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Biomedical subjects

R Brus

Publications and source records attributed to R Brus.

At least 109 records · Page 6Linked to original sources
PubMedDate not supplied

Interactive modulation by dopamine and serotonin neurons of receptor sensitivity of the alternate neurochemical system.

Ontogenetic dopaminergic denervation of rat forebrain is associated with latent supersensitization of dopamine (DA) receptors that is unmasked only by a priming process entailing repeated DA agonist treatments. Similar denervation supersensitivity holds for serotonin (5-HT) and most other neurochemical systems. Because DA and 5-HT neurons compete for target sites in the brain and mimic or replicate actions of the others, we investigated the modulatory influence of DA neurons on 5-HT receptor sensitivity; and role of 5-HT neurons in modulating DA receptor sensitivity. In these studies rats were lesioned with the DA neurotoxin 6-hydroxydopamine (6-OHDA, i.c.v.; desipramine pretreatment) or 5-HT neurotoxin 5,7-dihydroxytryptamine (5,7-DHT, i.c.v.; desipramine pretreatment) either at 3 days after birth or in adulthood. Responses to DA and 5-HT agonists were determined in several behavioral paradigms in adulthood. In assessing oral responses to agonists, we found that the D1 agonist (+/-)-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol (SKF 38393) profoundly induced activity if rats were lesioned neonatally with 6-OHDA, but not if rats were co-lesioned as neonates or as adults with 5,7-DHT. The D2 agonist quinpirole induced profound oral activity, but only if rats were lesioned as neonates with 5,7-DHT; or if rats were lesioned with both 6-OHDA (neonatally administered) and 5,7-DHT (adult stage). In all rats lesioned as neonates with 6-OHDA, the 5-HT2 agonist m-chlorophenylpiperazine produced enhanced activity, regardless of 5,7-DHT treatment. These findings demonstrate that DA neurons modulate receptor sensitivity status of both DA and 5-HT receptors; and 5-HT neurons do so similarly. This phenomenon is pertinent to animal models of human disorders and in the syndrome spectrum and treatment approach of human neurodegenerative disorders (e.g. parkinsonism, tardive dyskinesia), developmental disorders (e.g. hyperkinetic activity) and psychiatric disorders.

Animals↗
PubMedDate not supplied

[The role of nitric oxide (NO) in central nervous system (CNS)].

Nitric oxide (NO), the smallest known bioactive product of mammalian cells, can be produced by most cell types. In the central nervous system NO acts as intracellular and extracellular messenger of a novel generation. NO plays important physiologic role, mediates learning, memory, regulates food intake, drinking and other. Under conditions of excessive formation, NO is emerging as important mediator of neurotoxicity in a variety disorders of the nervous system.

Arginine↗
PubMedDate not supplied

Acetylcholine content in the brain and heart of developing rats.

Acetylcholine content in the brain and heart of developing rats. Acta Physiol. Pol. 1975, 26 (1): 41-44. The content of acetylcholine was determined in four parts of the brain and in the heart of developing rats. It was found that changes in acetylcholine level were not parallel in the examined brain stuctures and in the heart in the time period from birth to 18 months of age of the rats.

Acetylcholine↗
PubMedDate not supplied

Amphetamine-induced enhancement of neostriatal in vivo microdialysate dopamine content in rats, quinpirole-primed as neonates.

Amphetamine (AMPH)-induced sensitization of central dopamine (DA) receptors, produced by repeated AMPH treatments, is associated with increased AMPH-induced DA release in the rat forebrain. However, for DA receptor sensitization produced by repeated DA receptor agonist treatments, the effects on forebrain DA release are not known. The objective of our study was to determine this. DA receptor sensitization was produced by administering the DA D2 agonist quinpirole (50 microg/kg/day) to rats, from the 1st to 11th days after birth - a process known as 'priming'. When these rats were tested at 3 months, DA receptor sensitization was manifested as increased quinpirole-induced yawning. We also found that AMPH (1.0 mg/kg, ip) acutely induced a 5-fold greater increase in DA content in the neostriatal in vivo microdialysate of these quinpirole-primed rats (vs. controls), accompanied by a reduction in dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels in the microdialysate. Conversely, an acute injection of quinpirole x HCl (100 microg/kg, ip) reduced the microdialysate contents of DA, DOPAC and HVA to comparable levels in quinpirole-primed and control rats. Therefore, we can conclude that long-lived DA receptor sensitization, produced by repeated DA D2 agonist treatments in ontogeny, is associated with enhanced AMPH-induced DA release in the neostriatum in adulthood, but is not accompanied by evident alteration in quinpirole-induced DA release.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

D-Ala2,F5Phe4-dynorphin amide, an opiate with analgesic and toxic properties.

