Lack of sprouting and its presence after lesions of the cat spinal cord

Degeneration methods were used to study the dorsal root and descending projections after chronic partial denervation of adult cat spinal cord. Conventional mapping methods were used, supplemented in some cases by densitometric measurements of the amounts of degeneration present. The amount of shrinkage of spinal gray matter in some sections was estimated by planimetric measurement. Two preparations were used: (1) partial unilateral rhizotomy in which all dorsal roots caudal to T4 were cut except L6 (spared root preparation); (2) complete unilateral deafferentation. The projection of L6 dorsal roots was examined in spared root preparations. T13 dorsal root projections were examined in deafferented preparations in which T13 was the lowest remaining root. The projection of descending systems was mapped in spared root and deafferented preparations. The spared root displayed an increased projection in the lateral portion of the dorsal horn, in the zona intermedia, Clarke's nucleus and in the base and reticular zone of nucleus gracilis. The lowest remaining root (T13) increased its projection to laminae VII and VIII and to the base and reticular zone of nucleus gracilis. In all cases, when an increased projection resulted from prior denervation, the increase never exceeded the boundaries of the normal projection. No sprouting was observed in those regions with the strictest topographical organization, the cell nests of nucleus gracilis or lamina IX of the spinal cord, even though these regions were partially denervated by the chronic lesions. Descending projections were increased on the experimental side of deafferented preparations12 but not of spared root preparations, suggesting that the presence of the spared root may prevent sprouting by descending systems. Because measurements of gray matter indicated that maximal sprouting occurred in segments showing least shrinkage (sprouting of L6 spared root into L6 segment), in this case shrinkage cannot account for the increased density of degeneration. These results suggest that certain conditions are important for the regulation of sprouting in the adult CNS. Firstly, sprouting is limited by a requirement for proximity and/or overlap. Secondly, the strictness of topographical localization within a particular region may limit the likelihood of sprouting into that region. Finally, a competitive or hierarchical relationship among the remaining systems may modify the capacity of a particular system to sprout.

[1]  F. W. Kerr The potential of cervical primary afferents to sprout in the spinal nucleus of V following long term trigeminal denervation. , 1972, Brain research.

[2]  G Raisman,et al.  Neuronal plasticity in the septal nuclei of the adult rat. , 1969, Brain research.

[3]  E. Perl,et al.  Distribution of primary afferent fibers within the sacrococcygeal dorsal horn: An autoradiographic study , 1979, The Journal of comparative neurology.

[4]  O. Steward,et al.  Behavioral correlates of denervation and reinnervation of the hippocampal formation of the rat: Recovery of alternation performance following unilateral entorhinal cortex lesions , 1977, Brain Research Bulletin.

[5]  M. Goldberger,et al.  Restitution of function and collateral sprouting in the cat spinal cord: The deafferented animal , 1974, The Journal of comparative neurology.

[6]  M. Goldberger,et al.  Spinal neurons mediate return of substance P following deafferentation of cat spinal cord , 1981, Brain Research.

[7]  J. Sprague,et al.  THE TERMINAL FIELDS OF DORSAL ROOT FIBERS IN THE LUMBOSACRAL SPINAL CORD OF THE CAT, AND THE DENDRITIC ORGANIZATION OF THE MOTOR NUCLEI. , 1964, Progress in brain research.

[8]  R W Guillery,et al.  Experiments to determine whether retinogeniculate axons can form translaminar collateral sprouts in the dorsal lateral geniculate nucleus of the cat , 1972, The Journal of comparative neurology.

[9]  M. E. Goldberger Locomotor recovery after unilateral hindlimb deafferentation in cats , 1977, Brain Research.

[10]  Marion Murray,et al.  Recovery of substance P in the cat spinal cord after unilateral lumbosacral deafferentation , 1980, Brain Research.

[11]  G. Lynch,et al.  The Hippocampus as a Model for Studying Anatomical Plasticity in the Adult Brain , 1975 .

