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N K Popova - One of the best experts on this subject based on the ideXlab platform.
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on the association between lipopolysaccharide induced Catalepsy and serotonin metabolism in the brain of mice genetically different in the predisposition to Catalepsy
Pharmacology Biochemistry and Behavior, 2013Co-Authors: E Y Bazhenova, Maria A. Tikhonova, A. V. Kulikov, Daria V Bazovkina, Daria V Fursenko, N K PopovaAbstract:Abstract The study of the interaction between nervous and immune systems in the mechanism of psychopathology is an important problem of neuroscience. Catalepsy (freezing reaction) is a passive defensive strategy in response to threatening stimuli. An exaggerated form of Catalepsy is a syndrome of some grave mental disorders. Both the brain serotonin (5-HT) and immune systems were shown to be involved in the mechanism of Catalepsy. Here we compared the effects of two doses (50 or 200 μg/kg, ip) of innate immune system activator, bacterial lipopolysaccharide (LPS), on Catalepsy, 5-HT and its main metabolite, 5-hydroxyindole acetic acid (5-HIAA) in the hippocampus, striatum, and midbrain of mice of Catalepsy-prone (CBA/Lac and AKR.CBA-D13Mit76) and Catalepsy-resistant (AKR/J) strains. The expression of LPS-induced Catalepsy as well as 5-HIAA/5-HT ratio in the midbrain and striatum were significantly higher in mice of the Catalepsy-prone strains compared with animals of the Catalepsy-resistant strains. These results indicated an involvement of the brain 5-HT system in the cataleptogenic effect of LPS and open up new vistas for understanding the nervous–immune mechanism of behavioral disorders.
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hereditary Catalepsy in mice is associated with the brain dysmorphology and altered stress response
Behavioural Brain Research, 2013Co-Authors: Maria A. Tikhonova, A. V. Kulikov, Daria V Bazovkina, Elizabeth A Kulikova, A S Tsybko, E Y Bazhenova, V S Naumenko, A E Akulov, M P Moshkin, N K PopovaAbstract:Abstract Catalepsy is a passive defensive strategy in response to threatening stimuli. In exaggerated forms it is associated with brain dysfunctions. The study was aimed to examine (1) possible association of the hereditary Catalepsy with neuroanatomical characteristics and (2) sensitivity of the Catalepsy expression, HPA and brain serotonin (5-HT) systems to restraint stress (for one hour) in mice of Catalepsy-prone (CBA/Lac, ASC (Antidepressant Sensitive Catalepsy), congenic AKR.CBA-D13M76) and Catalepsy-resistant (AKR/J) strains. Magnetic resonance imaging showed that the Catalepsy-prone mice were characterized by the smaller size of the pituitary gland and the larger size of the thalamus. In ASC mice, diencephalon region (including hypothalamus) and striatum were significantly reduced in size. Restraint stress provoked Catalepsy in AKR mice and enhanced it in the Catalepsy-prone mice. Stress-induced corticosterone elevation was diminished, while 5-HT metabolism (5-HIAA level or 5-HIAA/5-HT ratio) in the midbrain was significantly augmented by stress in the Catalepsy-prone mice. The multivariate factor analysis revealed interactions between the basal levels and the stress-induced alterations of 5-HT metabolism in the hippocampus and midbrain suggesting the interaction between multiple alterations in 5-HT neurotransmission in several brain structures in the regulation of hereditary Catalepsy. The study indicated an association between the hereditary Catalepsy, neuroanatomical characteristics, and neurochemical responses to emotional stress. The Catalepsy-prone genotypes seem to be more susceptible to stress that suggests them as the adequate models to study the genetic predisposition to stress-based neuropathology. The data support the association of hereditary Catalepsy with the inherited brain dysfunction of a neurodegenerative nature.
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association of glycoprotein gp130 with hereditary Catalepsy in mice
Genes Brain and Behavior, 2010Co-Authors: A. V. Kulikov, V S Naumenko, D V Bazovkina, N. A. Sinyakova, N K PopovaAbstract:Glycoprotein gp130 is involved in the interleukin-6 (IL-6) and related cytokines' signaling. Linkage between the gp130 coding gene and freezing reaction (Catalepsy) was shown. Here, we compared the expression and function of the gp130 in male mice of Catalepsy-resistant AKR/J strain and Catalepsy-prone congenic AKR.CBA-D13Mit76 strain created by transferring the gp130 gene allele from Catalepsy-prone CBA/Lac to the genome of AKR/J strain. No difference in the gp130 expression in the frontal cortex, hippocampus and midbrain between AKR and AKR.CBA-D13Mit76 mice was found. However, AKR.CBA-D13Mit76 mice were more sensitive to bacterial lipopolysaccharide (LPS). The administration of LPS (50 µg/kg, ip) significantly increased mRNA level of the gene coding IL-6-regulated glial fibrillary acidic protein (GFAP) in the midbrain, induced Catalepsy and decreased locomotion in the open field and social investigation tests in AKR.CBA-D13Mit76, but not in AKR mice. The result indicates (1) the association between gp130 and hereditary Catalepsy, (2) increased functional activity rather than expression of gp130 in AKR.CBA-D13Mit76 mice and (3) the involvement of gp130 in the mechanism of LPS-induced alteration of behavior.
