphetamine, apomorphine and quinpirole (all those drugs added in concentrations of 10(-8)-10(-5) M), concentration-dependently increased the release of TRH, a more potent effect being observed in striatal slices. On the other hand, SKF-38393 (10(-6)-10(-5) M) was ineffective. Furthermore, the increases in the TRH release from the striatal slices, induced by 10(-5) M of amphetamine, apomorphine or quinpirole, were completely blocked by the selective D2 receptor antagonist sulpiride (10(-5) M), but not by the selective D1 receptors antagonist SCH-23390 (10(-5) M). These results indicate that stimulation of D2 receptors is responsible for the TRH release from the striatum and nucleus accumbens in vitro, and that this effect may be involved in the decrease in the peptide content in the striatum following DA stimulants, observed earlier in in vivo studies.

Animals↗
PubMed1992

The effect of p-chloroamphetamine and p-chlorophenylalanine on the level of thyrotropin-releasing hormone and its receptors in some brain structures and lumbar spinal cord of the rat.

The concentration of thyrotropin-releasing hormone (TRH) and the density and affinity of TRH receptors were examined in the ventral and dorsal lumbar spinal cord, nucleus accumbens and striatum of rats with the 5-hydroxytryptamine (5-HT) nerve terminal destroyed with p-chloroamphetamine (PCA), or in animals treated with the inhibitor of 5-HT synthesis p-chlorophenylalanine (PCPA). PCA (2 x 10 mg/kg i.p., 9 and 8 d before killing) and PCPA (3 x 300 mg/kg i.p., 72, 48 and 24 h before killing)--either of them dramatically diminishing the 5-HT and 5-HIAA concentrations in all the examined structures--reduced the TRH level and increased the density of TRH receptors in the ventral lumbar spinal cord. PCPA also reduced the TRH content in the nucleus accumbens. The PCA-induced reduction in the TRH level and increase in the density of TRH receptors in the ventral lumbar spinal cord were significantly attenuated by citalopram (2 x 20 mg/kg i.p., 30 min before PCA), a selective inhibitor of 5-HT uptake. Our results constitute a further proof that coexistence of TRH and 5-HT takes place in the ventral lumbar spinal cord and then indicate that other form(s) of relationship between 5-HT and TRH may exist in some parts of the central nervous system. They also suggest that an up-regulation of TRH receptors occurs in the spinal cord as a result of TRH depletion.

Animals↗
PubMed1991

The role of dopamine in regulation of thyrotropin-releasing hormone in the striatum and nucleus accumbens of the rat.

The effect of alpha-methyl-p-tyrosine (alpha-MT), FLA-63, amphetamine, apomorphine and quinpirole on the concentration of thyrotropin-releasing hormone (TRH) in the striatum and nucleus accumbens was studied in rats. It has been found that the TRH content was increased in both those structures after alpha-MT, an inhibitor of tyrosine hydroxylase which reduced the concentration of both dopamine (DA) and noradrenaline (NA), but not after FLA-63, an inhibitor of DA-beta-hydroxylase which decreased the NA level without affecting DA. On the other hand, the indirectly acting dopaminomimetic amphetamine, the non-selective DA receptor agonist apomorphine, and the selective D2 receptor agonist quinpirole reduced the TRH level in the striatum, but not in the nucleus accumbens. Moreover, the decrease in the striatal peptide content induced by DA-mimetics was antagonized by the selective D2-receptor antagonist sulpiride, but not by the selective D1 receptor antagonist SCH 23390. The effect of amphetamine was not modified by the selective alpha 1-adrenoceptor antagonist prazosin. These results indicate that DA and D2 receptors play a significant role in the regulation of the striatal TRH.

Amphetamine↗
PubMed1990

Repeated treatment with amitriptyline or electroconvulsive shock does not affect thyrotropin releasing hormone receptors in discrete rat brain structures.

