TY - JOUR
T1 - Age‐dependent cell death in the olfactory cortex
T2 - Lack of transneuronal degeneration in neonates
AU - Friedman, B.
AU - Price, Joseph L.
PY - 1986/4/1
Y1 - 1986/4/1
N2 - Adult olfactory cortical neurons in layer IIa undergo fulminant transneuronal degeneration after removal of afferent olfactory bulb fibers (Price, '76, Neurosci Abst. 2:161; Heimer and Kalil, '78, J. Comp. Neurol 178:559‐609). This provides an unusual example of dependence of a mature population of neurons on axonal input. In order to investigate whether similar transneuronal degeneration occurs in immature animals, a series of rats were subjected to unilateral olfactory bulb removal at various ages during the first 3 postnatal weeks. The brains were examined for degeneration after short survivals by use of the de Olmos cupric silver method, which selectively stains degenerating neurons. In addition, animals with long survivals were examined with the HRP retrograde tracing method, in order to determine if cells that survive the acute effects of deafferentation develop normal patterns of connections. Young neurons are more resistant to the effects of olfactory bulb removal than more mature neurons. There was little degeneration of cortical neurons after bulb ablation during the first 2 postnatal, weeks. Although layer IIa does not become distinct from layer IIb in, these experimental animals, cells that have connections normally characteristic of the cells of layer IIa, and are situated at the superficial edge of layer II, were identified with the HRP method. The severity of transneuronal degeneration increases and becomes adultlike between the second and third postnatal weeks. This increase in transneuronal degeneration is temporally associated with a progressive reduction in axonal sprouting following deafferentation during the first 3 postnatal weeks, as described in the companion paper (Friedman and Price, '86). Thus, axon sprouting may “protect” the immature IIa neurons from the effects of removal of the fibers from the olfactory bulb. A period of normal cell death has also been identified in olfactory cortex by the use of the de Olmos cupric silver method. This cellular degeneration is much less severe and has a different time course and laminar distribution than the transneuronal degeneration produced by olfactory bulb ablation in adults. Although normal cell death appears to be potentiated by removal of the olfactory bulb on postnatal day 1, it is clearly a different process from the transneuronal reaction.
AB - Adult olfactory cortical neurons in layer IIa undergo fulminant transneuronal degeneration after removal of afferent olfactory bulb fibers (Price, '76, Neurosci Abst. 2:161; Heimer and Kalil, '78, J. Comp. Neurol 178:559‐609). This provides an unusual example of dependence of a mature population of neurons on axonal input. In order to investigate whether similar transneuronal degeneration occurs in immature animals, a series of rats were subjected to unilateral olfactory bulb removal at various ages during the first 3 postnatal weeks. The brains were examined for degeneration after short survivals by use of the de Olmos cupric silver method, which selectively stains degenerating neurons. In addition, animals with long survivals were examined with the HRP retrograde tracing method, in order to determine if cells that survive the acute effects of deafferentation develop normal patterns of connections. Young neurons are more resistant to the effects of olfactory bulb removal than more mature neurons. There was little degeneration of cortical neurons after bulb ablation during the first 2 postnatal, weeks. Although layer IIa does not become distinct from layer IIb in, these experimental animals, cells that have connections normally characteristic of the cells of layer IIa, and are situated at the superficial edge of layer II, were identified with the HRP method. The severity of transneuronal degeneration increases and becomes adultlike between the second and third postnatal weeks. This increase in transneuronal degeneration is temporally associated with a progressive reduction in axonal sprouting following deafferentation during the first 3 postnatal weeks, as described in the companion paper (Friedman and Price, '86). Thus, axon sprouting may “protect” the immature IIa neurons from the effects of removal of the fibers from the olfactory bulb. A period of normal cell death has also been identified in olfactory cortex by the use of the de Olmos cupric silver method. This cellular degeneration is much less severe and has a different time course and laminar distribution than the transneuronal degeneration produced by olfactory bulb ablation in adults. Although normal cell death appears to be potentiated by removal of the olfactory bulb on postnatal day 1, it is clearly a different process from the transneuronal reaction.
KW - cortical lamination
KW - deafferentation
KW - development
KW - olfactory system
KW - rat
UR - http://www.scopus.com/inward/record.url?scp=0022701912&partnerID=8YFLogxK
U2 - 10.1002/cne.902460103
DO - 10.1002/cne.902460103
M3 - Article
C2 - 3700716
AN - SCOPUS:0022701912
SN - 0021-9967
VL - 246
SP - 20
EP - 31
JO - Journal of Comparative Neurology
JF - Journal of Comparative Neurology
IS - 1
ER -