In a recent issue of The Journal of Physiology, David Ritter (JCGS3, Covarrubias Lab) and colleagues reported the molecular and ionic bases of a mechanism that regulates the shape of the action potential in pain-sensing neurons. Previously, the Covarrubias lab showed that inactivation of the voltage-gated potassium channel Kv3.4 is eliminated by protein kinase C (PKC)-dependent phosphorylation in heterologous expression systems. David’s work shows that Kv3.4 channels are present in pain-sensing neurons and undergo modulation by PKC activation via endogenous G-protein coupled receptors. Furthermore, the study shows that Kv3.4 channels regulate the duration of the action potential in a manner that depends on the channel’s phosphorylation status. This work begins to shed light on the neurophysiological roles of Kv3.4 channels, which are down-regulated in chronic pain models.
Read more: http://jp.physoc.org/content/590/1/145.abstract
Celestine Wanjalla ( JMC3, Schnell Lab), in a recent publication in Virology, analyzed the impact of the pro-inflammatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) co-expressed with HIV-1 Gag by a recombinant rabies virus on the adaptive immune responses. Celestine was able to show a significant increase in antigen presenting cells (APCs) in response to GM-CSF expression. However, despite the increase in APCs, the primary and memory anti-HIV-1 CD8+ T cell response was significantly lower compared to controls not expressing the cytokine. The results indicate that this was likely due to lower levels of proliferation of CD8+ T cell. Animals treated with GM-CSF neutralizing antibodies restored the CD8+ T cell response. These data indicate an important role of CM-CSF in the regulation of the CD8+ and has implications in the use of GM-CSF as a molecular adjuvant in vaccine development.
Read more: Virology, In Press