It is possible that the changes in current amplitude that we have observed with a4b2 and a7 nAChRs may be a consequence of temperature-induced changes in single-channel conductance. Indeed, it has been reported that the conductance of muscle-type nAChRs increases with increasing temperature. As has been discussed previously in connection with the effects of temperature on Qingyangshengenin-B functional properties of acetylcholine-gated chloride channels from the pond snail Lymnaea, alternative possibilities for the effects that we have observed include temperature-dependent changes in single-channel kinetics and/ or changes in the affinity of agonist binding. Recently, evidence has been obtained indicating that the gating rate constants of muscle nAChRs are altered by temperature. Further work will be required to establish the precise mechanism of action of the temperature dependent effects that we have observed on the amplitudes of whole-cell responses in different subtypes of neuronal nAChRs. We can conclude, however, that changes in temperature can have opposing effects on the amplitude of nAChR whole-cell responses, whilst having a NSC 632839 similar effect on the rate of desensitization of the macroscopic agonist-evoked response. Within the nervous system, a good number of miRNAs exhibit developmentally-dependent and cell-type-specific, expression patterns. Further, recent work has shown that miRNAs can be expressed in an activity-dependent manner. Within this context, particular attention has been paid to the miRNA132. miR132 is processed from the intron of a small noncoding RNA gene and is robustly responsive to an array of physiological and pathophysiological stimuli. With respect to neuronal function, miR132 has been shown to influence dendritic growth and spinogenesis in cultured hippocampal neurons and in brain slices. Some of these effects appear to be mediated by the down regulation of the miR132 target p250GAP, which, in turn, allows for Rac1-PAK-mediated spinogenesis. Interestingly, expression of methyl CpG�Cbinding protein 2 is also tightly regulated by miR132, and altered expression of MeCP2 has been shown to be an underlying element in the development of Rett syndrome, a neuro-developmental disorder in which dendritic development and synaptogenesis are affected. Thus, miR132 appears to be well-positioned to couple synaptic activity to neuronal structural/functional plasticity. To begin to address the potential role of miR132 in vivo, we developed a transgenic mouse strain that over-expresses miR132 in forebrain neurons. Morphometric analysis revealed a marked effect of transgenic miR132 on hippocampal neuronal morphology. Concordant with this, there was a decrease in MeCP2 expression in hippocampus. Furthermore, we show that these mice have impaired hippocampal-dependent object recognition memory. Collectively, these data reveal miR132 as a potent regulator of neuronal structure and CNS function.