Katarzyna Ossowska - Academia.edu (original) (raw)

Papers by Katarzyna Ossowska

Przeglad Filozoficzny - Nowa Seria, 2014

Tetrahedron, 2005

The oxidation of sulfides to sulfoxides by halogen-mediated oxidation has been reviewed. The repo... more The oxidation of sulfides to sulfoxides by halogen-mediated oxidation has been reviewed. The report contains 180 references, 28 tables and 34 schemes.

Neuroscience, 2007

Group III metabotropic glutamate receptors (mGluRs) are widely distributed in the basal ganglia, ... more Group III metabotropic glutamate receptors (mGluRs) are widely distributed in the basal ganglia, especially on the terminals of pathways which seem to be overactive in Parkinson’s disease. The aim of the present study was to determine whether (1S,3R,4S)-1-aminocyclo-pentane-1,3,4-tricarboxylic acid (ACPT-1), an agonist of group III mGluRs, injected bilaterally into the globus pallidus (GP), striatum or substantia nigra pars reticulata (SNr), can attenuate the haloperidol-induced catalepsy in rats, and whether that effect was related to modulation of proenkephalin (PENK) or prodynorphin (PDYN) mRNA expression in the striatum. Administration of ACPT-1 (0.05–1.6 μg/0.5 μl/side) caused a dose-and-structure-dependent decrease in the haloperidol (0.5 mg/kg i.p. or 1.5 mg/kg s.c.)-induced catalepsy whose order was as follows: GP>striatum>SNr. ACPT-1, given alone to any of those structures, induced no catalepsy in rats. Haloperidol (3×1.5 mg/kg s.c.) significantly increased PENK mRNA expression in the striatum, while PDYN mRNA levels were not affected by that treatment. ACPT-1 (3×1.6 μg/0.5 μl/side) injected into the striatum significantly attenuated the haloperidol-increased PENK mRNA expression, whereas administration of that compound into the GP or SNr did not influence the haloperidol-increased striatal PENK mRNA levels. Our results demonstrate that stimulation of group III mGluRs in the striatum, GP or SNr exerts antiparkinsonian-like effects in rats. The anticataleptic effect of intrastriatally injected ACPT-1 seems to correlate with diminished striatal PENK mRNA expression. However, since the anticataleptic effect produced by intrapallidal and intranigral injection of ACPT-1 is not related to a simultaneous decrease in striatal PENK mRNA levels, it is likely that a decrease in enkephalin biosynthesis is not a necessary condition to obtain an antiparkinsonian effect.

Neuroscience, 1997

This study was aimed at assessing the contribution of reflex and non-reflex factors to the muscle... more This study was aimed at assessing the contribution of reflex and non-reflex factors to the muscle tone of old female Wistar rats. The hind foot of a rat was flexed or extended at the ankle joint by 25 degrees over 250 ms. The resistance of the foot to passive movements (torque, mechanomyogram), as well as the reflex electromyographic activity in the gastrocnemius and tibialis anterior muscles, were recorded simultaneously. Moreover, the impact of the blockade of the reflex activity caused by the local anesthetic lignocaine (1-2 ml of a 2% solution, injected in the vicinity of the sciatic nerve) on the muscle tone was investigated. Additionally, old rats' hind leg muscle samples were analysed using fluorescent microscopy for the expression of fibronectin, which is an early marker of connective tissue formation. It has been shown that old rats are characterized by (i) a substantially increased resistance of flexor muscle stiffness (measured during extension) and unchanged resistance of extensors (measured during flexion), (ii) the loss of a major part of the reflex electromyographic activity and (iii) the increased content of fibronectin in muscles. Moreover, it has been shown that lignocaine, which completely blocked the electromyographic reflex activity in the gastrocnemius and tibialis anterior muscles in young animals, was unable to counteract the resistance of these muscles to passive movements in old rats. The present results suggest that the muscle stiffness seen in old rats is not due to a reflex response, but depends mainly on non-reflex factors--chiefly on a large overgrowth of non-elastic connective tissue replacing degenerated active muscle fibers.

Naunyn-Schmiedeberg's Archives of Pharmacology, 1998

The aim of this study was to examine whether (+)-2-aminobicyclo[3.1.0]-hexane-2,6-dicarboxylate m... more The aim of this study was to examine whether (+)-2-aminobicyclo[3.1.0]-hexane-2,6-dicarboxylate monohydrate (LY354740), a selective agonist of group II metabotropic glutamate receptors, possesses antiparkinsonian properties. Parkinsonian-like muscle rigidity was induced by pretreatment with haloperidol (1 mg/kg i.p.). It was measured as increased resistance developed by the rat's hind leg to passive extension and flexion. LY354740 (5 and 10 mg/kg i.p.) dose-dependently diminished the haloperidol-induced muscle rigidity. The present results suggest that LY354740 counteracts the muscle rigidity in an animal model of parkinsonism.

Naunyn-Schmiedeberg's Archives of Pharmacology, 1999

The aim of the present study was to examine the influence of 3-month administration of haloperido... more The aim of the present study was to examine the influence of 3-month administration of haloperidol (1 mg/kg per day) and clozapine (30 mg/kg per day) in drinking water on cortical NMDA (N-methyl-D-aspartate) receptors in rats. On day 5 of withdrawal, the animals were killed and their brains were removed. The binding of [3H]MK-801 ([3H](5R, 10S)-(+)-5-methyl-10,1 11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine) and [3H]CGP 39653([3H]D,L-(E)-2-amino-4-propyl-5-phosphono-3-pentenoic acid) to NMDA receptors in different cortical areas, as well as the binding of [3H]spiperone to dopamine D2 receptors in the striatum, were analysed by quantitative autoradiography. Haloperidol increased the binding of [3H]CGP 39653 in frontal, insular and parietal cortices. Clozapine increased the binding of [3H]CGP 39653 in insular and parietal cortices. Haloperidol, but not clozapine, increased the binding of [3H]spiperone in the striatum. None of the neuroleptics influenced the binding of [3H]MK-801 to cortical NMDA receptors. An additional assay revealed an increase in the Bmax value, with no significant changes in the K(D) of [3H]CGP 39653 binding in parieto-insular cortical homo-genates as a result of haloperidol and clozapine administration. The present results suggest that long-term treatments with haloperidol and clozapine increase the number of NMDA receptors in different cortical regions.

