The persistent facilitatory effect of i.c.v. methoctramine in the CA1 region of urethane-anesthetized rats was mimicked by gallamine, an M2 receptor antagonist, selleck chemical supporting a role for this receptor subtype. Neither the N-methyl-D-aspartate (NMDA) receptor antagonists D-(-)-2-amino phosphonopentanoic acid (D-AP5) and memantine, nor the metabotropic glutamate receptor subtype la antagonist (S)-(+)-alpha-amino-4-carboxy-2-methylbenzeneacetic acid (LY367385) significantly affected the methoctramine-induced persistent

synaptic enhancement, indicating a lack of requirement for these glutamate receptors. The selective kinase inhibitors Rp-adenosine-3′, 5′-cyclic monophosphorothioate (Rp-cAMPS) EGFR inhibitor and the myrostylated pseudosubstrate peptide, Myr-Ser-Ile-Tyr-Arg-Arg-Gly-Ala-Arg-Arg-Trp-Arg-Lys-Leu-OH

(ZIP), were used to investigate the roles of protein kinase A (PKA) and the atypical protein kinase C, protein kinase M zeta (PKM zeta), respectively. Remarkably, pretreatment with either agent prevented the induction of the persistent synaptic enhancement by methoctramine and post-methoctramine treatment with Rp-cAMPS transiently reversed the enhancement. These findings are strong evidence that antagonism of M2 muscarinic ACh receptors in vivo induces an NMDA receptor-independent persistent synaptic enhancement that requires activation of both PKA and PKM zeta. (c) 2008 IBRO. Published by Elsevier

Ltd. All rights reserved.”
“Although predator-induced stress is a common biotic factor in aquatic communities that can strongly influence anuran development, there have been no studies to date that examined the interaction between this factor and atrazine, the most widely used pesticide in the United States. The potential synergistic effects of atrazine (0, 20, or 200 mu g/L) and predatory stress on the survival, growth, development, and reproductive Bcl-w development of Hyla versicolor (gray treefrog) tadpoles were investigated. Atrazine reduced the proportion of tadpoles reaching metamorphosis; however, this effect was modified by the presence of a nonlethal predator. The combined effects of predatory stress and exposure to 200 mu g/L atrazine resulted in the lowest proportion of tadpoles reaching metamorphosis. No treatment effects were observed for mass, snout-urostyle length, or the proportion of metamorphs that were male or female. No macroscopic gonadal anomalies were observed. Many gonads were underdeveloped; however, gonadal development was more advanced in metamorphs exposed to 200 mu g/L atrazine. This effect was modified by the presence of a nonlethal predator such that female gonadal development was further accelerated and male gonadal development was retarded by predatory stress.