Prevention of galanin upregulation following neonatal infraorbital nerve transection or attenuation of axoplasmic transport does not rescue central vibrissae-related patterns in the rat.
Neonatal transection of, or blockade of axoplasmic transport in, the infraorbital nerve [ION, the trigeminal (V) branch that supplies the mystacial vibrissae follicles] results in a loss of all central patterns corresponding to the vibrissae follicles in the brainstem, thalamus and cortex except for those of the central terminal arbors of ION primary afferents that survive this lesion. Both of these manipulations also result in a rapid and dramatic upregulation of at least two peptides, galanin and neuropeptide Y, in surviving vibrissae-related primary afferents. Galanin is of particular interest, because this peptide has effects on neuronal activity and growth, both factors which may be involved in the disappearance of central vibrissae-related patterns in rats that have sustained neonatal ION transection or axoplasmic transport blockade. The present study used antisense technology to determine whether the upregulation of galanin in the central terminals of ION primary afferents is necessary for the loss of central vibrissae-related patterns in rats. Newborn rats had their left ION transected or axoplasmic transport in this nerve blocked by application of a vinblastine-impregnated implant, and at the same time received an injection of commercially synthesized phosphorothioate oligodeoxynucleotide sequences (15-20 bases) directly into the V ganglion in order to block galanin upregulation. These injections effectively prevented the upregulation of this peptide which is normally associated with ION transection or axoplasmic transport blockade. Preventing galanin upregulation, however, did not prevent or attenuate the loss of central vibrissae-related patterns in the brainstem or cortex normally observed following ION transection or axoplasmic transport blockade in this nerve. These results are thus consistent with the conclusion that the upregulation of galanin in the central terminals of V primary afferents, observed after damage to or attenuation of axoplasmic transport in the ION, is not necessary for the reorganization that results in a disappearance of central vibrissae-related patterns in the V neuraxis.
Chiaia
N L
NL
Department of Anatomy and Neurobiology, Medical College of Ohio, PO Box 10008, Toledo, OH 43614-5804, USA. nchiaia@mco.edu
Shah
A
A
Crissman
R S
RS
Rhoades
R W
RW
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001370:Axonal Transport / Q000502:physiology*; D001921:Brain / Q000502:physiology*; D001933:Brain Stem / Q000201:enzymology; D003714:Denervation; D003576:Electron Transport Complex IV / Q000378:metabolism; D019004:Galanin / Q000235:genetics / Q000378:metabolism*; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D009915:Orbit / Q000294:innervation*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012701:Serotonin / Q000378:metabolism; D014276:Trigeminal Nerve / Q000187:drug effects / Q000502:physiology*; D015854:Up-Regulation; D014738:Vibrissae / Q000502:physiology*; D014747:Vinblastine / Q000494:pharmacology
D016376:Oligonucleotides, Antisense; D012701:Serotonin; D014747:Vinblastine; D019004:Galanin; D003576:Electron Transport Complex IV