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Tests of the regenerative capacity of tectal efferent axons in the frog, Rana pipiens
Author(s) -
Lyon Michael J.,
Stelzner Dennis J.
Publication year - 1987
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.902550404
Subject(s) - axoplasmic transport , tectum , biology , optic nerve , anatomy , diencephalon , efferent , brainstem , wheat germ agglutinin , rana , optic tract , optic chiasm , retrograde tracing , posterior commissure , midbrain , axon , nucleus , neuroscience , central nervous system , afferent , dorsum , lectin , biochemistry
Experiments were designed to determine if neurons of the ranid optic tectum, a major target of the optic nerve, possess the same regenerative potential as optic axons. Normal tectal efferent (TE) projections were reexamined by using the anterograde transport of 3 H‐proline and autoradiography (n = 18), bulk‐filling damaged TE axons with horseradish peroxidase (HRP; n = 18) and anterogradely transporting wheat germ agglutinin‐HRP (n = 8) to label TE axons. Results were similar to reports that used degeneration methods (Rubinson: Brain Behav. Evol. 1 :529–561, '68; Lazar: Acta. Biol. Hung. 20 :171–183, '69). Following a brainstem hemisection just caudal to the nucleus isthmi (1–20 weeks), the ipsilateral descending TE pathway was autoradiographically examined (n = 20). While all other TE projections appeared normal, there was no detectable ipsilateral descending projection beyond the lesion site. Ascending TE axons were cut at the anterior tectal border by hemisecting the left diencephalon (LDH)–a lesion that also cuts optic axons projecting to the left tectum. There was no indication of TE axonal regeneration with the aid of autoradiography or HRP histochemistry 1–30 weeks postlesion (n = 48) even when the medial diencephalon was intentionally left intact (n = 4). However, in all four cases examined, optic axons regenerated following the same LDH where TE axonal regeneration failed (also see Stelzner, Lyon, and Strauss: Anat. Rec. 205 :191A–192A, '83). Local effects of LDH should be similar for both the cut optic and cut TE axons. Other factors were tested that may contribute to the lack of TE axonal regeneration. Our results indicate that optic regeneration itself (n = 8), postaxotomy retrograde cell death of TE neurons (n = 6), deafferentation of the tectum of optic axons, and potential sprouting within tectal targets by intact contralateral TE axons (n = 10) are not critical factors aborting TE axonal regeneration. TE axons filled with HRP at chronic periods after LDH (n = 4) terminate anomalously near the LDH border. Many of these endings are similar to reactive endings or terminal clubs seen after axonal injury in the mammalian CNS. Our results suggest that this disparity in regenerative ability of optic and TE axons may be related to a difference in the responsive ability of these cell types to initiate or maintain axonal elongation after axotomy within the amphibian CNS environment.