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Biomedical subjects

N I Dubrovina

Publications and source records attributed to N I Dubrovina.

At least 19 recordsLinked to original sources

Characteristics of extinction of a conditioned passive avoidance reflex in mice with different levels of anxiety.

The relationship between the extinction of a conditioned passive avoidance reflex and the initial anxiety level was studied in mice. The time spent in the open arms of an elevated cross maze was used to classify the mice into high-, intermediate-and low-anxiety individuals. Each level of anxiety was found to correspond to a defined extinction dynamic. Highly anxious mice were characterized by the absence of extinction of the conditioned passive avoidance reflex and stability of good reproduction of the memory trace on testing to as long as 15 days. In intermediately anxious individuals, a deficit in performance of the avoidance reflex appeared from day 7 of extinction. In low-anxiety mice, memory trace reproduction deteriorated from test day 11.

Animals↗

Acquisition and extinction of a conditioned passive avoidance reflex in mice with genetic knockout of monoamine oxidase A.

We report here the results obtained from comparative analysis of learning and the dynamics of extinction of a conditioned passive avoidance response in mice with genetic knockout of monoamine oxidase A (MAO A) and the progenitor line C3H. Mice of both lines acquired the conditioned passive avoidance reaction efficiently. Mice with genetic knockout of MAO A were characterized by prolonged retention of reproduction of the memory trace, as compared with rapid extinction in C3H mice. Smaller numbers of transfers, and vertical rearings on days 7-13 and the numbers of glances into and rom the dark sector on days 11-13 of extinction in MAO A-knockout mice appear to reflect their more marked fear reactions when confronted with the "dangerous" sector, along with increased anxiety, these facilitating longer-lasting retention of the memory trace.

Analysis of Variance↗

Effects of activation of D1 dopamine receptors on extinction of a conditioned passive avoidance reflex and amnesia in aggressive and submissive mice.

The studies reported here demonstrate the relationship between the effect of activation of D1 dopamine receptors on the reproduction of a conditioned passive avoidance reflex during extinction and amnesia and the aggressive and submissive behavioral stereotypes. During extinction, the D1 receptor agonist SKF 38393 at a dose of 5 mg/kg given before acquisition of the conditioned reflex and on test day 12 suppressed the reproduction of the conditioned skill in aggressive mice and improved reproduction in submissive mice. The effects of activation of D1 receptors were also opposite relative to the stereotype in amnesia. In aggressive mice, SKF 38393 significantly decreased the resistance to amnesia characteristic of these animals; in submissive mice, SKF 38393 weakened the amnestic effects of the delay in the "dangerous" sector and restored memory traces. The possible mechanisms of the selectivity of the actions of D1 receptors in mice with alternative behavioral stereotypes in retaining memory traces related to aversive stimulation during extinction and amnesia are discussed.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

[Influence of activation and blockade of NMDA receptors on extinction of passive avoidance response in mice with different levels of anxiety].

Influence of agonist (D-cycloserine) and antagonist (dizocilpine) N-methyl-D-aspartate receptors on learning and extinction of passive avoidance response in medium-, high-, and low-anxious mice was studied. In medium-anxious mice, D-cycloserine (30 mg/kg) although not changing learning accelerated development of extinction, whereas dizocilpine (0.15 mg/kg), while impairing passive avoidance learning, detained the extinction. In high-anxious mice with good retrieval of memory trace and absence of extinction, D-cycloserine was ineffective, whereas dizocilpine reduced learning and promoted retention of memory trace retrieval at the generated level on extinction. In low-anxious mice, D-cycloserine impaired learning and accelerated extinction, whereas dizocilpine completely blocked learning and retention of passive avoidance response.

Animals↗

[Comparative analysis of conditioned passive avoidance retention in rats with different forms of inherited arterial hypertension].

Comparing behavioral traits of anxiety in elevated plus-maze and retention of passive avoidance response in two rat strains with hereditary arterial hypertension ISIAH (inherited stress induced arterial hypertension) and SHR (spontaneously hypertensive rats) has shown the following. The SHR rats demonstrate impairment in retrieval of passive avoidance, hyperactivity and low anxiety. ISIAH rats showned better avoidance performance, average level of anxiety and activity. The interdependence of two pathologies: hypertension and memory impairment is discussed.

Animals↗

[Features of a passive avoidance extinction of mice with a different level of anxiety].

