Biomedical subjects

K Ossowska

Publications and source records attributed to K Ossowska.

79 records · Page 5Linked to original sources

PubMedDate not supplied

Muscle rigidity induced by the opioid analgesic tramadol, but not by the non-opioid flupirtine.

The influence of high doses of two analgesic drugs, tramadol and flupirtine on the electromyographic activity in the gastrocnemius soleus muscles was examined. Tramadol (100-200 mg/kg po) dose-dependently induced a tonic electromyographic activity, which is generally accepted as a model of the opiate-induced muscle rigidity. That effect was antagonized by intraperitoneal injection of naloxone (0.8 mg/kg ip). On the other hand, flupirtine even in the high doses (100-200 mg/kg po) did not induce any tonic electromyographic activity. The obtained results confirm an opiate-like action of tramadol, but not that of flupirtine, on the muscle tension.

Administration, Oral↗

PubMedDate not supplied

Disturbances in neurotransmission processes in aging and age-related diseases.

This paper reviews the changes in dopaminergic, cholinergic and glutamatergic neurotransmission, which occur in the aging of the central nervous system (CNS) and in age-related diseases: Parkinson's disease (PD) and Alzheimer's disease (AD). Dopaminergic neurotransmission is impaired with age due to degeneration of the substantia nigra pars compacta neurons and reduction of the density of postsynaptic D1 and D2 dopamine receptors in the striatum. PD is believed to be caused by a severe loss of dopaminergic neurons, which leads to nearly complete depletion of dopamine in the striatum, particularly in the putamen. The supersensitivity of postsynaptic dopamine receptors, reported by some authors, may result from compensatory mechanisms to degeneration of dopaminergic neurons. The role of aging in PD is also discussed in the paper. An interest in the role of the cholinergic and glutamatergic systems in aging results from the concept that the development of AD is due to the pathology of these systems. The data on cholinergic neurotransmission are controversial and imply that aging affects rather slightly both neurons and cholinergic receptors. In AD, however, severe degeneration of cholinergic neurons of the basal nucleus of Meynert, leading to the impairment of cholinergic neurotransmission in the hippocampus and the cerebral cortex, has been observed. In AD degeneration of glutamatergic neurons and subsensitivity of some excitatory amino acids receptors in the hippocampus and the cerebral cortex may lead to dementia. However, an increase in the glutamate release from presynaptic glutamatergic terminals may be responsible for neuronal degeneration in AD. The role of the beta-amyloid protein in a neurodegenerative activity of glutamic acid is discussed.

Aged↗

PubMedDate not supplied

Specific involvement of striatal D1 and D2 dopamine receptors in the neuroleptic catalepsy in rats.

Since highly specific antagonists of D1 (SCH 39166) and D2 (raclopride) dopamine receptors have recently become available, we decided to investigate the role of striatal populations of these receptors in catalepsy - an animal model of neuroleptic-induced parkinsonism in humans. Injections of raclopride (2.5, 5 and 10 micrograms/0.5 microliters) into the ventro-rostral part of the striatum induced a strong, dose-dependent and long-lasting catalepsy. Intrastriatal injections of SCH 39166 (1.5 and 3.6 micrograms/ 0.5 microliters) also evoked a dose-dependent, but short-lasting catalepsy. The present results suggest, that neuroleptic side-effects are specifically dependent on the blockade of D2 and D1 dopamine receptors in the striatum.

Animals↗

PubMedDate not supplied

Lack of a strong influence of neuroleptic decanoates on dopaminergic and GABAergic functions.