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genetic structure of hereditary Catalepsy in mice
Genes Brain and Behavior, 2008Co-Authors: A. V. Kulikov, Daria V Bazovkina, E M Kondaurova, N K PopovaAbstract:Catalepsy or pronounced freezing is a natural passive defense strategy in animals and a syndrome of some mental disorders in human. Hereditary Catalepsy was shown to be associated with depressive-like features in rats and mice. The loci underlying the difference in predisposition to Catalepsy between Catalepsy-prone CBA/lacJ and Catalepsy-resistant AKR/J mice were mapped using congenic line and selective breeding approaches. Three congenic mouse lines (AKR.CBA-D13Mit76C, AKR.CBA-D13Mit76A and AKR.CBA-D13Mit78) carrying the 59- to 70-, 61- to 70- and 71- to 75-cm fragments of chromosome 13 transferred from the CBA to the AKR genome were created by nine successive backcrossing of (CBA × AKR)F1 on AKR strain. Because Catalepsy was found only in the AKR.CBA-D13Mit76C and AKR.CBA-D13Mit76A mice, the major gene of Catalepsy was mapped on the fragment of 61–70 cm. Selective breeding of the (CBA × (CBA × AKR))BC backcross generation for high predisposition to Catalepsy showed numerous genome-wide distributed CBA-derived alleles as well as the AKR-derived alleles mapped on chromosome 17 and on the proximal parts of chromosomes 10 and 19 that increased the cataleptogenic effect of the major gene.
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selective breeding for Catalepsy changes the distribution of microsatellite d13mit76 alleles linked to the 5 ht1a serotonin receptor gene in mice
Genes Brain and Behavior, 2006Co-Authors: E M Kondaurova, A. V. Kulikov, D V Bazovkina, N K PopovaAbstract:Catalepsy (pronounced motor inhibition) is a natural defensive reaction against predator. Recently, the quantitative trait locus for Catalepsy was mapped on mouse chromosome 13 near the 5-HT1A serotonin receptor gene. Here, the linkage between Catalepsy and the 5-HT1A receptor gene was verified using breeding experiment. Selective breeding for high predisposition to Catalepsy was started from backcross BC[CBA × (CBA × AKR)] generation between Catalepsy-prone (CBA) and Catalepsy-resistant (AKR) mouse strains. CBA and AKR strains also differed in the 5-HT1A receptor functional activity. A rapid increase of cataleptic percentage from 21.2% in the backcrosses to 71% in the third generation of selective breeding (S3) was shown. The fragment of chromosome 13 including the 5-HT1A receptor gene was marked with D13Mit76 microsatellite. Breeding for Catalepsy increased the concentration of CBA-derived and decreased the concentration of AKR-derived alleles of microsatellite D13Mit76 in the S1 and S2. All mice of the S9 and S12 were homozygous for CBA-derived allele of D13Mit76 marker. Mice of the S12 showed CBA-like receptor activity. These findings indicate that selective breeding for behavior can involve selection of polymorphic variants of the 5-HT1A receptor gene.
A. V. Kulikov - One of the best experts on this subject based on the ideXlab platform.
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expression of genes in the 111 35 116 16 million bp fragment of chromosome 13 in brain of mice with different predisposition to hereditary Catalepsy
Molecular Biology, 2014Co-Authors: N. A. Sinyakova, A. V. KulikovAbstract:Catalepsy is a pathological animal behavior that is usually associated with dysfunctions in the striatal pallidal system of the brain and can be caused by different reasons. It was previously demonstrated that hereditary Catalepsy is linked to the 111.35–116.16 million bp fragment of chromosome 13 in mice. The level of mRNA content in 42 genes localized in this fragment was determined in the study. Two brain departments that are functionally associated with Catalepsy (striatum and substantia nigra) were studied in mice from AKR line (resistant to Catalepsy), cataleptic CBA line, and recombinant cataleptic AKR.CBA-D13Mit76 (D13) line. The latter was obtained by the transfer of indicated fragment of chromosome 13 from the CBA line to the genome of the AKR line. It was found that two genes (Ndufs4 and Ppap2a) in the striatum and ten genes (Esm1, Fst, Gm10735, Gm15322, Gm15323, Gm15324, Gm15325, Il6st, Il31ra, and Itga1) in the substantia nigra differ in the level of mRNA expression in AKR and D13 lines. The Mcidas gene mRNA level is lower in both structures in D13 line mice than in the AKR line. The expression of the Hspb3 and Mocs2 genes (that encode heat shock protein and molybdenum cofactor synthesis, respectively) is lower in the substantia nigra of CBA and D13 cataleptic line mice than in the AKR line resistant to Catalepsy. These genes are considered to be the most likely candidate genes of the Catalepsy. The coexpression of a large amount of genes in these brain structures in sick animals indicates the existence of a complex gene network that regulates hereditary Catalepsy.