[12]  C. D'amato,et al.  Motor-sensory and visual behavior after hemispherectomy in newborn and mature rats. , 1970, Experimental neurology.

[13]  L. Pubols,et al.  Recovery of function in dorsal horn following partial deafferentation. , 1980, Journal of neurophysiology.

[14]  M. Murray,et al.  Restitution of function and collateral sprouting in the cat spinal cord: The partially hemisected animal , 1974, The Journal of comparative neurology.

[15]  G. Macchi,et al.  Distribution of dorsal root fibers in the medulla oblongata of the cat , 1968, The Journal of comparative neurology.

[16]  D. Ganchrow,et al.  Relationship of afferentation with soma size of nucleus gracilis neurons after bilateral dorsal column lesion in the rat , 1981, Experimental Neurology.

[17]  J. A. Horel,et al.  Sprouting of optic tract projections in the brain stem of the rat , 1966, The Journal of comparative neurology.

[18]  Carl W. Cotman,et al.  Selective reinnervation of hippocampal area CA1 and the fascia dentata after destruction of CA3-CA4 afferents with kainic acid , 1980, Brain Research.

[19]  R. Lund,et al.  Anomalous bilateral corticofugal pathways in albino rats after neonatal lesions. , 1973, Brain research.

[20]  D. Stelzner,et al.  A comparison of the effect of mid-thoracic spinal hemisection in the neonatal or weanling rat on the distribution and density of dorsal root axons in the lumbosacral spinal cord of the adult , 1979, Brain Research.

[21]  G. Raisman,et al.  Quantitative electron microscopic evidence for reinnervation in the adult rat interpeduncular nucleus after lesions of the fasciculus retroflexus , 1979, The Journal of comparative neurology.

[22]  G. Lynch,et al.  Rapid axon sprouting in the neonatal rat hippocampus , 1978, Brain Research.

[23]  G. Raisman,et al.  Synapse formation after injury in the adult rat brain: preferential reinnervation of denervated fimbrial sites by axons of the contralateral fimbria , 1980, Brain Research.

[24]  J. Crabtree,et al.  Anomalous uncrossed retinal projections fail to activate superior colliculus neurons in rabbits unilaterally enucleated by fetal surgery , 1981, The Journal of comparative neurology.

[25]  P. Brown,et al.  Somatotopic representation of hindlimb skin in cat dorsal horn. , 1975, Journal of neurophysiology.

[26]  S. Siegel,et al.  Nonparametric Statistics for the Behavioral Sciences , 2022, The SAGE Encyclopedia of Research Design.

[27]  W. Chambers,et al.  Intraspinal sprouting of dorsal root axons; development of new collaterals and preterminals following partial denervation of the spinal cord in the cat. , 1958, A.M.A. archives of neurology and psychiatry.

[28]  P. Hand Lumbosacral dorsal root terminations in the nucleus gracilis of the cat. Some observations on terminal degeneration in other medullary sensory nuclei , 1966, The Journal of comparative neurology.

[29]  G. Schneider Early Lesions of Superior Colliculus: Factors Affecting the Formation of Abnormal Retinal Projections; pp. 91–109 , 1973 .

[30]  P M Field,et al.  A quantitative investigation of the development of collateral reinnervation after partial deafferentation of the septal nuclei. , 1973, Brain research.

[31]  C. P. Baker,et al.  Effects of heavy, ionizing, monoenergetic particles on the cerebral cortex. II. Histological appearance of laminar lesions and growth of nerve fibers after laminar destructions , 1960, The Journal of comparative neurology.

[32]  F. W. Kerr,et al.  Electrophysiologic evidence that neither sprouting nor neuronal hyperactivity occur following long term trigeminal or cervical primary deafferentation , 1976, Experimental Neurology.

[33]  N. Mizuno,et al.  Synaptic reorganization of the red nucleus after chronic deafferentation from cerebellorubral fibers: an electron microscope study in the cat. , 1974, Brain research.

[34]  G. McCouch,et al.  Sprouting as a cause of spasticity. , 1958, Journal of neurophysiology.