Distribution of glycine-immunoreactive profiles in the monkey spinal cord: A light microscopic and ultrastructural study

Abstract

The present study analyzed the relationships of glycine (GLY)-immunoreactive (-IR) and unlabeled profiles in the primate spinal cord. Light microscopic analysis demonstrated GLY-IR profiles in laminae III-VII, with fewer labeled profiles in laminae I, II, VIII, IX and X. The dorsal part of the lateral funiculus and the dorsal funiculus contained few labeled axons, in contrast to all other areas of white matter, which were heavily labeled. At the electron microscopic level, GLY-IR terminals in monkeys contained mainly round, with occasional pleomorphic, clear vesicles; however, F-type GLY-IR terminals synapsing on motoneurons contained pleomorphic vesicles. This seems to be an important species difference because vesicles in GLY-IR terminals in rat and cat are predominantly oval or elliptical. GLY-IR terminals synapsed on unlabeled as well as GLY-IR cell bodies and dendrites. This is morphological evidence that GLY may be both an inhibitor (GLY-IR terminals synapse on and presumably inhibit non-GLY cell bodies and dendrites) and a disinhibitor (GLY-IR terminals synapse on and presumably inhibit other GLY elements) of spinal activity. Also noteworthy was the conspicuous absence of axoaxonic interactions involving GLY-IR terminals. A related finding was that GLY profiles were always postsynaptic, never presynaptic, to glomerular primary afferent terminals. The functional implications would seem to be that primary afferent input can activate the spinal GLY system but that there is little GLY presynaptic control of afferent input in monkeys. This is in contrast to rats and cats, in which axoaxonic interactions involving GLY-IR terminals have been observed and where it is common to find GLY-IR terminals presynaptic to glomerular primary afferent terminals.

Neurotransmitter signaling in white matter

“…High concentrations of neurotransmitter such as GABA and glycine are also present in a sub-population of mature WM axons in several species (Carlton et al, 1996;Davanger et al, 1991;Rogers and Pow, 1995;Todd and Sullivan, 1990;van den Pol and Gorcs, 1988;Wilson et al, 1996). Block of GABA uptake mimics the effects of GABA upon axon conduction in the neonatal rat optic nerve (Sakatani et al, 1991), while block of catecholamine uptake mimics the effect of nor-adrenaline (Nikolaeva et al, 2009); observations consistent with tonic operation of functional neurotransmitter uptake in the tissue.…”

“…GABA is localized in neonatal rat optic nerve glia, with expression down-regulated with maturation (Ochi et al, 1993;Sakatani et al, 1992), although this may be due to increased rates of GABA degradation since numerous GABA1 WM astrocytes are apparent in adult rat following inhibition of the catabolic enzyme GABA-alpha-ketoglutaric acid aminotransferase (Bull and Blomqvist, 1991). High concentrations of neurotransmitter such as GABA and glycine are also present in a sub-population of mature WM axons in several species (Carlton et al, 1996;Davanger et al, 1991;Rogers and Pow, 1995;Todd and Sullivan, 1990;van den Pol and Gorcs, 1988;Wilson et al, 1996).…”

Synaptic relationships between hair follicle afferents and neurones expressing GABA and glycine‐like immunoreactivity in the spinal cord of the rat

“…Afferent terminals may therefore act directly on GABAergic interneurones mediating PAD (Zou et al, 2001). GABA‐like immunoreactivity (albeit often rather weak) has frequently been reported in dendrites postsynaptic to the central terminals of glomeruli in laminae I and II (Carlton and Hayes, 1990; Todd and Lochhead, 1990; Carlton et al, 1996; Todd, 1996) and to intracellularly labelled C and Aδ fibres (Alvarez et al, 1992, 1993; Bernardi et al, 1995). Only rarely did we see this in dendrites postsynaptic to hair follicle afferents, and immunoreactivity for GABA has not been reported by other immunohistochemical studies of physiologically identified Aα or Aβ fibres such as hair follicle afferents (Maxwell and Noble, 1987), type Ia or type II muscle spindle afferents (Maxwell et al, 1990; Maxwell and Riddell, 1999; Watson and Bazzaz, 2001), slowly adapting periodontal afferents (Bae et al, 1997), or for terminals of large‐diameter myelinated afferents labelled by retrograde transport of Cholera toxin B (Bae et al, 2000).…”

Glycine, glycine receptor subunit and glycine transporters in the rat parabrachial and Kölliker-Fuse nuclei

“…The PBil receives afferents predominantly from the spinal cord, in particular from the lateral reticulated area and the lateral spinal nucleus (Feil and Herbert 1995). However, these spinal areas apparently contain no glycinergic neurons (Todd and Sullivan 1990;Carlton et al 1996). The possibility remains that the glycinergic input to the PBil originates laterally in the medullary reticular formation that has recently been shown to project also to the PBil (Feil and Herbert 1996) and that contains glycinergic neurons in abundance (Rampon et al 1996).…”