Summary: Below is an exercise designed for (1) introducing students to reading scientific papers & (2) providing relevance of intro neurobiology to clinical research/work. The exercise questions themselves will not make much sense unless you have access to the figures in the journal article referenced.

The material in a .docx format: Discussion_5_Paper_Questions

Paper Title: “An SCN9A channelopathy causes congenital inability to experience pain” Cox, 2006.

Purpose: The goal of this exercise is to (1) introduce students to the structure of scientific papers & (2) evidence of neurobiological research that is relevant to material they have just learned about regarding the electrophysiology of neurons and its clinical impact.
Activity 1: Discuss the structure and purpose of the sections in the paper.The structure of this paper is organized into:

  1. Abstract
  2. Introduction
  3. Results
  4. Discussion/Conclusion
  5. Methods
  6. Supplemental Data
An overview of Nav1.7:
SCN9a encodes the alpha subunit of the Nav1.7 voltage-gated Na+ channel. Together with SCN1b & SCN2b, these create a functional Nav1.7 channel. Nav1.7 is expressed in 2 tissues, nociceptive DRG neurons and sympathetic ganglion neurons. For the detection of pain, the nociceptive DRG neurons are essential.
The Nav1.7 gene functions as an “amplifier” of nociception. Nociception is the detection/perception of pain, and is activated by nociceptors in nerve fibers. Nociceptors are a type of sensory receptor which responds to pain. In response to pain, nociceptors produce “generator potentials.” In this case, they are small voltage depolarizations across the neuronal membrane in DRG neurons. When there are small depolarizations from nociceptors, the Nav1.7 channel amplifies the initial generator potential, further depolarizing the neuron. If enough depolarization is reached, an AP is initiated. To clarify, the Nav1.7 does not detect the painful stimuli, it amplifies the initial detection, thus an “amplifier.”
Activity 2: Questions are included in the .docx file above.