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Biomedical subjects

K Wiśniewski

Publications and source records attributed to K Wiśniewski.

At least 163 records · Page 9Linked to original sources

The participation of prostaglandins in the action of kinins on the central dopaminergic system in the rat. II. Participation of PGF2 alpha in the action of kinins on the central dopaminergic system.

Administration of prostaglandin F2 alpha (PGF2 alpha) in the presence of kinins did not change or potentiated the action of amphetamine (AMPH). Depending on the dose, PGF2 alpha could antagonize or potentiate the effect of kinins on the apomorphine (APO)-induced stereotypy. A combined treatment with PGF2 alpha and kinins did not affect or potentiate the haloperidol (HAL)-induced catalepsy. Bradykinin (BRS) and PGF2 alpha given separately or in combination did not change the levels of dopamine (DA), homovanillic acid (HVA) and noradrenaline (NA) after administration of AMPH, but given in combination elevated the striatal level of DA after treatment with APO. PGF2 alpha given in combination with BRS to rats receiving alpha-methyl-p-tyrosine (alpha-MT) increased the DA turnover in the striatum, while combined treatment with PGF2 alpha BRS, APO and alpha-MT depressed the turnover rate.

Animals↗

The participation of prostaglandins in the action of kinins on the central dopaminergic system in the rat. III. Participation of PGE1 in the action of kinins on the central dopaminergic system.

Prostaglandin E1 (PGE1) slightly inhibited the amphetamine (AMPH) induced stereotypy after administration of bradykinin (BRS) or stimulation the activity of kininogenic enzymes of the cerebral tissue by kallikrein administration. After administration of PGE1, BRS did not affect the apomorphine (APO)-induced stereotypy. The effect of kinins on catalepsy induced by haloperidol (HAL) was changed depending on the dose of PGE1. PGE1 given in combination with BRS increased the NA turnover in the rat striatum in comparison with the group receiving BRS, and given together with BRS and APO depressed the NA turnover in comparison with the group BRS and APO. A combined administration of PGE1 and BRS did not change the DA and HVA content under the experimental conditions used.

Animals↗

2-amino-3-phosphonopropionic acid (AP3) and its N-methyl analog improve learning and memory in rats.

The influence of 2-amino-3-phosphonopropionic acid (AP3), an antagonist of metabotropic glutamate receptors and its N-methyl analog (N-methyl AP3) on acquisition, consolidation and recall of information in a passive avoidance situation was tested. Both compounds improved three examined parameters. The significant effect of AP3 appeared at the icv dose of 12.5 micrograms per rat when its influence on acquisition and consolidation was tested, and at the icv dose of 100 micrograms when its influence on retrieval process was evaluated. The significant improvement of acquisition of information was observed at the icv dose of 50 micrograms per rat of N-methyl AP3, but significant facilitation of consolidation and retrieval processes appeared at the higher dose of 100 micrograms per rat. Significant improvement of performance in a passive avoidance situation persisted in all experiments to the highest used dose of both compounds, 250 micrograms.

Alanine↗

Central activity of 2-amino-4-phosphonobutyric acid (AP4).

The influence of intracerebroventricular (icv) injections of 2-amino-4-phosphonobutyric acid (AP4) on the activity of central nervous system was examined in rats. The compound (100 and 200 micrograms icv) significantly enhanced apomorphine stereotypy, in doses of 50, 75, and 100 micrograms decreased haloperidol-induced catalepsy and did not change motility of rats estimated in the "open field" test. AP4 significantly improved learning and memory processes in passive and learning in active avoidance situation. The highest significant effect was observed after icv dose of 100 micrograms per rat, when acquisition, consolidation and recall of information was evaluated in the passive avoidance behavior. AP4 significantly improved only acquisition of information in active avoidance situation at the icv dose of 50 micrograms per rat. The mechanism of the positive effect of AP4 on learning and memory is at present unclear, and its explanation needs future investigations.

Aminobutyrates↗

Central activity of 2-amino-3-phosphonopropionic acid (AP3) and its N-methyl analog.

