Cognitive Test Solution in Mice with Different Brain Weights after Atomoxetine

In this paper, the data are presented concerning different reactions to seven daily injections of atomoxetine in two mouse strains differing in relative brain weight. Atomoxetine affected the performance in a puzzle-box cognitive test in a complicated way—the large brain mice were less successful at task solutions (presumably because they were not afraid of the brightly lit test box), while the small brain strain of atomoxetine treated mice solved the task more successfully. The behavior of all atomoxetine treated animals was more active in an aversive situation (an unescapable slippery funnel, (analogous to the Porsolt test) and the time of immobility decreased significantly in all atomoxetine treated mice. The general patterns of behavioral reactions to atomoxetine in the cognitive test and other interstrain differences demonstrated in these experiments made it possible to suggest that differences in ascending noradrenergic projections between the two strains used exist. Further analysis of the noradrenergic system in these strains is needed (and further analysis of the effects of drugs which affect noradrenergic receptors)

Characteristic Features of the Transcriptome in a Rat Strain with Audiogenic Epilepsy

Audiogenic epilepsy (AE), developing in rodent strains in response to sound, is widely used as the model of generalized convulsive epilepsy, while the molecular mechanisms determining AE are currently poorly understood. The brain region that is crucial for AE development isthe inferior and superior colliculi (IC, SC). We compared IC-SC gene expression profiles in rats with different AE susceptibility using transcriptome analysis.The transcriptomes were obtained from the IC-SC of Wistar rats (with no AE), Krushinsky-Molodkina (KM) strain rats (100% AE susceptible), and ”0” strain rats (with no AE) selected from F2 KM x Wistar hybrids for AE absence. KM gene expression displayed characteristic differences inboth of the strains that were not susceptible to AE. There was increased expression of a number of genes responsible for positive regulation of the MAPK signaling cascade, as well as of genes responsible for the production of interferon and several other cytokines. An increase in the expression levels of theTTR gene was found in KM rats, as well as significantly lower expression of the Msh3 gene (involved in post-replicative DNA repair systems). AE was also describedin the 101/HY mouse strain with a mutation in the locus controlling DNA repair. The DNA repair system defects could be the primary factor leading to the accumulation of mutations, which, in turn, promote AE. Keywords: udiogenic seizure, KM strain, transcriptome, TTR gene, Msh3 gene, DNA repai

Rodent Models of Audiogenic Epilepsy: Genetic Aspects, Advantages, Current Problems and Perspectives

Animal models of epilepsy are of great importance in epileptology. They are used to study the mechanisms of epileptogenesis, and search for new genes and regulatory pathways involved in the development of epilepsy as well as screening new antiepileptic drugs. Today, many methods of modeling epilepsy in animals are used, including electroconvulsive, pharmacological in intact animals, and genetic, with the predisposition for spontaneous or refractory epileptic seizures. Due to the simplicity of manipulation and universality, genetic models of audiogenic epilepsy in rodents stand out among this diversity. We tried to combine data on the genetics of audiogenic epilepsy in rodents, the relevance of various models of audiogenic epilepsy to certain epileptic syndromes in humans, and the advantages of using of rodent strains predisposed to audiogenic epilepsy in current epileptology

Recolonization of mutans streptococci after application of chlorhexidine gel

Streptococcus mutans is specifically suppressed by intensive treatment with chlorhexidine gel, but the time for recolonization and the effect on other oral bacteria are not totally clear. In this study, recolonization of mutans streptococci was evaluated in nine healthy adult volunteers, who were highly colonized with this microorganism. Stimulated saliva was collected before (baseline) and at 1, 7, 14, 21 and 28 days after application of 1% chlorhexidine gel on volunteers’ teeth for two consecutive days. On each day, the gel was applied using disposable trays for 3 x 5 min with intervals of 5 min between each application. Saliva was plated on blood agar to determine total microorganisms (TM); on mitis salivarius agar to determine total streptococci (TS) and on mitis salivarius agar plus bacitracin to determine mutans streptococci (MS). Chlorhexidine was capable of reducing the counts of MS and the proportion of MS with regard to total microorganisms (%MS/ TM) (p0.05) after 14 days for MS and 21 days for %MS/TM. The counts of TM and TS and the proportion of MS to total streptococci did not differ statistically from baseline (p>0.05) after chlorhexidine treatment. The results suggest that the effect of chlorhexidine gel treatment on suppression of mutans streptococci is limited to less than a month in highly colonized individuals.Streptococcus mutans é especificamente suprimido pelo tratamento intensivo com clorexidina em gel, mas o tempo de recolonização e o efeito em outras bactérias orais não está totalmente claro. Nesse estudo, a recolonização de estreptococos do grupo mutans foi avaliado em nove voluntários adultos saudáveis, os quais eram altamente colonizados por esse microrganismo. Saliva estimulada foi coletada antes (baseline) e 1, 7, 14, 21 e 28 dias após a aplicação de clorexidina em gel a 1% nos dentes dos voluntários por dois dias consecutivos. Em cada dia, o gel foi aplicado utilizando moldeiras descartáveis por 3 x 5 min com intervalos de 5 min entre cada aplicação. A saliva foi inoculada em ágar sangue para determinação dos microrganismos totais (MT); em mitis salivarius ágar para determinação dos estreptococos totais (ET) e em meio mitis salivarius com bacitracina para determinar a contagem de estreptococos do grupo mutans (EGM). O tratamento com clorexidina foi capaz de reduzir as contagens de EGM e a proporção de EGM em relação aos microrganismos totais (%EGM/MT) (p0,05) após 14 dias para EGM e 21 dias para %EGM/MT. As contagens de MT e ET e a proporção de EGM em relação a estreptococos totais não difereriram estatisticamente do baseline (p>0,05) após o tratamento com clorexidina. Os resultados sugerem que o efeito do tratamento com clorexidina em gel na supressão de estreptococos do grupo mutans é limitado a menos de um mês em indivíduos altamente colonizados

Characteristic Features of the Transcriptome in A Rat Strain with Audiogenic Epilepsy

Audiogenic epilepsy (AE), developing in rodent strains in response to sound, is widely used as the model of generalized convulsive epilepsy, while the molecular mechanisms determining AE are currently poorly understood. The brain region that is crucial for AE development isthe inferior and superior colliculi (IC, SC). We compared IC-SC gene expression profiles in rats with different AE susceptibility using transcriptome analysis.The transcriptomes were obtained from the IC-SC of Wistar rats (with no AE), Krushinsky-Molodkina (KM) strain rats (100% AE susceptible), and ”0” strain rats (with no AE) selected from F2 KM x Wistar hybrids for AE absence. KM gene expression displayed characteristic differences inboth of the strains that were not susceptible to AE. There was increased expression of a number of genes responsible for positive regulation of the MAPK signaling cascade, as well as of genes responsible for the production of interferon and several other cytokines. An increase in the expression levels of theTTR gene was found in KM rats, as well as significantly lower expression of the Msh3 gene (involved in post-replicative DNA repair systems). AE was also describedin the 101/HY mouse strain with a mutation in the locus controlling DNA repair. The DNA repair system defects could be the primary factor leading to the accumulation of mutations, which, in turn, promote AE. Keywords: udiogenic seizure, KM strain, transcriptome, TTR gene, Msh3 gene, DNA repai