Skip to main content
. 2013 Jan 16;304(8):C693–C714. doi: 10.1152/ajpcell.00350.2012

Fig. 5.

Fig. 5.

Nociception phenotype in NKCC1 knockout mice. A: model of sensory circuitry in the spinal cord. Nociceptive signals are carried by unmyelinated (C) and thinly myelinated (Aδ) afferent fibers that synapse onto spinal cord lamina I and II neurons. Interneurons (orange), which are activated by projection neurons in deeper spinal cord layers, release GABA at the terminals of the C and Aδ fibers. Because the Cl concentration is high in these afferent neurons, GABA produces a depolarization of the nerve terminal and inhibition of incoming pain signals from the periphery. B: withdrawal latencies for hot plate and tail flick assays in wild-type, heterozygous, and homozygous NKCC1 knockout mice. Both tests were performed at 52°C. Data represent means ± SE. *Significant difference with P < 0.05. Hot plate and tail flick data were taken from references 136 and 74, respectively.