The absence of helplessness in females was neither dependent on organizational effects of testosterone during the day of birth, because masculinized females did not express helplessness as adults. Thus, sex differences in helplessness behavior are independent of gonadal hormones in adulthood and testosterone exposure during perinatal development. Learned helplessness may not constitute a valid model for depressive behavior in women, at least as reflected by the response of female rats to operant conditioning procedures

after stressful experience.”
“Gamma interferon receptor a (IFN-gamma R alpha) is stable but posttranslationally modified in herpes simplex virus 1(F) [HSV-1(F)]-infected cells. Studies with antibody directed to the phosphorylation site indicate that IFN-gamma R alpha is phosphorylated by the U(S)3 kinase. The modification is abolished in cells infected with Delta U(S)3, Delta U(L)13, or Delta(U(S)3/U(L)13) mutant virus. Transcripts learn more of the IFN-gamma-dependent genes do not accumulate in cells transduced with the U(S)3 protein kinase and treated with IFN-gamma. In contrast, the accumulation of IFN-gamma dependent gene transcripts is suppressed in cells infected with the wild-type virus, in cells infected with the Delta U(S)3 mutant virus, and to a lesser extent in the Delta U(L)41 virus-infected cells. The accumulation selleck products of IFN-gamma dependent gene transcripts

in Delta U(L)41-infected cells could be due at least in part to a significant delay and reduction in the accumulation of the U(S)3 protein. The results suggest that the expression of IFN-gamma-dependent genes is blocked independently by the degradation of IFN-gamma-dependent gene transcripts-a function of the virion host shutoff RNase-and by posttranslational modification of the IFN-gamma R alpha protein.”
“Human anxiety is frequently accompanied by depression, and when they co-occur both conditions exhibit greater severity and resistance to treatment. Little is known, however, about the molecular processes linking these emotional and mood disorders. Based on previously reported phosphorylation patterns of extracellular signal-regulated kinase

(ERK) in the brain, Selleckchem CA3 we hypothesized that ERK’s upstream activators intertwine fear and mood regulation through their hippocampal actions. We tested this hypothesis by studying the upstream regulation of ERK signaling in behavioral models of fear and depression. Wild-type and ERK1-deficient mice were used to study the dorsohippocampal actions of the putative ERK activators: mitogen-activated and extracellular signal-regulated kinase (MEK), protein kinase C (PKC), and cAMP-dependent protein kinase (PKA). Mice lacking ERK1 exhibited enhanced fear extinction and reduced depression caused by overactivation of ERK2. Both behaviors were reversed by inhibition of MEK, however the extinction phenotype depended on hippocampal, whereas the depression phenotype predominantly involved extrahippocampal MEK.