We studied the effect of repeated treatment with amitriptyline (10 mg/kg, p.o., twice daily for 14 days) or electroconvulsive shock (ECS) (once daily for 10 days) on the thyrotropin-releasing hormone (TRH) content and TRH receptors in the cerebral cortex, nucleus accumbens, striatum and septum of the rat. Repeated amitriptyline did not significantly affect the density or affinity of TRH receptors in the examined structures, but caused a marked increase in the TRH content in the striatum and nucleus accumbens. Long-term treatment with ECS reduced the density and affinity of TRH receptors in the septum only, but it increased the TRH concentration in the cerebral cortex and striatum. These results, together with the literature data, indicate that there is no simple relationship between the brain content (and release) of TRH and the functional sensitivity of TRH receptors on one hand, and the density of these receptors on the other.

Amitriptyline↗
PubMed1990

The effect of fenfluramine on the thyrotropin-releasing hormone (TRH) content in the rat brain structures and lumbar spinal cord.

The effect of fenfluramine (20 mg/kg i.p.) was studied on the thyrotropin-releasing hormone (TRH) content in several brain structures and the ventral part of the lumbar spinal cord of the rat. The effect of fenfluramine on the concentration of 5-hydroxytryptamine (5-HT) in some brain structures and the lumbar spinal cord was also examined. It was found that fenfluramine had no effect on the TRH level in the hypothalamus, hippocampus, occipital cortex, septum, nucleus accumbens and ventral part of the lumbar spinal cord, though the drug produced a profound depletion (by more than 60%) of 5-HT in the hypothalamus, nucleus accumbens, striatum and lumbar spinal cord. On the other hand, fenfluramine significantly increased the TRH content in the striatum, this effect was completely abolished by citalopram (20 mg/kg i.p.) or metergoline (10 mg/kg i.p.) Citalopram also prevented the fenfluramine-induced depletion of the striatal 5-HT. These results indicate a separate neuronal storage of TRH and 5-HT in the structures (ventral part of the lumbar spinal cord, nucleus accumbens, septum) in which the peptide and indoleamine coexist in 5-HT neurons. They also suggest that the fenfluramine-induced increase in the striatal TRH concentration is due to 5-HT release and stimulation of 5-HT receptors.

Animals↗
PubMed1990

The effect of repeated administration of antidepressant drugs on the thyrotropin-releasing hormone (TRH) content of rat brain structures.

The present study investigated the effect of repeated treatment with the antidepressant drugs imipramine, amitryptyline, citalopram and mianserin (10 mg/kg PO, twice daily for 14 days) on levels of thyrotropin-releasing hormone (TRH) in several brain structures (cerebral cortex, amygdala + pyriform cortex, hippocampus, nucleus accumbens, striatum and hypothalamus) of the rat. Amitriptyline caused a marked increase in the TRH content in the striatum and nucleus accumbens. Citalopram and mianserin produced a smaller but significant increase in the TRH content in the striatum only, while imipramine did not significantly affect the TRH concentrations in any of the brain structures. None of the antidepressant drugs administered acutely significantly affected the TRH concentrations in the nucleus accumbens or the striatum. These results indicate that changes in brain TRH induced by antidepressant drugs are not related to their therapeutic activity.

Amitriptyline↗
PubMed1984

[Anaerobic microbes in perimandibular inflammation].

Studies conducted in 16 patients with perimandibular inflammation included bacteriological examinations and tests of the resistance of the bacterial flora to 6 antibiotics:davercin, erythromycine, penicillin, ampicillin, tetracycline and chloramphenicol. A total of 73 strains (47 anaerobic and 26 aerobic) were isolated, including 47 Gram - and 26 Gram's strain +. Anaerobic Gram - ve bacteria appear to be the principal cause of perimandibular inflammatory lesions, streptococcus viridans being identified more frequently in these cases than in the normal buccal cavity. Bacterial flora of dental origin was more sensitive to davercin than to the other 5 antibiotics tested.

Female↗