The dependence of the passive avoidance extinction from a level of mice initial anxiety is investigated. Mice were classified as high-, medium- and low-anxious by time spent in the open area of the elevated plus-maze. It is revealed that to each from levels of anxiety there corresponds certain dynamics of extinction. The high-anxious mice are characterized absence of the passive avoidance extinction and stability of good retrieval of memory trace for want of testing down to 15 days. At medium-anxious mice the deficit of avoidance habit performance developed since the 7th day of extinction. At low-anxious mice since the 11th day of testing the deterioration of retrieval was observed.

Animals↗

The effects of the duration of adaptation to laboratory conditions on the formation of a passive avoidance reflex in rats.

The level of adaptation of rats to their new living conditions was studied during formation of a passive avoidance habit using a single combination. A short acclimation period (3 days) had positive influences on the ability of rats to retain a memory trace. There was a negative correlation between step-through latency and measures of anxiety behavior in the elevated cross maze. A change in the adaptation period to nine days decreased the state of anxiety and the level of performance of the conditioned response. There were no correlations between these measures. The modulating role of the level of adaptation to living conditions, associated with different levels of anxiety, in a passive one-session avoidance learning model was assessed.

Adaptation, Psychological↗

The effects of novelty and behavioral stereotype on the development of amnesia in mice.

The aim of the present study was to analyze the significance of the interaction between the basic behavioral strategy, the extinction of the novelty of information, and the efficacy of amnesia-inducing influences. Using a combination of training to passive avoidance with holding the animal in the unsafe sector of the apparatus, comparative analysis was performed of the reproduction of a memory trace in aggressive and submissive mice of line C57BL/6J with and without six sessions of familiarization with the apparatus. These experiments showed that preliminary habituation prevented the development of amnesia in submissive but not aggressive individuals. The cause of these differences in the effects of preexposure on the development of amnesia involves the selectivity of the process of extinction of information novelty characteristic for the behavioral stereotype.

Aggression↗

[Effect of forced swimming on the memory track retention in mice with various behavioral stereotypes].

The effects of forced swimming on retrieval of the passive avoidance during its extinction were found to depend on aggressive and submissive behavior. In mice without generated behavioral stereotypes, swim stress applied before or after training stabilized retention of the memory trace retrieval. The similar improved influence of forced swimming on memory storage is revealed in submissive, but not aggressive mice. The increase of resistance against extinction under the swim stress can be connected to facilitation of emotional processes.

Aggression↗

[Effect of novelty and behavioral stereotype on development of amnesia in mice].

The research was aimed at analysis of interaction of basic behavioural strategy, extinction of information novelty and efficiency of amnesic influence. It is shown that preliminary habituation to the task apparatus prevented development of amnesia, induced detention of the animal in a dangerous compartment in submissive rather than aggressive mice C57BL/6J. The findings suggest that revealed distinctions in effects of pre-exposure on development of amnesia are essentially predetermined by selectivity of extinction of the information novelty specific to a stereotype of behaviour.

Aggression↗

[The effect of the duration of adaptation to laboratory conditions on the passive avoidance reflex in rats].

Influence of adaptation degree in new conditions on the passive avoidance was studied. The short period of habituation (3 days) positively influenced the rats' ability for memory trace retrieval. A negative correlation between the step through latency and anxiety in the elevated plus-maze, was shown. Prolongation of adaptation up to 9 days reduced levels of anxiety and retrieval of conditioned response. Modulating role of adaptation degree causing various anxiety levels in passive avoidance, is discussed.

Adaptation, Physiological↗

[Effects of pre-exposure to an experimental chamber on memory trace retrieval in aggressive and submissive mice during extinction of conditioning].

Mice with a submissive stereotype of behaviour developed a fast habituation to novelty of environment. A subsequent training revealed a deficit of passive avoidance learning and prolongation of the memory trace extinction. Aggressive mice are characterised by a delay of the habituation and absence of any significant changes in the memory trace retrieval. The findings suggest that responses to environmental novelty and use of its estimation in learning and retention of memory traces are essentially predetermined by the basic strategy of behaviour.

Aggression↗

[The mechanisms of the emotiogenic regulation of memory].

The determining mechanism of memory regulation is a system involving the right temporal region and two anterior frontal regions. This is a cortical part of the integral system of the emotional regulation of memory. The dopaminergic mechanism forms the basis for fortifying the emotiogenic memory system, promoting the facilitation of retrieval. The selective emotional set of aggressive and submissive mice determines both the processes of extinction, development of amnesia, and subsequent reactivation of a memory trace induced by neuropharmacological agents. The GABA system is shown to enter the mechanism that controls the activity of dopamine system--dopamine release from the terminals of the nigrostriatal and mesolimbic dopaminergic systems is stimulated. The neurochemical background in the development of amnesia or forgetting determines the subsequent retrieval of a memory trace. The dopamine and GABA systems are common links in the retrieval of amnestic and forgetting memory traces, respectively. A substantial rise of met-enkephaline levels along with the maximum increase of D2-receptor density in the frontal cortex, amygdala, striatum, and hippocampus were observed in rats after learning. In vitro experiments indicated that met-enkephaline and beta-endorphine stabilized the kinetics of dopamine-receptor interactions.