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on the association between lipopolysaccharide induced Catalepsy and serotonin metabolism in the brain of mice genetically different in the predisposition to Catalepsy
Pharmacology Biochemistry and Behavior, 2013Co-Authors: E Y Bazhenova, Maria A. Tikhonova, A. V. Kulikov, Daria V Bazovkina, Daria V Fursenko, N K PopovaAbstract:Abstract The study of the interaction between nervous and immune systems in the mechanism of psychopathology is an important problem of neuroscience. Catalepsy (freezing reaction) is a passive defensive strategy in response to threatening stimuli. An exaggerated form of Catalepsy is a syndrome of some grave mental disorders. Both the brain serotonin (5-HT) and immune systems were shown to be involved in the mechanism of Catalepsy. Here we compared the effects of two doses (50 or 200 μg/kg, ip) of innate immune system activator, bacterial lipopolysaccharide (LPS), on Catalepsy, 5-HT and its main metabolite, 5-hydroxyindole acetic acid (5-HIAA) in the hippocampus, striatum, and midbrain of mice of Catalepsy-prone (CBA/Lac and AKR.CBA-D13Mit76) and Catalepsy-resistant (AKR/J) strains. The expression of LPS-induced Catalepsy as well as 5-HIAA/5-HT ratio in the midbrain and striatum were significantly higher in mice of the Catalepsy-prone strains compared with animals of the Catalepsy-resistant strains. These results indicated an involvement of the brain 5-HT system in the cataleptogenic effect of LPS and open up new vistas for understanding the nervous–immune mechanism of behavioral disorders.
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hereditary Catalepsy in mice is associated with the brain dysmorphology and altered stress response
Behavioural Brain Research, 2013Co-Authors: Maria A. Tikhonova, A. V. Kulikov, Daria V Bazovkina, Elizabeth A Kulikova, A S Tsybko, E Y Bazhenova, V S Naumenko, A E Akulov, M P Moshkin, N K PopovaAbstract:Abstract Catalepsy is a passive defensive strategy in response to threatening stimuli. In exaggerated forms it is associated with brain dysfunctions. The study was aimed to examine (1) possible association of the hereditary Catalepsy with neuroanatomical characteristics and (2) sensitivity of the Catalepsy expression, HPA and brain serotonin (5-HT) systems to restraint stress (for one hour) in mice of Catalepsy-prone (CBA/Lac, ASC (Antidepressant Sensitive Catalepsy), congenic AKR.CBA-D13M76) and Catalepsy-resistant (AKR/J) strains. Magnetic resonance imaging showed that the Catalepsy-prone mice were characterized by the smaller size of the pituitary gland and the larger size of the thalamus. In ASC mice, diencephalon region (including hypothalamus) and striatum were significantly reduced in size. Restraint stress provoked Catalepsy in AKR mice and enhanced it in the Catalepsy-prone mice. Stress-induced corticosterone elevation was diminished, while 5-HT metabolism (5-HIAA level or 5-HIAA/5-HT ratio) in the midbrain was significantly augmented by stress in the Catalepsy-prone mice. The multivariate factor analysis revealed interactions between the basal levels and the stress-induced alterations of 5-HT metabolism in the hippocampus and midbrain suggesting the interaction between multiple alterations in 5-HT neurotransmission in several brain structures in the regulation of hereditary Catalepsy. The study indicated an association between the hereditary Catalepsy, neuroanatomical characteristics, and neurochemical responses to emotional stress. The Catalepsy-prone genotypes seem to be more susceptible to stress that suggests them as the adequate models to study the genetic predisposition to stress-based neuropathology. The data support the association of hereditary Catalepsy with the inherited brain dysfunction of a neurodegenerative nature.
