Protein kinase C gamma interneurons in the rat medullary dorsal horn: Distribution and synaptic inputs to these neurons, and subcellular localization of the enzyme

Cédric Peirs, Sudarshan Patil, Rabia Bouali-Benazzouz, Alain Artola, Marc Landry, Radhouane Dallel
J. Comp. Neurol.. 2013-12-06; 522(2): 393-413
DOI: 10.1002/cne.23407

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1. J Comp Neurol. 2014 Feb 1;522(2):393-413. doi: 10.1002/cne.23407.

Protein kinase C gamma interneurons in the rat medullary dorsal horn:
distribution and synaptic inputs to these neurons, and subcellular localization
of the enzyme.

Peirs C(1), Patil S, Bouali-Benazzouz R, Artola A, Landry M, Dallel R.

Author information:
(1)Inserm/UdA U1107, Neuro-Dol: Trigeminal Pain and Migraine, Université
d’Auvergne, Faculté de Chirurgie Dentaire, Clermont-Ferrand, 63000, France.

The γ isoform of protein kinase C (PKCγ), which is concentrated in interneurons
in the inner part of lamina II (IIi ) of the dorsal horn, has been implicated in
the expression of tactile allodynia. Lamina IIi 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 IIi raise the general
issue of synaptic inputs to lamina IIi 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
IIi 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 GABAA 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.

Copyright © 2013 Wiley Periodicals, Inc.

DOI: 10.1002/cne.23407
PMID: 23818225 [Indexed for MEDLINE]

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