Journal of Neural Transmission - Parkinson's Disease and Dementia Section, 1994

MK-801, a non-competitive antagonist of NMDA receptors, is known to exhibit a beneficial action i... more MK-801, a non-competitive antagonist of NMDA receptors, is known to exhibit a beneficial action in many animal models of Parkinson's disease. The aim of this study was to examine the influence of MK-801 on the reserpine-induced muscle rigidity. The rigidity was estimated by a direct mechanomyographic method. This method consists in successive bending and straightening of a rat's hind foot in the ankle joint and measuring the resistance of the foot to passive movements. Reserpine in doses of 5-10 rag/ kg ip, given alone or in combination with Gt-methyl-p-tyrosine (ctMT, 250 mg/kg ip), induced rigidity. The strongest muscle rigidity was induced by 10mg/kg of reserpine 1 hour after administration. MK-801 (0.32-1.28mg/kg sc) injected 70min after reserpine (10mg/kg ip) decreased the rigidity induced by the latter compound. Similarly, MK-801 (1.28 mg/kg sc), administered 27h40' after joint treatment with reserpine (10mg/kg ip) and aMT (250 mg/kg ip), strongly inhibited the reserpine-induced muscle rigidity. The obtained results show that the glutamatergic hyperactivity plays a significant role in the reserpine-induced rigidity. As the reserpineinduced motor disturbances are commonly accepted to be an animal model of parkinsonian symptoms, it may be assumed that the NMDA receptor blocking component may contribute substantially to the therapeutic action of antiparkinsonian drugs.

Neuroscience, 2006

A deficiency of the dopaminergic transmission in the mesocortical system has been suggested to co... more A deficiency of the dopaminergic transmission in the mesocortical system has been suggested to contribute to cognitive disturbances in Parkinson&amp;#39;s disease. Therefore, the aim of the present study was to examine whether the long-term administration of a commonly used herbicide, paraquat, which has already been found to induce a slowly progressing degeneration of the nigrostriatal neurons, influences mesocortical dopaminergic neurons in rats. Paraquat at a dose of 10 mg/kg i.p. was injected either acutely or once a week for 4, 8, 12 and 24 weeks. Acute treatment with this pesticide increased the level of homovanillic acid (HVA) and HVA/dopamine ratio in the prefrontal cortex. After 8 weeks of administration paraquat increased the number of stereologically counted tyrosine hydroxylase-immunoreactive (TH-ir) neurons and their staining intensity in the ventral tegmental area (VTA), which is a source of the mesocortical dopaminergic projection. At the same time, few TH-ir neurons appeared in different regions of the cerebral cortex: in the frontal, cingulate, retrosplenial and parietal cortices. Chronic paraquat administration did not influence the level of dopamine in the prefrontal cortex but increased the levels of its metabolites: 3,4-dihydroxyphenylacetic acid (after 8-12 weeks), HVA (after 4 and 12 weeks) and HVA/dopamine ratio (4 weeks). After 24 weeks this pesticide reduced the number of TH-ir neurons in the VTA by 42% and of the Nissl-stained neurons by 26%, and induced shrinkage of this structure by ca. 25%. Moreover, TH-ir neurons in the cortex were no more visible after such a long period of administration and levels of dopamine metabolites returned to control values. The present results suggest that the long-term paraquat administration destroys dopaminergic neurons of the VTA. However, compensatory activation of the VTA neurons and cortex overcomes progressing degeneration and maintains cortical dopaminergic transmission.

European Journal of Neuroscience, 2005

The aim of the present study was to examine the influence of the long-term paraquat administratio... more The aim of the present study was to examine the influence of the long-term paraquat administration on the dopaminergic nigrostriatal system in rats. Paraquat was injected at a dose of 10 mg/kg i.p. for 4–24 weeks. We found that this pesticide reduced the number of tyrosine hydroxylase-immunoreactive neurons of the substantia nigra; after the 4-week treatment the reduction (17%, nonsignificant) was confined to the rostrocentral region of this structure but, after 24 weeks, had spread along its whole length and was ≈ 37%. Moreover, it induced a biphasic effect on dopaminergic transmission. First, levels of dopamine, its metabolites and turnover were elevated (4–8 weeks) in the caudate–putamen, then all these parameters returned to control values (12 weeks) and dropped by 25–30% after 24 weeks. The binding of [3H]GBR 12,935 to dopamine transporter in the caudate–putamen was decreased after 4–8 weeks, then returned to control values after 12 weeks but was again decreased after 24 weeks. Twenty-four-week paraquat administration also decreased the level of tyrosine hydroxylase (Western blot) in the caudate–putamen. In addition, paraquat activated serotonin and noradrenaline transmission during the first 12 weeks of treatment but no decreases in levels of these neurotransmitters were observed after 24 weeks. The above results seem to suggest that long-term paraquat administration produces a slowly progressing degeneration of nigrostriatal neurons, leading to delayed deficits in dopaminergic transmission, which may resemble early, presymptomatic, stages of Parkinson's disease.

European Neuropsychopharmacology, 2005

Behavioural Pharmacology, 2000