Biomedical subjects
Publications and source records attributed to N A Krupina.
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The levels of anxiety were determined in male Wistar rats using a complex multiparameter method for evaluating anxiety-phobic states in rats based on ranged scale. The effects of psychotropic drugs differed in rats with innate high and low levels of anxiety. Anxiolytics sodium valproate (200 mg/kg), phenazepam (0.05 mg/kg) and diazepam (0.1 and 0.6 mg/kg) reduced anxiety in rats with innate high level of anxiety and prevented increase of anxiety induced by saline in rats with innate low level of anxiety. Pentylenetetrazol (10 mg/kg) and haloperidol at a large dose (0.5 mg/kg) increased anxiety in rats with either high or low innate levels of anxiety. However sodium lactate (600 mg/kg) increased anxiety only in rats with innate high level of anxiety. Haloperidol at a small dose (0.01 mg/kg) and melipramin (10 mg/kg) were uneffective in rats with innate high level of anxiety. Results believed the rats with innate high level of anxiety to be used as a new natural animal model of anxiety.
A new multiparameter method for evaluating anxiety-phobic states in rats is elaborated. The method is based on the ranged scale consisting of parameters which characterize the species-specific rat response to the series of ethologically adequate test-stimuli inducing manifestation of the anxiety-phobic states. The method makes it possible to evaluate individual anxiety-phobic level in rats, to form experimental groups with rats of known individual anxiety-phobic level, to conduct repeated observations in the same animals. The method is easy to perform in laboratory and makes it possible to get the results quickly.
The injection of subconvulsive doses of pentylenetetrazol (corazol, 10 mg/kg, intraperitoneally) leads to the appearance of a complex of the emotional-behavioral disturbances in rats which consists of three main syndromes: anxiety, pathologically enhanced fear and inactivation state. Each of syndromes is characterized, by a particular pattern of electrical activity (EA) recorded from brain structures. The bursts of EA (10-11 oscillations per s) with maximum amplitude and duration in locus coeruleus (LC) correspond to the syndrome of anxiety. The wave EA of a frequency coincident with a frequency of rat respiration corresponds to the syndrome of pathologically enhanced fear. The appearance of spindle-like EA (6 oscillations per s) in striatum (STR) corresponds to the syndrome of inactivation state. The amplitude and duration of generalized spindle-like EA are maximum in STR. The change from anxiety to inactivation state is accompanied by the change of corresponding EA patterns. It can be suggested that the injection of subconvulsive doses of pentylenetetrazol in rats leads to LC and STR hyperactivation because of which LC and STR acquired the properties of a pathological determinant whose appearance induces the formation of pathological systems with corresponding clinical manifestations. The relationship between the systems created by LC and STR hyperactivation is of antagonistic character.
Penicillin administration into the bed nucleus of stria terminalis (BNST) in the rat brain caused epileptiform activity (EpA)--the formation of the generator of pathologically enhanced excitation (GPEE) in the nucleus. GPEE was registered during the first 3 days. EpA was also detected in the amygdala during 5-8 days, and in the hippocamp during the whole period of registration (2-3 weeks). There was the generalized enhancement of synchronized EpA in the range of 6-10 oscillations per s., in some cases with high-amplitude spindle (7-8 oscillations per s.). 50% of animals had emotional behavioural disorders, a marked fear reaction was observed for a month and more. Some animals demonstrated psychotic-like paroxysms with the elements of stereotypy accompanied by high-frequency low-amplitude EpA. It is suggested that when a primary GPEE in BNST is formed, the structures of septo-hippocampal system (BNST, amygdala, hippocamp) play a role of pathological determinants under the influence of which the pathological system consisting of a number of limbic and extrapyramidal structures is formed. Its activity is clinically manifested in the complex polymorphic neuropathological syndrome.
Dynamics of appearance and maintenance of emotional-behavioural disorders in male Wistar rats was studied on and after repeated neurotoxin MPTP injection at a dose of 15 mg/kg intraperitoneally daily for 18 days MPTP caused suppression of locomotion and rearing in open field test, decrease of daily liquid consumption and lowering of preference for the sucrose over water, increase of immobility time and depression index simultaneously with disadaptation in forced swimming test. Behavioural alterations were maintained for not less than a week after abolition of MPTP injection. Data improved the appearance and development of the state of decreased motivation simultaneously with anhedonia and behavioural despair in rats in response to MPTP injection. The state can be considered as a new model of DA-depended depression-like syndrome in rats.
Sensorimotor response was measured by acoustic startle reflex in Wistar male rats with innate high and low levels of anxiety. The levels of anxiety were determined using a complex multiparameter method for evaluating anxiety-phobic states in rats by a ranged scale. Amplitude and prepulse inhibition of the acoustic startle response were increased, but latency of the startle reflex was decreased in rats with innate high level of anxiety as compared with those with innate low level. In rats with innate high level of anxiety injection of subconvulsive doses of pentylenetetrazol (10 and 15 mg/kg i.p.) resulted in an increase of the amplitude of the acoustic startle response and, additionally (under the dose 10 mg/kg) in a decrease of its latency. Facilitation of acoustic startle in rats with innate high level of anxiety is suggested to reflect either a deficit of inhibitory, or intensification of excitatory modulating influences on signal transmission in nerve circuit of acoustic startle. Studies of the sensorimotor response by acoustic startle in rats with innate high level of anxiety are believed to be useful for elucidating basic mechanisms of anxiety and phobia.
A new multiparameter method is elaborated for evaluating the anxiety-phobic states in rats. The method is based on a ranged scale of parameters which characterize the species-specific responses of an animal to the series of ethologically adequate test-stimuli inducing manifestation of the anxiety-phobic states. The method makes it possible to evaluate an individual anxiety-phobic level of a rat, to form experimental groups of rats with known individual anxiety-phobic levels, to conduct repeated observations of the same animals. The method is easy to introduce into laboratory practice and makes it possible to obtain results quickly.
Bilateral destruction of the Locus coeruleus in rats was carried out by means of 6-hydroxydopamine injections. Sham-operated animals served as control ones. Electrical activity was recorded in the region of the Locus coeruleus, the dorsal hippocampus, and in the caudatus-putamen complex. Beginning from the second week after surgery in experimental rats was observed a generalization of the theta-rhythm (7-9 Hz) in electrical activity of the Locus coeruleus, hippocampus and the caudatus-putamen complex during orienting-exploratory activity. At the same time such a rhythm was enhanced in animals with motor and orienting-exploratory agitation. In comparison to the sham-operated animals there were no changes in expression in the electrical activity of the subcortical structures of the rhythm of 5-6 Hz, accompanying immobilization state as well as that of 9-11 Hz, accompanying teeth chattering. The dynamics of changes of subcortical electrical activity of rats after the Locus coeruleus destruction may serve an index of the functional state of the animals under the conditions of noradrenergic deficiency. Changes of the brain electrical activity and behaviour of the animals revealed are considered to be a consequence of a relative enhancement of the central serotoninergic regulation of the subcortical structures being caused by a weakening of noradrenergic influences.