A novel analog of dynorphin (1-13), D-Ala2,F5Phe4-dynorphin amide, was prepared and its pharmacological spectrum of activity was investigated. In a hot plate test on Swiss Webster and C57Bl mice, a 20 micrograms intracerebroventricular (icv) dose of the analog produced analgesia, which was greater in potency and duration than the parent dynorphin. This action of D-Ala2,F5Phe4-dynorphin amide was antagonized by the opiate receptor antagonist naloxone (2 mg/kg ip), administered either before or after the peptide. In addition to its analgesic action in mice, D-Ala2,F5Phe4-dynorphin amide produced a Straub tail and a catatonic-like state, both of which were also attenuated by naloxone. On the electrically-stimulated mouse vas deferens preparation, in vitro, D-Ala2,F5Phe4-dynorphin amide inhibited contractile activity and had an IC50 of 108.2 +/- 34.7 nM (SEM), about 4-fold weaker than that of dynorphin. This action was also attenuated by naloxone. An icv dose of 150 micrograms of D-Ala2,F5Phe4-dynorphin amide in mice, and a cumulative series of icv doses up to 2600 micrograms in anesthetized rats, failed to produce a lethal effect. No pathological changes were observed in mouse liver and kidney at 24 h after a 50 mg/kg dose of the peptide analog. In rats anesthetized with diallylbarbital (70 mg/kg ip) and urethane (280 mg/kg ip), D-Ala2,F5Phe4-dynorphin amide did not modify blood pressure, heart rate and respiratory rate. However, when mice were injected peripherally with single doses of D-Ala2,F5Phe4-dynorphin amide, convulsive episodes were produced, and lethal effects were observed with an LD50 of 60.0 mg/kg (95% confidence limits: 49.7-70.2 mg/kg) at 48 h. This action of D-Ala2,F5Phe4-dynorphin amide was not attenuated by naloxone (2.0 mg/kg, ip). Although analgesic and behavioral effects of D-Ala2,F5Phe4-dynorphin amide (e.g. Straub tail and catatonic-like state) are opiate-like, the lethal effect may be the consequence of actions of the peptide on non-opiate systems, Thus, the novel fluorinated dynorphin analog, D-Ala2,F5Phe4-dynorphin amide, may be a useful chemical tool for the study of opiate systems and their occasionally unanticipated biological or toxic actions.

Analgesics↗
PubMedDate not supplied

Conopressins and their analogs: synthesis, antidiuretic and behavioral effects.

[Lys8]-Conopressin G (L1), and [Arg8]-Conopressin S (A1) and their four analogs were synthesized using solid phase procedure. These analogs are [2-thiopropionic acid1, lys8]-conopressin (L2), [2-thiopropionic acid1, Arg8]-conopressin (A2), [cis-4-methyl-1-thiocyclohexaneacetic acid1, Lys8], conopressin (L3), and [cis-4-methyl-1-thiocyclohexaneacetic acid1, ARg8]-conopressin (A3). Behavioral and diuretic effects of all six peptides were compared with these of [Arg8]-vasopressin (AVP). Conopressin A1, and L1 and their analogs A2, A3, L2, L3, induced antidiuretic effects. After icv injection of some conopressins, barrel rotatory behavior of rats was observed.

Amino Acid Sequence↗
PubMedDate not supplied

Central action of catecholamines on the cardiovascular system in rats.

Central action of catecholamines on the cardiovascular system in rats. Acta Physiol Pol., 1978, 29 (2): 123--130. It was demonstrated that noradrenaline, adrenaline, dopamine and isoproterenol as well as normethanephrine administered into the lateral ventricle of the rat brain, under urethane anaesthesia, caused significant changes in arterial blood pressure. This action is due to stimulation of central adrenergic receptors. Arterial blood pressure rise after intraventricular administration of noradrenaline is caused by activation of the renin-angiotensin system in the periphery. The results of these experiments point to a role of central catecholamines in functional regulation ofthe cardiovascular system.

Animals↗
PubMedDate not supplied

[The role of arachidonic acid metabolites in the skin].

The metabolism of the arachidonic acid (AA) in normal skin is presented, and the role of its metabolites (eicosanoids) in pathogenesis of psoriasis is reviewed. Beside, possibility of the treatment of psoriasis by means of fish oil and eicosapentaenoic acid (EPA) is discussed.

Arachidonic Acids↗
PubMedDate not supplied

Effect of ethanol and diazepam given to pregnant rats on the behavior and catecholamine content in the brain of offspring.

Effect of separate and combined treatment with ethanol and diazepam applied to pregnant rats upon the behavior of 3- and 6-week old and 3 month old rats, as well as on the content of noradrenaline (NA), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) in various brain areas was investigated. It has been shown that separate application of ethanol and diazepam causes slight changes in the behavior and content of amines on the brain of offsprings. Combined application of ethanol and diazepam to pregnant rats exerts marked effects upon the behavior of offsprings and causes a decreased content mainly of 5-HT and 5-HIAA in the investigated areas of the brain.

Animals↗
PubMedDate not supplied

Influence of H2 receptors blockade upon some central effects of prostacyclin in rats.

Prostacyclin (PGI2) administered icv into the lateral rat brain ventricle in a dose of 1 and 10 micrograms caused hypothermia and catalepsy. Joint administration of PGI2 and chlorpromazine produced a greater cataleptic effect than that observed after the neuroleptic alone. Cimetidine (CMT) 2 g/kg po administered 60 min before PGI2 icv injection inhibited hypothermic and cataleptogenic action of PGI2. CMT blocked the cataleptogenic effect of chlorpromazine as well as combination of it with PGI2. CMT inhibited cataleptogenic effect of haloperidol, but it did not block the catalepsy induced by joint administration of haloperidol and PGI2. PGI2 did not change concentration of noradrenaline and dopamine in different brain areas. The results indicate that H2 receptors take part in some central pharmacological effects of PGI2 in rats.

Animals↗