Protein kinase C gamma interneurons in the rat medullary dorsal horn: Distribution and synaptic inputs to these neurons, and subcellular localization of the enzyme. Issue 2 (February 2014)
- Record Type:
- Journal Article
- Title:
- Protein kinase C gamma interneurons in the rat medullary dorsal horn: Distribution and synaptic inputs to these neurons, and subcellular localization of the enzyme. Issue 2 (February 2014)
- Main Title:
- Protein kinase C gamma interneurons in the rat medullary dorsal horn: Distribution and synaptic inputs to these neurons, and subcellular localization of the enzyme
- Authors:
- Peirs, Cédric
Patil, Sudarshan
Bouali‐Benazzouz, Rabia
Artola, Alain
Landry, Marc
Dallel, Radhouane - Abstract:
- <abstract abstract-type="main"> <title>ABSTRACT</title> <p>The γ isoform of protein kinase C (PKCγ), which is concentrated in interneurons in the inner part of lamina II (II<sub>i</sub>) of the dorsal horn, has been implicated in the expression of tactile allodynia. Lamina II<sub>i</sub> PKCγ interneurons were shown to be activated by tactile inputs and to participate in local circuits through which these inputs can reach lamina I, nociceptive output neurons. That such local circuits are gated by glycinergic inhibition and that A‐ and C‐fibers low threshold mechanoreceptors (LTMRs) terminate in lamina II<sub>i</sub> raise the general issue of synaptic inputs to lamina II<sub>i</sub> PKCγ interneurons. Combining light and electron microscopic immunochemistry in the rat spinal trigeminal nucleus, we show that PKCγ‐immunoreactivity is mostly restricted to interneurons in lamina II<sub>i</sub> of the medullary dorsal horn, where they constitute 1/3 of total neurons. The majority of synapses on PKCγ‐immunoreactive interneurons are asymmetric (likely excitatory). PKCγ‐immunoreactive interneurons appear to receive exclusively myelinated primary afferents in type II synaptic glomeruli. Neither large dense core vesicle terminals nor type I synaptic glomeruli, assumed to be the endings of unmyelinated nociceptive terminals, were found on these interneurons. Moreover, there is no vesicular glutamate transporter 3‐immunoreactive bouton, specific to C‐LTMRs, on PKCγ‐immunoreactive<abstract abstract-type="main"> <title>ABSTRACT</title> <p>The γ isoform of protein kinase C (PKCγ), which is concentrated in interneurons in the inner part of lamina II (II<sub>i</sub>) of the dorsal horn, has been implicated in the expression of tactile allodynia. Lamina II<sub>i</sub> PKCγ interneurons were shown to be activated by tactile inputs and to participate in local circuits through which these inputs can reach lamina I, nociceptive output neurons. That such local circuits are gated by glycinergic inhibition and that A‐ and C‐fibers low threshold mechanoreceptors (LTMRs) terminate in lamina II<sub>i</sub> raise the general issue of synaptic inputs to lamina II<sub>i</sub> PKCγ interneurons. Combining light and electron microscopic immunochemistry in the rat spinal trigeminal nucleus, we show that PKCγ‐immunoreactivity is mostly restricted to interneurons in lamina II<sub>i</sub> of the medullary dorsal horn, where they constitute 1/3 of total neurons. The majority of synapses on PKCγ‐immunoreactive interneurons are asymmetric (likely excitatory). PKCγ‐immunoreactive interneurons appear to receive exclusively myelinated primary afferents in type II synaptic glomeruli. Neither large dense core vesicle terminals nor type I synaptic glomeruli, assumed to be the endings of unmyelinated nociceptive terminals, were found on these interneurons. Moreover, there is no vesicular glutamate transporter 3‐immunoreactive bouton, specific to C‐LTMRs, on PKCγ‐immunoreactive interneurons. PKCγ‐immunoreactive interneurons contain GABA<sub>A</sub>ergic and glycinergic receptors. At the subcellular level, PKCγ‐immunoreactivity is mostly concentrated on plasma membranes, close to, but not within, postsynaptic densities. That only myelinated primary afferents were found to contact PKCγ‐immunoreactive interneurons suggests that myelinated, but not unmyelinated, LTMRs play a critical role in the expression of mechanical allodynia. J. Comp. Neurol. 522:393–413, 2014. © 2013 Wiley Periodicals, Inc.</p> </abstract> … (more)
- Is Part Of:
- Journal of comparative neurology. Volume 522:Issue 2(2014:Feb. 01)
- Journal:
- Journal of comparative neurology
- Issue:
- Volume 522:Issue 2(2014:Feb. 01)
- Issue Display:
- Volume 522, Issue 2 (2014)
- Year:
- 2014
- Volume:
- 522
- Issue:
- 2
- Issue Sort Value:
- 2014-0522-0002-0000
- Page Start:
- 393
- Page End:
- 413
- Publication Date:
- 2014-02
- Subjects:
- Comparative neurobiology -- Periodicals
Neurology -- Periodicals
616 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1096-9861 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/cne.23407 ↗
- Languages:
- English
- ISSNs:
- 0021-9967
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4962.000000
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 3599.xml