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effect of selective agonist of serotonin 5 ht1a receptors on defensive behavior in mice with different predisposition to Catalepsy
Bulletin of Experimental Biology and Medicine, 2010Co-Authors: D V Bazovkina, Elena Terenina, A. V. KulikovAbstract:We studied the effect of activation of serotonin 5-HT1A receptors with selective agonist 8-OHDPAT (0.1, 0.5, and 1.0 mg/kg) on intraspecies aggression and freezing reaction (Catalepsy) in male mice of Catalepsy-resistant AKR/J and two Catalepsy-prone strains CBA/Lac and congenic AKR.CBA-D13Mit76. The latter strain differs from AKR strain only by terminal chromosome 13 fragment transferred from CBA strain and containing a locus determining predisposition to Catalepsy and a gene encoding 5-HT1A receptor. 8-OH-DPAT in a low dose (0.1 mg/kg) affecting primarily presynaptic receptors suppressed aggressive behavior in CBA mice, but had no effect on the time of cataleptic freezing. At the same time, this dose of the drug produced no significant effect on aggression in AKR and AKR.CBA-D13Mit76 mice, but significantly attenuated freezing in AKR.CBA-D13Mit76 mice. High doses of 8-OHDPAT (0.5 and 1 mg/kg) which affected mainly postsynaptic receptors inhibited Catalepsy in CBA and AKR.CBA-D13Mit76 mice and in a dose of 1 mg/kg it suppressed aggression in all tested mouse strains. We concluded that the genome of the recipient strain (AKR) modulated the involvement of 5-HT1A receptors into the regulation of aggression and Catalepsy in mice.
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association of glycoprotein gp130 with hereditary Catalepsy in mice
Genes Brain and Behavior, 2010Co-Authors: A. V. Kulikov, V S Naumenko, D V Bazovkina, N. A. Sinyakova, N K PopovaAbstract:Glycoprotein gp130 is involved in the interleukin-6 (IL-6) and related cytokines' signaling. Linkage between the gp130 coding gene and freezing reaction (Catalepsy) was shown. Here, we compared the expression and function of the gp130 in male mice of Catalepsy-resistant AKR/J strain and Catalepsy-prone congenic AKR.CBA-D13Mit76 strain created by transferring the gp130 gene allele from Catalepsy-prone CBA/Lac to the genome of AKR/J strain. No difference in the gp130 expression in the frontal cortex, hippocampus and midbrain between AKR and AKR.CBA-D13Mit76 mice was found. However, AKR.CBA-D13Mit76 mice were more sensitive to bacterial lipopolysaccharide (LPS). The administration of LPS (50 µg/kg, ip) significantly increased mRNA level of the gene coding IL-6-regulated glial fibrillary acidic protein (GFAP) in the midbrain, induced Catalepsy and decreased locomotion in the open field and social investigation tests in AKR.CBA-D13Mit76, but not in AKR mice. The result indicates (1) the association between gp130 and hereditary Catalepsy, (2) increased functional activity rather than expression of gp130 in AKR.CBA-D13Mit76 mice and (3) the involvement of gp130 in the mechanism of LPS-induced alteration of behavior.
Maria A. Tikhonova - One of the best experts on this subject based on the ideXlab platform.
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on the association between lipopolysaccharide induced Catalepsy and serotonin metabolism in the brain of mice genetically different in the predisposition to Catalepsy
Pharmacology Biochemistry and Behavior, 2013Co-Authors: E Y Bazhenova, Maria A. Tikhonova, A. V. Kulikov, Daria V Bazovkina, Daria V Fursenko, N K PopovaAbstract:Abstract The study of the interaction between nervous and immune systems in the mechanism of psychopathology is an important problem of neuroscience. Catalepsy (freezing reaction) is a passive defensive strategy in response to threatening stimuli. An exaggerated form of Catalepsy is a syndrome of some grave mental disorders. Both the brain serotonin (5-HT) and immune systems were shown to be involved in the mechanism of Catalepsy. Here we compared the effects of two doses (50 or 200 μg/kg, ip) of innate immune system activator, bacterial lipopolysaccharide (LPS), on Catalepsy, 5-HT and its main metabolite, 5-hydroxyindole acetic acid (5-HIAA) in the hippocampus, striatum, and midbrain of mice of Catalepsy-prone (CBA/Lac and AKR.CBA-D13Mit76) and Catalepsy-resistant (AKR/J) strains. The expression of LPS-induced Catalepsy as well as 5-HIAA/5-HT ratio in the midbrain and striatum were significantly higher in mice of the Catalepsy-prone strains compared with animals of the Catalepsy-resistant strains. These results indicated an involvement of the brain 5-HT system in the cataleptogenic effect of LPS and open up new vistas for understanding the nervous–immune mechanism of behavioral disorders.