The influence of 2-amino-3-phosphonopropionic acid (AP3) an antagonist of metabotropic glutamate receptors and its N-methyl analog (N-methyl AP3) on locomotor activity in the "open field" test, apomorphine stereotypy and haloperidol catalepsy were tested. Both compounds had not any influence on spontaneous crossings of squares, number of rearings and bar approaches in the "open field" test. AP3 and its N-methyl analog significantly enhanced apomorphine stereotypy at the intracerebroventricular (icv) doses of 100 and 200 micrograms per rat respectively. Although, both compounds significantly diminished haloperidol catalepsy at the icv doses of 50, 100 and 200 micrograms per rat. All observed effects of AP3 and N-methyl AP3 were dose independent. Methyl substitution at the N-position in AP3 did not change pharmacological properties of this compound i.e. its influence on behavior mainly dependent on dopaminergic systems.

Alanine↗

Effect of vasopressin analog [d(CH2)1(5),Tyr(Me)2]AVP on learning and memory in rats chronically treated with ethanol.

The effect of single 2 micrograms dose of vasopressin (AVP) and analog [d(CH2)1(5),Tyr(Me)2]AVP on processes of retrieval, acquisition and consolidation of conditioned reflexes in rats chronically alcoholized was studied. Long term (9 weeks) ethanol intoxication profoundly impaired learning and memory processes in all tests used. The AVP analog [d(CH2)1(5), Tyr(Me)2]AVP facilitated retrieval of passive avoidance, improved consolidation of active avoidance of rats previously treated with alcohol, but did not affect the acquisition of active avoidance. [d(CH2)1(5), Tyr(Me)2]AVP did not affect the motor and exploratory activity of rats in open field.

Animals↗

A search for new active amino acids responsible for pharmacological activity of collagen degradation products.

The pharmacological activity of glycine (Gly), proline (Pro) and hydroxyproline (Hyp)--the main amino acids in collagen degradation products--was studied in comparison to the activity of all mixture of DPTC (degradation products of trihelical collagen). The investigated amino acids decreased psychomotor activity of rats, enhanced apomorphine- and amphetamine-induced stereotypy. Pro and Hyp enhanced also catalepsy, but Gly decreased the haloperidol action. Each amino acid was given adequately to its contents in DPTC. Our results indicated that hydroxyproline revealed the action on the central nervous system (CNS) in each aspect most similar to the action of DPTC mixture.

Animals↗

The effect of vasopressin analog: [d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP on learning and memory processes in rats with experimental amnesia.

We investigated the effect of a single 2 micrograms dose of a vasopressin (AVP) analog, [d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP on processes of retrieval, consolidation and acquisition of conditioned reflexes in rats with experimentally induced amnesia. The investigated amnesia models were: long term ethanol intoxication, electroconvulsive shocks (ECS), and hypoxia. They all profoundly impaired the learning and memory processes in all tests used. The AVP analog-[d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP facilitated retrieval of passive avoidance in all amnesia models. It improved consolidation of active avoidance of rats previously treated with alcohol, but did not affect the acquisition of active avoidance. [d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP lack antidiuretic properties.

Alcoholism↗

The effect of angiotensin II and its fragments on post-alcohol impairment of learning and memory.

Angiotensin II(1-8) (A II) and its fragments: angiotensin III(2-8) (A III), angiotensin IV(3-8) (AIV), angiotensin V (4-8) (A V) and angiotensin VI(3-7) (A VI) accelerate acquisition of avoidance response and prolong their extinction. A II fragments are devoid classical A II activities such as the effects on blood pressure and thirst. Alcohol administered chronically (for 9 weeks) depresses the ability to retrieve and acquire avoidance responses. The investigated A II fragments counteract the post-alcohol impairment of learning and memory processes (A V being somewhat less active). Fragments A IV and A VI normalize the retrieval in offspring of mothers exposed to alcohol pre- and post-natally.

Alcoholism↗

Psychotropic effects of angiotensin II N-terminal fragments: Asp-Arg-Val-Tyr-Ile-His and Arg-Val-Tyr-Ile-His in rats.

