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• W1975571417 abstract "It is generally accepted that presynaptic transmitter release is mainly regulated by subtypes of neuronal high-voltage-activated Ca²⁺ channels. Here for the first time, we examined the role of T-type Ca²⁺ 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_V3.2 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." @default.
• W1975571417 created "2016-06-24" @default.
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• W1975571417 date "2012-07-04" @default.
• W1975571417 modified "2023-10-18" @default.
• W1975571417 title "Presynaptic CaV3.2 Channels Regulate Excitatory Neurotransmission in Nociceptive Dorsal Horn Neurons" @default.
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• W1975571417 doi "https://doi.org/10.1523/jneurosci.0068-12.2012" @default.
• W1975571417 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3398424" @default.
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