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hereditary Catalepsy in mice is associated with the brain dysmorphology and altered stress response
Behavioural Brain Research, 2013Co-Authors: Maria A. Tikhonova, A. V. Kulikov, Daria V Bazovkina, Elizabeth A Kulikova, A S Tsybko, E Y Bazhenova, V S Naumenko, A E Akulov, M P Moshkin, N K PopovaAbstract:Abstract Catalepsy is a passive defensive strategy in response to threatening stimuli. In exaggerated forms it is associated with brain dysfunctions. The study was aimed to examine (1) possible association of the hereditary Catalepsy with neuroanatomical characteristics and (2) sensitivity of the Catalepsy expression, HPA and brain serotonin (5-HT) systems to restraint stress (for one hour) in mice of Catalepsy-prone (CBA/Lac, ASC (Antidepressant Sensitive Catalepsy), congenic AKR.CBA-D13M76) and Catalepsy-resistant (AKR/J) strains. Magnetic resonance imaging showed that the Catalepsy-prone mice were characterized by the smaller size of the pituitary gland and the larger size of the thalamus. In ASC mice, diencephalon region (including hypothalamus) and striatum were significantly reduced in size. Restraint stress provoked Catalepsy in AKR mice and enhanced it in the Catalepsy-prone mice. Stress-induced corticosterone elevation was diminished, while 5-HT metabolism (5-HIAA level or 5-HIAA/5-HT ratio) in the midbrain was significantly augmented by stress in the Catalepsy-prone mice. The multivariate factor analysis revealed interactions between the basal levels and the stress-induced alterations of 5-HT metabolism in the hippocampus and midbrain suggesting the interaction between multiple alterations in 5-HT neurotransmission in several brain structures in the regulation of hereditary Catalepsy. The study indicated an association between the hereditary Catalepsy, neuroanatomical characteristics, and neurochemical responses to emotional stress. The Catalepsy-prone genotypes seem to be more susceptible to stress that suggests them as the adequate models to study the genetic predisposition to stress-based neuropathology. The data support the association of hereditary Catalepsy with the inherited brain dysfunction of a neurodegenerative nature.
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effect of imipramine on the behavior and cerebral 5 ht1a serotonin receptors in mice genetically predisposed to Catalepsy
Bulletin of Experimental Biology and Medicine, 2006Co-Authors: Maria A. Tikhonova, A. V. Kulikov, D V Bazovkina, V V Lebedeva, N K PopovaAbstract:Acute injection of imipramine to NPK mice hereditary predisposed to pinching Catalepsy reduced immobility in the forced swimming test, but had no effect on Catalepsy. Chronic treatment with imipramine reduced the severity of Catalepsy and functional activity of 5-HT1A serotonin receptors, but did not modify their expression in the hippocampus. NPK mice can be a convenient model for studies of the effects of antidepressant.
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Effects of Experimental Increases and Decreases in Thyroxine Levels on the Extent of Cataleptic Freezing Reactions in Rats
Neuroscience and Behavioral Physiology, 2005Co-Authors: A. V. Kulikov, Maria A. Tikhonova, E. I. Lebedeva, V. F. Chugui, Nina K. PopovaAbstract:Numerous clinical observations have provided evidence for a tight connection between impairments in the functions of the hypothalamo-hypophyseal-thyroid system and nervous and mental disorders. The aim of the present work was to compare the effects of experimental decreases and increases in blood thyroxine levels on the extents of two types of pathological freezing reaction in male Wistar rats — spontaneous Catalepsy and Catalepsy evoked by pinches at the nape of the neck (pinch-induced Catalepsy). Chronic administration of the thyroxine synthesis inhibitor propylthiouracil (5 mg/kg/day for 28 days) significantly decreased the blood hormone level and sharply increased the proportion of animals showing spontaneous Catalepsy and the immobility time, but had no effect on the extent of pinch-induced Catalepsy. At the same time, chronic administration of thyroxine (0.1 mg/kg/day for 28 days), which produced significant increases in blood hormone levels, had no effect on the extent of spontaneous Catalepsy but significantly increased the proportion of animals showing pinch-induced Catalepsy and the duration of this type of Catalepsy. It is concluded that both insufficiency and excess of thyroid hormones have cataleptogenic actions, but enhance different types of Catalepsy.