Data concerning the incidence of extrapyramidal symptoms and the development of the supersensitivity to dopamine after administration of depot neuroleptics are controversial. The aim of the study was to examine the influence of depot neuroleptics on the sensitivity of dopamine receptors and GABA nigral receptors. Haloperidol decanoate (30 or 60 mg/kg im) and fluphenazine decanoate (12.5 or 25 mg/kg im) were injected twice at a 15 day interval. These treatments induced weak but very long-lasting catalepsy (60-105 days depending on the neuroleptic and its dose). The only significant enhancement of the apomorphine (0.25 mg/kg sc) stereotypy was observed 135 days after the lower dose of haloperidol and 230 days after the lower dose of fluphenazine. Haloperidol decanoate (30 mg/kg) did not influence the number of contralateral rotations induced by muscimol (10 or 25 ng/0.5 microliter) injected into the substantia nigra pars reticulata 35, 55 and 135 days after the first injection. Present results indicate that the dopaminergic supersensitivity after administration of depot neuroleptics is weak and appears very late, and that haloperidol decanoate does not induce nigral supersensitivity to GABA. It is suggested that the depot neuroleptics might induce less extrapyramidal symptoms in the clinic than the daily neuroleptic treatment.

Animals↗

PubMedDate not supplied

Dopamine receptors--the present state of research and perspectives.

The aim of the review is a brief description of the present status of research and perspectives in the field of multiple dopamine receptors, as well as of the importance of new discoveries for the treatment of schizophrenic psychoses and Parkinson's disease. Since the discovery of D1 and D2 dopamine receptors in the seventhies, evidence has accumulated for the existence of some new dopamine receptors. Among them the D3, D4 and D5 receptors, as well as their isoforms have been cloned. Molecular biology and pharmacology of these receptors have been exhaustively studied in recent years. These studies have prompted a number of hypotheses which open new perspectives for investigation into pathophysiology and therapy of schizophrenia and Parkinson's disease.

Antiparkinson Agents↗

PubMedDate not supplied

NMDA receptors in the rostral and intermediate-caudal striatum play an opposite role in regulation of the muscle tone in rats.

The aim of the study was to assess the contribution of the NMDA receptors in the caudate-putamen to the regulation of the muscle tone. The experiment was carried out on male Wistar rats. The hind foot of a rat was flexed or extended at the ankle joint by 25 degrees and the resistance of the foot to passive movements was measured. Haloperidol (1 mg/kg ip) induced the muscle rigidity. The competitive antagonist of NMDA receptors, (+/-)-2-amino-5-phosphonopentanoic acid (AP-5), injected in doses of 2 and 5 micrograms/0.5 microliter bilaterally into rostral regions of the caudate-putamen, inhibited the muscle rigidity induced by haloperidol. In contrast, AP-5 injected bilaterally in the same doses into the intermediate-caudal region of the caudate-putamen in rats not pretreated with haloperidol, induced muscle rigidity. The present results seem to suggest that NMDA receptors localized in the rostral and intermediate-caudal regions of the caudate-putamen play an opposite role in regulation of the muscle tone in rats.

2-Amino-5-phosphonovalerate↗

PubMedDate not supplied

Age-related changes in glutamate receptors: an autoradiographic analysis.

The aim of the present study was to evaluate age-related changes in NMDA and AMPA receptors in old female rats. To this end a quantitative autoradiography of [3H]-MK-801 and [3H]-AMPA binding was performed in the brain of young (3-month-old), middle-aged (12-month-old) and old (36-month-old) rats. Moreover, the binding of [3H]-spiperone to D2 dopamine receptors was also examined. No changes were observed in the binding of [3H]-MK-801 or [3H]-AMPA in middle-aged rats compared to young ones. In the caudate-putamen and shell and core of the nucleus accumbens septi of old rats, a pronounced decrease in the [3H]-MK-801 binding and a decreasing tendency in the [3H]-AMPA binding were observed. Furthermore, the binding of [3H]-MK-801 and [3H]-AMPA was reduced in the hippocampal formation and, additionally, a marked decline in the [3H]-MK-801 binding in different parts of the cerebral cortex including the frontal, parietal, cingulate, pyriform and insular cortices was found. The [3H]-spiperone binding progressively decreased with age in the dorsolateral, ventrolateral and medial caudate-putamen. The present results show that aging processes lead to changes in the binding of both [3H]-MK-801 to NMDA and [3H]-AMPA to AMPA receptors in a number of structures, a phenomenon which may reflect motor and memory disturbances found in old rats and elderly humans.

Aging↗