In this study the effects of angiotensin II (AII) angiotensin II hexapeptide [AII(1-6)] and angiotensin II pentapeptide [AII(2-6)] on the motility, stereotypy, learning of conditioned avoidance responses (CARs) and recall of a passive behavior making it possible to avoid aversive stimulation in rats, were compared. All the peptides were injected into the lateral cerebral ventricle (icv) in a dose of 1 nmol. AII caused a statistically significant increase in the number of crossings, rearings, and bar approaches in an open field whereas [AII(1-6)] and [AII(2-6)] were inactive in this test. The stereotypic behavior induced by an intraperitoneal (ip) injection of apomorphine (1 mg/kg) and amphetamine (7.5 mg/kg) was statistically significantly enhanced only in the rats which received AII icv. The application of AII, but not that of [AII(1-6)] and [AII(2-6)] resulted in a quicker acquisition of the CARs. A better recall of passive avoidance was achieved only by AII, while the fragments [AII(1-6)] and [AII(2-6)] had no effect. These findings indicate that the 1-6 and 2-6 fragments of AII do not possess a psychotropic activity like that of the parent octapeptide.

Amino Acid Sequence↗

Estimation of central activity of hydroxyproline--the amino acid characteristic for collagen degradation products.

The central activity of hydroxyproline - the amino acid characteristic for collagen degradation products was studied. The levels of urinary and serum hydroxyproline are elevated in many disturbances, among them is a mental deficiency connected with hydroxyprolinemia. Previous studies showed that the mixture of collagen degradation products is biologically active and exerts and effect on central nervous system. In our study hydroxyproline significantly decreased the psychomotor activity of rats in Lat's test, enhanced amphetamine stereotypy in lower doses, and enhanced catalepsy in one of used doses. It prolonged the time of thiopental sleeping. The pentylenetetrazole seizures latency was not significantly prolonged and duration of seizures was shorter after injection (icv) of hydroxyproline. Our investigations show, that hydroxyproline is the active amino acid in the mixture of collagen degradation products and may be responsible for central activity of this mixture.

Animals↗

Interaction of bradykinin with dopaminergic receptors in the CNS.

The influence of bradykinin on the action of compounds affecting predominantly the dopaminergic receptor was studied in behavioral tests (Lat test and sterotypy) and biochemically (estimation of the level of biogenic amines--noradrenaline, dopamine and serotonin, and their metabolites--normetanephrine, homovanillic and 5-hydroxyindoleacetic acids in the brain tissue). Bradykinin potentiated the action of nialamide with L-dopa, dopamine, 1,3-dimethyl-5-aminoadamantane, apomorphine and noradrenaline. Spiroperidol abolished potentializing effect of bradykinin on the central action of nialamide with L-DOPA and of noradrenaline. In animals receiving spiroperidol with bradykinin psychostimulatory action of noradrenaline was also not observed. FLA-63--inhibitor of dopamine beta-hydroxylase--increased the potentializing effect of bradykinin on the central action of dopamine. Most significant biochemical changes between the group receiving nialamide alone and the group given nialamide together with bradykinin have been observed in corpus striatum, where the level of dopamine and its metabolite--homovanillic acid--increased. The results obtained point out that the potentiation of the central effects of catecholamines by kinins depends mainly on the interaction of this peptide with dopaminergic receptor.

Animals↗

Interaction of cholecystokinin (CCK-8) with agonist and antagonist of beta-adrenergic receptors in circulatory system of diabetic rats.

The interaction of C-terminal cholecystokinin octapeptide (CCK-8) with beta-adrenoceptors agonist (isoprenaline-ISO) and antagonist (propranolol) and their influence on arterial blood pressure and function of isolated heart in rats with streptozotocin-induced diabetes mellitus (DM) was studied. After blockade of beta-adrenoceptors with propranolol, the hypertensive effect of CCK-8 was observed in the control group but not in DM-group, whereas CCK-8 had no effect on arterial blood pressure in the both studied groups. Stimulation of beta-adrenoceptors with ISO exerted the hypotensive effect of CCK-8 similar as after administration of the amine alone in the control and diabetic rats. CCK-8 increased the cardiac contraction amplitude and had no effect on heart rate and coronary outflow in control hearts. The positive inotropic effect of the peptide was abolished in DM-group. After blockade of beta-adrenoceptors, CCK-8 decreased all studied parameters of isolated hearts, the effect was similar as after infusion of propranolol alone. In DM group, after blockade of beta-adrenoceptors CCK-8 evoked decrease in the cardiac contraction amplitude (as during infusion of propranolol) and heart rate (the effect was greater than that after beta-adrenoceptors antagonist). CCK-8 administrated with ISO increased amplitude, heart rate and decreased coronary outflow of isolated control heart as after administration of ISO alone: in DM-group only the positive inotropic effect was observed. DM modified the effect of CCK-8 in circulatory system of rats. CCK-8 evoked bradycardia independent of stimulation or blockade of beta-adrenoceptors, mainly in DM.

