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Biomedical subjects

A I Gromov

Publications and source records attributed to A I Gromov.

At least 19 recordsLinked to original sources
PubMed1992

[Effects of haloperidol on extracellular contents of dopamine and its metabolites in the septum of rats during interspecies aggression].

The extracellular levels of dopamine (DA) and its metabolites in the septum of freely moving rats were studied using "push-pull" method during muricidal aggression before and after haloperidol (2 mg/kg, i. p.) treatment. Mouse-killing activity of the rats was accompanied by significant reduction of the output of DA and metabolites in this brain area. Haloperidol suppressed muricidal activity of the rats and increased the extracellular levels of DA metabolites. In contrast, the decrease of DA release monitoring during killing activity was not affected by haloperidol administration. Possible role of the septal dopaminergic mechanisms underlying muricidal behaviour and the drug effects is discussed.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

[The determination of the nociceptive thresholds in freely moving rats].

A simple method for determination of nociceptive thresholds in free-moving rats is put forward. The method is based on the registration of vocalization reaction caused by the feed through the lungs connected with the stimulator by thin wires electrodes of gradually increasing impulses of constant electric current. The examples of effect of morphin and naloxone on the nociceptive thresholds as well the alteration of thresholds during predatory aggression are given.

Aggression↗
PubMed1987

[Detection of ligand-induced conformation changes in lactate dehydrogenase by using fluorescent probes].

The binding of ANS to apolactate dehydrogenase (apo-LDH) is accompanied by a 300-fold increase in dye fluorescence with a shift of the emission maximum from 515 to 479 nm, as well as by quenching of intrinsic protein fluorescence. A tetrameric LDH molecule has 6.4 +/- 1.6 non-interacting dye-binding sites with an association constant equal to (4.3 +/- 1.6) X 10(3) M-1. NAD+ added at saturating concentrations does not alter the number of ANS binding sites or the association constant value. The formation of binary LDH.NAD+, LDH.NADH, LDH.AMP and LDH.pyruvate complexes causes the quenching of fluorescence of the enzyme-bound ANS. The extent of quenching observed at ligand saturating concentrations differs for each ligand. Pyruvate added to the binary LDH.AMP complex exerts no effect on the fluorescence of protein-bound ANS; this indicates that the binding of AMP causes some alterations in the microenvironment of the substrate-binding site. Nicotinamide mononucleotide (NMN) can act as a coenzyme in the LDH-catalyzed reaction. AMP added together with NMN displays an inhibitory effect. The cationic (auramine O) and anionic (ANS) fluorescent probes bound to LDH exhibit different responses to conformational changes accompanying the transition from the apoenzyme to the LDH X NAD-pyruvate complex.

Anilino Naphthalenesulfonates↗
PubMed1983

[Effect of prostaglandins on the sensitivity of cerebral cortical neurons in rabbits to cholinoreceptor agonists].

The effect of prostaglandins F2a and E2 on the reaction of rabbit's brain cortex neurons provoked by arecoline and nicotine (stimulators of M- and N-cholinereceptors) has been investigated by using a microionophoretic technique. As a rule, prostaglandin F2a decreased and prostaglandin E2 increased the effects of arecoline. Prostaglandins rarely changed the effect of nicotine. The data obtained confirms the supposition that prostaglandin F2a has inhibitory effects on the synthesis in neurons of the cyclical guanosinemonophosphate. Some hypothesis of the prostaglandins participation in integrative activity mechanisms of neurons are supposed.

Action Potentials↗
PubMed1982

[Effect of inhibition of prostaglandin biosynthesis on the spike activity and chemical sensitivity of cortical neurons in the rabbit].

Inhibition of prostaglandins synthesis by non-narcotic analgetics--aspirin, butadion and indometacin--produces an over effect of the background firing activity of the cortical units and on their sensitivity to microiontophoretic application of acetylcholine and norepinephrine in acute experiments on unanesthetized and unrestrained rabbits. As a rule, non-narcotic analgetics depressed background firing and reinforced responses to the neuro-mediators. Some neurons showed complete, but reversible inhibition of discharge activity and chemical sensitivity. Participation of prostaglandins in activity of the nerve cells is discussed.

Acetylcholine↗
PubMed1980

[Effect of prostaglandins F2alpha and E2 on the sensitivity of rabbit cerebral cortex neurons to acetylcholine and noradrenaline].

Effects of microiontophoretically applied prostaglandins F2 alpha and E2 on the activity pattern and sensitivity of single neurons to acetylcholine and norepinephrine were investigated in the rabbit somatosensory cortex. F2 alpha generally inhibited and E2 increased the firing rate of the neurons. F2 alpha usually changed the sensitivity of the neurons acetylcholine, while E2 realized its effects upon norepinephrine-sensitive units. F2 alpha influence on the excitatory effects of acetylcholine and E2 influence on the norepinephrine inhibition were characterized as a rule by decreasing the mediator actions or by changing the initial responses sign to the opposite one. It is assumed that prostaglandins of group F take part in cholinergic transmission while those of group E -- in the adrenergic transmission. The investigated prostaglandin action is likely to be realized by selective inhibition of the adenilate or guanilate cyclase activity with subsequent decrease in synthesis of cyclic adenosine monophosphate and cyclic guanosine monophosphate.

Acetylcholine↗