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Effect of experimental elevation and decrease of thyroxine level on Catalepsy in rats
Fiziologicheskiĭ zhurnal, 2004Co-Authors: Alexander V. Kulikov, Maria A. Tikhonova, E. I. Lebedeva, Chuguĭ Vf, Nina K. PopovaAbstract:: Thyroid dysfunction is associated with mental disorders. The present study was aimed to reveal the effects of experimental decrease and increase of thyroxine level on expression of two types of extensive freezing: spontaneous and pinch-induced Catalepsy, in Wistar rat males. Chronic administration of thyroxine synthesis inhibitor, propylthiouracil (5 mg/kg/day, 28 days), markedly decreased plasma hormone level and at the same time produced a significant increase in percentage of spontaneously cataleptic animals and immobility time, but had no effect on the expression of pinch-induced Catalepsy. On the contrary, chronic thyroxin (0.1 mg/kg/day, 28 days) treatment produced no effect on spontaneous Catalepsy expression, although it significantly increased percentage of cataleptic animals and immobility time of pinch-induced Catalepsy. The results suggest that both the thyroid hormone deficit and excess provoke Catalepsy in rats but enhance different forms of freezing reaction.
D V Bazovkina - One of the best experts on this subject based on the ideXlab platform.
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effect of selective agonist of serotonin 5 ht1a receptors on defensive behavior in mice with different predisposition to Catalepsy
Bulletin of Experimental Biology and Medicine, 2010Co-Authors: D V Bazovkina, Elena Terenina, A. V. KulikovAbstract:We studied the effect of activation of serotonin 5-HT1A receptors with selective agonist 8-OHDPAT (0.1, 0.5, and 1.0 mg/kg) on intraspecies aggression and freezing reaction (Catalepsy) in male mice of Catalepsy-resistant AKR/J and two Catalepsy-prone strains CBA/Lac and congenic AKR.CBA-D13Mit76. The latter strain differs from AKR strain only by terminal chromosome 13 fragment transferred from CBA strain and containing a locus determining predisposition to Catalepsy and a gene encoding 5-HT1A receptor. 8-OH-DPAT in a low dose (0.1 mg/kg) affecting primarily presynaptic receptors suppressed aggressive behavior in CBA mice, but had no effect on the time of cataleptic freezing. At the same time, this dose of the drug produced no significant effect on aggression in AKR and AKR.CBA-D13Mit76 mice, but significantly attenuated freezing in AKR.CBA-D13Mit76 mice. High doses of 8-OHDPAT (0.5 and 1 mg/kg) which affected mainly postsynaptic receptors inhibited Catalepsy in CBA and AKR.CBA-D13Mit76 mice and in a dose of 1 mg/kg it suppressed aggression in all tested mouse strains. We concluded that the genome of the recipient strain (AKR) modulated the involvement of 5-HT1A receptors into the regulation of aggression and Catalepsy in mice.
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association of glycoprotein gp130 with hereditary Catalepsy in mice
Genes Brain and Behavior, 2010Co-Authors: A. V. Kulikov, V S Naumenko, D V Bazovkina, N. A. Sinyakova, N K PopovaAbstract:Glycoprotein gp130 is involved in the interleukin-6 (IL-6) and related cytokines' signaling. Linkage between the gp130 coding gene and freezing reaction (Catalepsy) was shown. Here, we compared the expression and function of the gp130 in male mice of Catalepsy-resistant AKR/J strain and Catalepsy-prone congenic AKR.CBA-D13Mit76 strain created by transferring the gp130 gene allele from Catalepsy-prone CBA/Lac to the genome of AKR/J strain. No difference in the gp130 expression in the frontal cortex, hippocampus and midbrain between AKR and AKR.CBA-D13Mit76 mice was found. However, AKR.CBA-D13Mit76 mice were more sensitive to bacterial lipopolysaccharide (LPS). The administration of LPS (50 µg/kg, ip) significantly increased mRNA level of the gene coding IL-6-regulated glial fibrillary acidic protein (GFAP) in the midbrain, induced Catalepsy and decreased locomotion in the open field and social investigation tests in AKR.CBA-D13Mit76, but not in AKR mice. The result indicates (1) the association between gp130 and hereditary Catalepsy, (2) increased functional activity rather than expression of gp130 in AKR.CBA-D13Mit76 mice and (3) the involvement of gp130 in the mechanism of LPS-induced alteration of behavior.
