The final step in this cascade is the activation of adenosine A(1

The final step in this cascade is the activation of adenosine A(1) receptors which results in protein kinase A- and phosphoinositide 3-kinase-mediated opening of potassium and chloride channels. EPO receptor protein was immunohistochemically localized to VX-661 in vivo the inner retina and photoreceptor inner segments. In isolated glial cells, EPO receptor protein is selectively localized to fibers which traverse the inner nuclear layer in situ. Inhibition of glial

swelling might contribute to the neuroprotective action of EPO in the retina under pathological conditions. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Dopamine (DA) neurons in the ventral tegmental area (VTA) constitute the origin of major dopaminergic neural pathways associated with essential functions including reward, motivation and cognition. Hence, regulation of VTA DA neurons’ excitability is of important significance. Like other neurons, the activity level of VTA DA neurons is considerably determined by excitatory and inhibitory

synaptic inputs. Here we show that DA itself, the most available modulator in the VTA, causes an inhibition of GABA receptor type A (GABA(A)R)-mediated evoked-IPSC (eIPSC) recorded from rat VTA DA neurons. The DA-induced inhibition was accomplished by activation of DA receptors, known to inhibit adenylyl cyclase p38 MAPK inhibitor activity (D2-like receptors), and was absent when these receptors were blocked. Moreover, blocking of either GABA receptor type B (GABA(B)R) or G-protein coupled inwardly-rectifying potassium (GIRK) channels was also Tanespimycin price found to effectively prevent the DA-induced inhibition of GABA(A)R

eIPSC. In addition, we found that DA changes the values of both paired-pulse ratio (PPR) and coefficient of variation (CV) of GABA(A)R eIPSC amplitude, similar to the changes obtained by lowering the extracellular calcium concentration. Taken together, we propose that activation of D2-like receptors and GABA(B)R in the VTA enhances presynaptic GIRK channels activity, which in turn leads to reduced GABA release. The consequence of reduced GABA release on VTA DA neurons may contribute to their increased activity. Accordingly, a novel potential regulatory form of VTA DA neurons’ excitability, which involves presynaptic potassium channels, is proposed. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Long-term morphological synaptic changes associated with homosynaptic long-term potentiation (LTP) and heterosynaptic long-term depression (LTD) in vivo, in awake adult rats were analyzed using three-dimensional (3-D) reconstructions of electron microscope images of ultrathin serial sections from the molecular layer of the dentate gyrus.

Comments are closed.