| First Author | Jacus MO | Year | 2012 |
| Journal | J Neurosci | Volume | 32 |
| Issue | 27 | Pages | 9374-82 |
| PubMed ID | 22764245 | Mgi Jnum | J:185954 |
| Mgi Id | MGI:5430671 | Doi | 10.1523/JNEUROSCI.0068-12.2012 |
| Citation | Jacus MO, et al. (2012) Presynaptic CaV3.2 Channels Regulate Excitatory Neurotransmission in Nociceptive Dorsal Horn Neurons. J Neurosci 32(27):9374-82 |
| abstractText | It is generally accepted that presynaptic transmitter release is mainly regulated by subtypes of neuronal high-voltage-activated Ca(2+) channels. Here for the first time, we examined the role of T-type Ca(2+) channels (T-channels) in synaptic transmission in the dorsal horn (DH) of the spinal cord using patch-clamp recordings from acute spinal cord preparations from both rat and mouse. We found that selective pharmacological antagonism of T-channels inhibited spontaneous synaptic release of glutamate in superficial laminae I-II of the DH, while GABA release was spared. We found similar effect in identified nociceptive projection neurons of lamina I of the DH, but not in inhibitory DH interneurons. In comparison, antagonism of T-channels did not affect excitatory transmission in deeper non-nociceptive DH laminae. Furthermore, we used isoform-specific agents, knock-out mice and immunohistochemistry to specifically implicate presynaptic Ca(V)3.2 channels. We also used an animal model of painful diabetic neuropathy to demonstrate that blocking T-channels in superficial DH neurons suppressed spontaneous excitatory synaptic transmission in diabetic rats in greater degree than in healthy age-matched animals. These studies provide previously unknown information regarding the role of presynaptic T-channels in nociceptive signaling in the spinal cord. |