Amnesia↗

Dopamine and opioid regulation of the memory retrieval recovery in mice.

The reactivation effects of the delta-opioid receptor blockade and D2 dopamine receptor activation on the detention-induced memory deficit in mice were investigated, in order to study possible interactions between opioid and dopamine systems in memory retrieval. Animals were trained in a one-trial passive-avoidance task. Pretesting treatment with ICI 174,864 (1, 3 or 5 mg/kg, i.p.) or quinpirole (0.5, 1 or 2 mg/kg, i.p.) facilitated retrieval of memory trace in saline-pretreated mice. Pretraining injection of the dopamine autoreceptor agonist, (+)-3PPP (2 mg/kg), having no effect alone in learning, prevented the ability of ICI 174,864 to produce the memory-enhancing effect. It is suggested that the normal functioning of the dopamine system was critical for the facilitation of retrieval by delta-antagonist. Quinpirole-induced reactivátion of memory retrieval was enhanced by pretreatment with Leu-enkephalin (0.2 mg/kg), inducing increased retention. We discuss these results in the context of an important interactions between D2 dopamine and delta-opioid receptors.

Animals↗

Effect of Leu-enkephalin on the memory reactivation produced by blockade of the benzodiazepine/GABA-chloride ionophore receptor complex.

This investigation sought to characterize the interaction between GABA/benzodiazepine and opioid systems in memory retrieval deficit induced by detaining an animal in the training apparatus after acquisition. Mice pretreated with saline or Leu-enkephalin (0.2 mg/kg) were trained in one-trial passive avoidance test with following detention. Pre-testing administration of bicuculline (1 mg/kg), picrotoxin (1 mg/kg), or flumazenil (10 mg/kg) produced the memory-enhancing effect in the saline-pretreated mice. Pretraining treatment with Leu-enkephalin blocked the reactivation of memory produced by bicuculline and picrotoxin, but not flumazenil. The present investigation suggest that both benzodiazepine/GABA and opioid systems are important modulators of memory retrieval and that a specific interaction between these systems is responsible for the observed recovery of impaired memory trace.

Analysis of Variance↗

Memory retrieval enhancement by kappa opioid agonist and mu, delta antagonists.

The present study sought to identify specific opioid receptor subtypes involved in the modulation of reactivation of amnesic or forgotten memory traces by use of a one-trial inhibitory avoidance training procedures in mice. The effects of naloxone, ICI 174,864 (mu and delta opioid receptor antagonists, respectively) and dynorphin (kappa agonist) were investigated. The results indicated that preretention test administration of naloxone (2 mg/kg) or ICI 174,864 (3 mg/kg) attenuated the amnesia and forgetting as indicated by prolongation of step-through latency. On the other hand, the activation of kappa opioid receptors by dynorphin (1 mg/kg) also showed reactivating effects both after amnesia and forgetting. On the basis of the parallelism of the effects for mu and delta opioid receptor antagonists and kappa agonist, and on the finding that all three opioids demonstrated a different degree of reactivation of amnesic and forgotten memory traces, it was concluded that mu, delta, and kappa opioid receptors contribute to the modulation of amnesia and forgetting by independent mechanisms.

Analysis of Variance↗

[Forgetfulness and amnesia: receptor mechanisms and brain mapping].

Inability to remember and amnesia have been shown to be active neurochemical processes. The coupled processes (blockade of the triggering DA stimulating system and activation of the inhibitory GABA-ergic system with the predominant value of postsynaptic D-2 receptors) are a neurochemical basis for development of amnesia. The mechanisms of spontaneous forgetting is provided by a decrease in the activity of the dopaminergic system along with the enhancement of benzodiazepine-GABA-ergic interferentional inhibition. The observed changes in dopamine metabolism, para-tyramine appearance, as well as restructure of D-2 receptors provide the activity of dopamine increasing mechanism which determines the retention of memory traces. A computer model of the spatial interaction of the dopamine membrane-receptor complex was constructed by scanning the samples of synaptic membranes after learning and amnesia. A new method of inducing psychogenic amnesia in human beings has been elaborated. Amnesia is characterized by the absence of increases in the number of cortical connections reflecting the emotional factor of information.

Amnesia↗