Characteristics, Emergent Properties and Functions of Somato-dendritic T- and L-Type Calcium Channels.

The primary literature, as an adjunct to textbooks, lectures, problem sets, and laboratories, has become integral to most undergraduate neuroscience courses by extending learning to topics outside the scope of introductory textbooks, providing insight into experimental methods and design, and offering a platform for critical thinking, independent learning, and student presentations. While introductory and intermediate textbooks cover "Hodgkin-Huxley" (H-H) Na and K channels thoroughly, the characteristics of diverse calcium, chloride, and other sodium and potassium channels, and especially the resulting emergent cellular properties and their functional consequences, receive far less coverage. The specific aim of this report is to identify, summarize, and pedagogically evaluate six articles that describe the biophysical channel properties, resulting cellular emergent properties, and potential functions of two types of somato-dendritic calcium channels: type T- and L- type channels. The three-tier vertical organization (channel, emergence, function) across multiple channels (T-, L-type) will help students connect information across parallel and hierarchical levels of analysis.

TNF-α/TNFR1 signaling is required for the development and function of primary nociceptors.

Primary nociceptors relay painful touch information from the periphery to the spinal cord. Although it is established that signals generated by receptor tyrosine kinases TrkA and Ret coordinate the development of distinct nociceptive circuits, mechanisms modulating TrkA or Ret pathways in developing nociceptors are unknown. We have identified tumor necrosis factor (TNF) receptor 1 (TNFR1) as a critical modifier of TrkA and Ret signaling in peptidergic and nonpeptidergic nociceptors. Specifically, TrkA+ peptidergic nociceptors require TNF-α-TNFR1 forward signaling to suppress nerve growth factor (NGF)-mediated neurite growth, survival, excitability, and differentiation. Conversely, TNFR1-TNF-α reverse signaling augments the neurite growth and excitability of Ret+ nonpeptidergic nociceptors. The developmental and functional nociceptive defects associated with loss of TNFR1 signaling manifest behaviorally as lower pain thresholds caused by increased sensitivity to NGF. Thus, TNFR1 exerts a dual role in nociceptor information processing by suppressing TrkA and enhancing Ret signaling in peptidergic and nonpeptidergic nociceptors, respectively.