Glutamate and aspartate immunoreactivity in dorsal root ganglion cells supplying visceral and somatic targets and evidence for peripheral axonal transport.
Glutamate (Glu) is released by primary sensory neurons at their central synapses, although immunohistochemical studies have shown that only a proportion of these cell bodies are Glu-immunoreactive. Antisera raised against Glu or aspartate (Asp) were used to investigate whether neurons that store high levels of these substances have a unique neuropeptide content or target projection. In male rats, many lumbar and sacral dorsal root ganglion cells and their associated glia show high levels of Glu or Asp immunoreactivity, and fewer than half of these also express substance P or calcitonin gene-related peptide. Conversely, only a minority of peptide-containing neurons store high levels of excitatory amino acids. When neurons that were labelled retrogradely from somatic (skin, gastrocnemius muscle) or visceral (bladder, rectum) targets were immunostained for peptides or amino acids, there was some variation in the peptide expression of their sensory nerve supply, but there was very little or no difference in the prevalence of Glu- or Asp-immunoreactive neurons. In vitro studies on isolated lumbar dorsal root ganglia showed that, after crushing nerve roots, Glu and Asp were transported in both central and peripheral directions, similar to substance P. These studies showed that primary afferent neurons store different levels of Glu and Asp in their somata but that this is not correlated with their target tissue or peptide content. This suggests that both visceral and somatic sensory neurons may vary considerably in the way they release, store, or metabolise amino acids. Peripheral and central transport of amino acids suggests that, in some neurons, reuptake at the synapse may need to be supplemented by amino acids that are produced or accumulated in the soma.
Department of Physiology and Pharmacology, University of Queensland, Brisbane, Queensland 4072, Australia. j.keast@unsw.edu.au
J R
JR
Keast
T M
TM
Stephensen
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism*; D001370:Axonal Transport / Q000502:physiology*; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D005727:Ganglia, Spinal / Q000166:cytology / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism*; D008297:Male; D018482:Muscle, Skeletal / Q000166:cytology / Q000294:innervation / Q000378:metabolism; D009475:Neurons, Afferent / Q000166:cytology / Q000378:metabolism*; D010525:Peripheral Nerves / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012867:Skin / Q000166:cytology / Q000294:innervation / Q000378:metabolism; D013373:Substance P / Q000378:metabolism; D014781:Viscera / Q000166:cytology / Q000294:innervation / Q000378:metabolism
D001224:Aspartic Acid; D013373:Substance P; D018698:Glutamic Acid; D015740:Calcitonin Gene-Related Peptide