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the role of 5 ht2a receptor and 5 ht2a 5 ht1a receptor interaction in the suppression of Catalepsy
Genes Brain and Behavior, 2010Co-Authors: V S Naumenko, E M Kondaurova, D V Bazovkina, E A Zubkov, A. V. KulikovAbstract:In the present study, the 5-HT2A and 5-HT1A receptors functional activity and 5-HT2A receptor gene expression were examined in the brain of ASC/Icg and congenic AKR.CBAD13Mit76C mouse strains (genetically predisposed to Catalepsy) in comparison with the parental Catalepsy-resistant AKR/J and Catalepsy-prone CBA/Lac mouse strains. The significantly reduced 5-HT2A receptor functional activity along with decreased 5-HT2A receptor gene expression in the frontal cortex was found in all mice predisposed to Catalepsy compared with Catalepsy-resistant AKR/J. 5-HT2A agonist DOI (0.5 and 1 mg/kg, i.p.) significantly reduced Catalepsy in ASC/Icg and CBA/Lac, but not in AKR.CBAD13Mit76C mice. Essential increase in 5-HT1A receptor functional activity was shown in Catalepsy-prone mouse strains in comparison with Catalepsy-resistant AKR/J mice. However, in AKR.CBAD13Mit76C mice it was lower than in ASC/Icg and CBA/Lac mice. The inter-relation between 5-HT2A and 5-HT1A receptors in the regulation of Catalepsy was suggested. This suggestion was confirmed by prevention of DOI anticataleptic effect in ASC/Icg and CBA/Lac mice by pretreatment with 5-HT1A receptor antagonist p-MPPI (3 mg/kg, i.p.). At the same time, the activation of 5-HT2A receptor led to the essential suppression of 5-HT1A receptor functional activity, indicating the opposite effect of 5-HT2A receptor on pre- and postsynaptic 5-HT1A receptors. Thus, 5-HT2A/5-HT1A receptor interaction in the mechanism of Catalepsy suppression in mice was shown.
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Epileptiform activity in the hippocampus of mice with different predisposition to pinch Catalepsy
Bulletin of Experimental Biology and Medicine, 2008Co-Authors: P. D. Lisachev, Alexander V. Kulikov, D V Bazovkina, T. A. Zapara, Nina K. PopovaAbstract:Experiments on hippocampal slices of CBA mice showed that the probability of spontaneous epileptiform discharges recorded in the field CA1 pyramidal layer is higher in animals predisposed to Catalepsy compared to mice with low predisposition to Catalepsy. Presumably, some factors determining predisposition to Catalepsy modulate synchronization of neuronal activity in the hippocampus; this suggests using hippocampal slices as a model for studies of neurophysiological mechanisms of hereditary predisposition to Catalepsy.
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selective breeding for Catalepsy changes the distribution of microsatellite d13mit76 alleles linked to the 5 ht1a serotonin receptor gene in mice
Genes Brain and Behavior, 2006Co-Authors: E M Kondaurova, A. V. Kulikov, D V Bazovkina, N K PopovaAbstract:Catalepsy (pronounced motor inhibition) is a natural defensive reaction against predator. Recently, the quantitative trait locus for Catalepsy was mapped on mouse chromosome 13 near the 5-HT1A serotonin receptor gene. Here, the linkage between Catalepsy and the 5-HT1A receptor gene was verified using breeding experiment. Selective breeding for high predisposition to Catalepsy was started from backcross BC[CBA × (CBA × AKR)] generation between Catalepsy-prone (CBA) and Catalepsy-resistant (AKR) mouse strains. CBA and AKR strains also differed in the 5-HT1A receptor functional activity. A rapid increase of cataleptic percentage from 21.2% in the backcrosses to 71% in the third generation of selective breeding (S3) was shown. The fragment of chromosome 13 including the 5-HT1A receptor gene was marked with D13Mit76 microsatellite. Breeding for Catalepsy increased the concentration of CBA-derived and decreased the concentration of AKR-derived alleles of microsatellite D13Mit76 in the S1 and S2. All mice of the S9 and S12 were homozygous for CBA-derived allele of D13Mit76 marker. Mice of the S12 showed CBA-like receptor activity. These findings indicate that selective breeding for behavior can involve selection of polymorphic variants of the 5-HT1A receptor gene.
Nina K. Popova - One of the best experts on this subject based on the ideXlab platform.
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Epileptiform activity in the hippocampus of mice with different predisposition to pinch Catalepsy
Bulletin of Experimental Biology and Medicine, 2008Co-Authors: P. D. Lisachev, Alexander V. Kulikov, D V Bazovkina, T. A. Zapara, Nina K. PopovaAbstract:Experiments on hippocampal slices of CBA mice showed that the probability of spontaneous epileptiform discharges recorded in the field CA1 pyramidal layer is higher in animals predisposed to Catalepsy compared to mice with low predisposition to Catalepsy. Presumably, some factors determining predisposition to Catalepsy modulate synchronization of neuronal activity in the hippocampus; this suggests using hippocampal slices as a model for studies of neurophysiological mechanisms of hereditary predisposition to Catalepsy.
