Publications by authors named "Inna Midzyanovskaya"

Behavioral copying is a key process in group actions, but it is challenging for individuals with autism spectrum disorder (ASD). We investigated behavioral contagion, or instinctual replication of behaviors, in Krushinky-Molodkina (KM) rats ( = 16), a new potential rodent model for ASD, compared to control Wistar rats ( = 15). A randomly chosen healthy Wistar male ("demonstrator rat") was introduced to the homecage of experimental rats ("observers") 10-14 days before the experiments to become a member of the group.

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This study aimed to investigate the role of the nigrostriatal dopaminergic system in the modulation of absence epilepsy. Immunochemical analysis of the rostral pole of the substantia nigra pars compacta (SNpc) was conducted on 13 adult male Wistar Albino rats from Rijswijk rats. The rostral pole of the SNpc included the dorsal and lateral parts.

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Epilepsy or epileptic syndromes affect more than 70 million people, often comorbid with autism spectrum disorders (ASD). Seizures are concerned as a factor for social regression in ASD. A stepwise experimental approach to this problem requires an animal model to provoke seizures and monitor subsequent behavior.

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Binding densities to dopamine D1-like and D2-like receptors (D1DR and D2DR) were studied in brain regions of animals with genetic generalized audiogenic (AGS) and/or absence (AbS) epilepsy (KM, WAG/Rij-AGS, and WAG/Rij rats, respectively) as compared to non-epileptic Wistar (WS) rats. Convulsive epilepsy (AGS) exerted a major effect on the striatal subregional binding densities for D1DR and D2DR. An increased binding density to D1DR was found in the dorsal striatal subregions of AGS-prone rats.

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Article Synopsis
  • Epilepsy is often found alongside autism spectrum disorders (ASDs), prompting researchers to look for animal models that share similar brain mechanisms.
  • The study utilized the KM rat strain, known for its convulsive epilepsy, to assess their social behavior in tests that measure social preference, revealing that these rats showed decreased social interaction and unusual responses when exposed to unfamiliar social stimuli.
  • Results indicated that KM rats had a significantly reduced inclination for social engagement despite not having lower overall activity levels, supporting the idea that this strain could serve as a new model for studying the co-occurrence of ASDs and epilepsy.
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Blind walks of previsual rat pups in the open field test were analyzed for random components and/or strategies of locomotion. Wistar infants (n = 51) on their 13th postnatal day was tracked in the open field test for 2 minutes. At this age, immature rats should rely only on non-visual modalities in their navigation.

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Distributions of brain H3 histamine receptors in regions of the prefrontal cortex were studied by assessing regional binding densities for [3 H](R)α-methylhistamine in coronal brain slices of normal rats and rats with genetically determined absence and/or audiogenic epilepsies. The three groups of epileptic rats displayed widespread significant decreases in H3 histamine receptor binding densities. A 20-25% decline was seen in the rostral aspects of the lateral prefrontal cortex, namely the granular, dysgranular, and dorsal agranular insular regions.

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Genetic animal models for convulsive, non-convulsive and mixed types of generalized epilepsies were used to establish putative histaminergic brain sites involved in the control of different types of epilepsy. Age matched rats of the KM strain (audiogenic seizures, AGS), WAG/Rij strain (absence seizures) and the WAG/Rij-AGS substrain (mixed model) were compared with a control group of Wistar rats on regional binding densities of H1 histamine receptors. Coronal slices of adult brains of the four groups were labeled with 3H pyrilamine, an antagonist of H1 histamine receptor and density of receptors was quantified with image analyses.

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The effects of metoprine, an inhibitor of histamine N-methyltransferase, on open field activity and brain regional histamine (HA) content were examined in rats with mixed, absence and audiogenic, epilepsy (WAG/Rij-AGS), rats with audiogenic epilepsy (Wistar-AGS) and in non-epileptic control rats (Wistar-nAGS). HA content was increased by metoprine (20mg/kg, i.p.

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The effects of vigabatrin, which increases GABA concentrations by inhibiting GABA transaminase, on spike and wave discharges (SWDs) in the electroencephalogram of WAG/Rij rats were studied. Vigabatrin increased the incidence and duration of the SWDs, suggesting a quantitative GABA(A)ergic involvement in the mechanism(s) underlying the starting and stopping of an ongoing SWD. Also, vigabatrin decreased the SWD peak frequency, suggesting an important role of GABA(B) in the mechanism(s) underlying the peak frequency of the SWDs.

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Spike-wave discharges (SWDs) characterizing absence epilepsy appear in closely packed aggregated sequences, which gave rise to the name "pyknolepsy" for this disease. In WAG/Rij rats, genetically prone to absence epilepsy, spontaneous SWDs seem to occur in clusters as well. Here, we aimed to quantify the seizures' clusters.

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The continuous Morlet wavelet transform was used for the analysis of the time-frequency pattern of spike-wave discharges (SWD) as can be recorded in a genetic animal model of absence epilepsy (rats of the WAG/Rij strain). We developed a new wavelet transform that allows to obtain the time-frequency dynamics of the dominating rhythm during the discharges. SWD were analyzed pre- and post-administration of certain drugs.

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Mixed forms of epilepsy in patients are often refractory. Therefore, animal models of comorbid convulsive and nonconvulsive seizure are needed for experimental research. Susceptibility to audiogenic convulsions was studied in a large group of young and adult WAG/Rij rats with inherited absence epilepsy.

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