Adrenergic beta-Agonists↗

Psychotropic activity of N-methyl-2-amino-4-phosphonobutyric acid (N-methyl AP4).

We have previously reported that 2-amino-4-phosphonobutyric acid (AP4), an agonist of presynaptically located metabotropic glutamate receptors, administrated at a single intracerebroventricular (icv) injection facilitated learning and memory in a passive- and learning in an active avoidance situation, enhanced apomorphine stereotypy, and attenuated haloperidol catalepsy in rats. In the present study the effect of a single icv injection of N-methyl analogue of AP4 (N-methyl AP4), in the same behavioral tests was investigated in rats. The compound at the doses of 100 and 200 micrograms per rat significantly enhanced apomorphine stereotypy, at the dose of 75 micrograms per rat attenuated haloperidol-induced catalepsy, without having any influence on spontaneous locomotor activity estimated in the open field test. N-methyl AP4 at the doses of 75 and 100 micrograms per rat significantly facilitated acquisition of information, consolidation, and retrieval process in a passive avoidance situation. The compound significantly improved only acquisition of conditioned avoidance responses (CARs) at the doses of 50 and 75 micrograms per rat; the positive effect of N-methyl AP4 on consolidation and recall of CARs was insignificant. Methyl-substitution at N-position in AP4 did not change its effects in the performed behavioral tests.

Aminobutyrates↗

Role of NMDA receptor in the effects of arginine-vasopressin on memory processes.

The mechanism of facilitatory action of vasopressin on memory processes, dependent probably on different neurotransmitter systems, remains unclear. We decided to study the interactions between arginine-vasopressin and ionotropic NMDA receptor. We estimated the influence of various antagonists of NMDA receptor on beneficial effect of arginine-vasopressin on consolidation of conditioned avoidance responses and on retrieval of memory in passive avoidance situation. We have shown that effect of vasopressin on consolidation is significantly reduced by noncompetitive antagonist of ion channel in the NMDA receptor--dizocilpine (MK-801) and competitive antagonist of glycine recognization site--HA-966. Distinctly, effect of the peptide on retrieval is decreased by competitive antagonist of glutamate recognition site--AP-7, competitive antagonist of polyamines site-arcaine and noncompetitive antagonist--MK-801. This suggests that NMDA receptor may participate in the action of vasopressin on memory, but it plays different roles in consolidation and retrieval processes.

Animals↗

Effect of bicuculline and angiotensin II fragment 3-7 on learning and memory processes in rats chronically treated with ethanol.

The aim of this study was to determine the possible influence of bicuculline, the antagonist of GABA-A receptor on behavioral activity (recall, acquisition of conditioned reflexes) of angiotension II fragment 3-7 (A II 3-7) in rats chronically treated with ethanol. Long term (9 weeks) ethanol intoxication profoundly impaired learning and memory processes in all testes used. The GABA-A receptor antagonist bicuculline (0.5 mg/kg ip) did not influence exploratory and motor activity in the control rats, but we observed tendency (without significance) to decrease the locomotor activity, in the alcohol-intoxicated groups of animals, when the drug was injected together with A II 3-7 (2 microgram icv). Bicuculline did not influence retrieval process in passive avoidance recall in both investigated groups, and when the drug was given together with AII 3-7 significantly enhanced its action in the control group and in rats chronically treated with ethanol. Bicuculline significantly improved acquisition in the active avoidance test in the control and alcohol-intoxicated groups. Bicuculline injected together with A II 3-7 significantly decreased its action in the control group. Coadministration of bicuculline with A II 3-7 did not significantly change the activity of A II 3-7 in the acquisition of active avoidance test in the alcohol-intoxicated groups of rats.

Angiotensin II↗