Late differentiation contributes to the apparent increase in sensory neuron number in juvenile rat

• Published in: Brain research. Developmental brain research 2003-08, Vol.144 (1), p.91-98
• Main Author: Farel, Paul B.
• Format: Article
• Language: English
• Subjects: Animals; Animals, Newborn; Axons - metabolism; Axons - ultrastructure; Bromodeoxyuridine - pharmacokinetics; Cell Count - methods; Dorsal root ganglion; Ganglia, Spinal - growth & development; Ganglia, Spinal - ultrastructure; Horseradish Peroxidase - pharmacokinetics; Immunohistochemistry - methods; In Vitro Techniques; Microscopy, Electron - methods; Neurofilament Proteins - metabolism; Neurons, Afferent - classification; Neurons, Afferent - physiology; Neurons, Afferent - ultrastructure; Postnatal differentiation; Radiation-Sensitizing Agents; Rat; Rats; Rats, Sprague-Dawley; Sural Nerve - growth & development; Sural Nerve - metabolism; Sural Nerve - ultrastructure; Time Factors; Tubulin - metabolism
• ISSN: 0165-3806
• DOI: 10.1016/S0165-3806(03)00163-9

Using both profile counts and unbiased stereological methods, estimates of neuron number in the lumbar dorsal root ganglia of the rat have been shown to increases approximately 35% during postnatal life [J. Comp. Neurol. 386 (1997) 8–15; J. Comp. Neurol. 449 (2002) 158–165]. The mechanism underlying this addition of neurons was investigated. No evidence of incorporation of (BrdU), a mitotic marker, was found. Similarly, counts of myelinated and unmyelinated axons in the sural nerve were the same in neonates and adults. These results are not consistent with the possibility that neurogenesis accounts for neuron addition. A population of neurons that stains with TuJ1, an antibody against neuronal class III β tubulin, but not with an antibody against the phosphorylated and non-phosphorylated forms of heavy chain neurofilament protein (NF-H) was found in neonates, but not adults. These less-differentiated (type-L) neurons are not detected by either profile counts or unbiased stereology and do not transport HRP retrogradely. Maturation of this pool of incompletely differentiated neurons appears to be one mechanism whereby neuron number is augmented during postnatal life.