Spinal axonal injury transiently elevates the level of metabotropic glutamate receptor 5, but not 1, in cord-projection central neurons.
In investigating the effect of spinal injury on cord-projection central neurons, we found that rat rubrospinal neurons retained glutamatergic afferents and, in general, ionotropic glutamate receptor expression following spinal axotomy. Since glutamate also acts on second-messenger-coupled metabotropic receptors, the expression of group I metabotropic glutamate receptors, mGluR1 and mGluR5, was examined following similar treatment. mGluR1 expression began to decline in the perikarya 2 days postlesion and a day later in the neuropil. The decline slowed down by the fifth day and recovered in both the perikarya and neuropil 1 week postlesion. However, expression in both the perikarya and neuropil declined again and persisted up to 2 years postlesion. Similarly, the mGluR5 displayed an early transient decrease and returned to normal levels by 7 days post-lesion. However, rather than progressing to a secondary decline, the expression of mGluR5 increased to levels dramatically higher than those of control nuclei at 2-4 weeks postlesion, subsiding again by 8 weeks, and remaining low up to 2 years postinjury. Although mGluR5 has been shown to save cultured neurons from excitotoxic cell death, its elevated expression in the present model corresponds in time to an increased input/output relationship and excitability of the injured neurons as well as a period of maximal somatic shrinkage and cell loss. In addition to the cell bodies and dendrites, axon-like profiles also contain mGluR1. Their decrease following rubrospinal axotomy suggests that axonal injury may also compromise the presynaptic regulation of afferent activities onto injured cord-projection central neurons.
Wang
Yueh-Jan
YJ
Department of Anatomy, College of Medicine, Tzu-Chi University, Taiwan. chris@mail.tcu.edu.tw
Tseng
Guo-Fang
GF
D000818:Animals; D001369:Axons / Q000378:metabolism / Q000648:ultrastructure; D004195:Disease Models, Animal; D004525:Efferent Pathways / Q000293:injuries* / Q000503:physiopathology; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism; D007150:Immunohistochemistry; D009498:Neurotoxins / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000502:physiology; D064529:Receptor, Metabotropic Glutamate 5; D018094:Receptors, Metabotropic Glutamate / Q000378:metabolism*; D012012:Red Nucleus / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D012183:Retrograde Degeneration / Q000378:metabolism* / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009435:Synaptic Transmission / Q000502:physiology; D015854:Up-Regulation / Q000502:physiology
C578937:Grm5 protein, rat; D009498:Neurotoxins; D064529:Receptor, Metabotropic Glutamate 5; D018094:Receptors, Metabotropic Glutamate; C104077:metabotropic glutamate receptor type 1; D018698:Glutamic Acid