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Effects of Experimental Increases and Decreases in Thyroxine Levels on the Extent of Cataleptic Freezing Reactions in Rats
Neuroscience and Behavioral Physiology, 2005Co-Authors: A. V. Kulikov, Maria A. Tikhonova, E. I. Lebedeva, V. F. Chugui, Nina K. PopovaAbstract:Numerous clinical observations have provided evidence for a tight connection between impairments in the functions of the hypothalamo-hypophyseal-thyroid system and nervous and mental disorders. The aim of the present work was to compare the effects of experimental decreases and increases in blood thyroxine levels on the extents of two types of pathological freezing reaction in male Wistar rats — spontaneous Catalepsy and Catalepsy evoked by pinches at the nape of the neck (pinch-induced Catalepsy). Chronic administration of the thyroxine synthesis inhibitor propylthiouracil (5 mg/kg/day for 28 days) significantly decreased the blood hormone level and sharply increased the proportion of animals showing spontaneous Catalepsy and the immobility time, but had no effect on the extent of pinch-induced Catalepsy. At the same time, chronic administration of thyroxine (0.1 mg/kg/day for 28 days), which produced significant increases in blood hormone levels, had no effect on the extent of spontaneous Catalepsy but significantly increased the proportion of animals showing pinch-induced Catalepsy and the duration of this type of Catalepsy. It is concluded that both insufficiency and excess of thyroid hormones have cataleptogenic actions, but enhance different types of Catalepsy.
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Effect of experimental elevation and decrease of thyroxine level on Catalepsy in rats
Fiziologicheskiĭ zhurnal, 2004Co-Authors: Alexander V. Kulikov, Maria A. Tikhonova, E. I. Lebedeva, Chuguĭ Vf, Nina K. PopovaAbstract:: Thyroid dysfunction is associated with mental disorders. The present study was aimed to reveal the effects of experimental decrease and increase of thyroxine level on expression of two types of extensive freezing: spontaneous and pinch-induced Catalepsy, in Wistar rat males. Chronic administration of thyroxine synthesis inhibitor, propylthiouracil (5 mg/kg/day, 28 days), markedly decreased plasma hormone level and at the same time produced a significant increase in percentage of spontaneously cataleptic animals and immobility time, but had no effect on the expression of pinch-induced Catalepsy. On the contrary, chronic thyroxin (0.1 mg/kg/day, 28 days) treatment produced no effect on spontaneous Catalepsy expression, although it significantly increased percentage of cataleptic animals and immobility time of pinch-induced Catalepsy. The results suggest that both the thyroid hormone deficit and excess provoke Catalepsy in rats but enhance different forms of freezing reaction.
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Genetic relationships between Catalepsy and pendulum movements in rats
Genetika, 1999Co-Authors: V. G. Kolpakov, Chuguĭ Vf, Nina K. Popova, Barykina Nn, T. A. Alekhina, Zorkol'steva, Aksenovich TiAbstract:: Predispositions to pendulum movements (PMs) and Catalepsy was studied in rat strains selected for predisposition to Catalepsy and for enhanced or suppressed PMs. Positive correlation between PMs and Catalepsy at earlier stages of selection changed to negative at later stages. Based on these data, it was hypothesized that the genes that determine the predisposition to Catalepsy affect the expression of the gene determining PMs in such a way that different PM alleles become dominant in the cases of moderate and strong effects of the Catalepsy genes.
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Involvement of striatum serotonergic system in the expression of genetically defined Catalepsy.
Fiziologicheskiĭ zhurnal, 1997Co-Authors: Nina K. Popova, Alexander V. Kulikov, Damira F. Avgustinovich, Barykina NnAbstract:: The activity of the rate-limiting enzyme of serotonin biosynthesis, tryptophan hydroxylase, and specific binding of [3H]ketanserin to 5-HT2A receptors and [3H]8-OH-DPAT to 5-HT1A receptors in the striatum of genetically predisposed to Catalepsy rats and mice have been studied. The activity of tryptophan hydroxylase in the striatum of rats bred for many generations for predisposition to Catalepsy was higher than in nonselected rats. Mice of highly susceptible to pinch-induced Catalepsy CBA strain also differed from noncataleptic AKR and C57BL mouse strains by higher activity of tryptophan hydroxylase in striatum. Inhibition of tryptophan hydroxylase with p-chlorophenylalanine or p-chloromethamphetamine significantly decreased immobility time in genetically predisposed to Catalepsy rats and mice. A decrease in the [3H]ketanserin specific binding in the striatum of cataleptic rats and CBA mice was found indicating a decrease in 5-HT2A receptor density. A decrease in [3H]8-OH-DPAT binding in striatum of cataleptic rats but not in CBA mice was shown. These results indicate that serotonergic system of striatum is involved in the expression of hereditary Catalepsy and suggest that hereditary Catalepsy may result from genetic changes in the regulation of serotonin metabolism and reception in striatum.