Axonal regeneration from GABAergic neurons in the adult rat thalamus

Benfey, M.; Bünger, U. R.; Vidal‐Sanz, Manuel; Bray, Garth M.; Aguayo, Albert J.

doi:10.1007/bf01258453

Cited by 79 publications

(31 citation statements)

References 36 publications

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“…We have shown that the axons regenerating into tibial nerve autografts placed in the dorsal thalamus originate predominantly from neurons in the TRN, confirming previous observations (Benfey et al, 1985;Morrow et al, 1993) and attesting to the strong regenerative propensity of this nucleus. The TRN forms a sheet of variable thickness partially enveloping the dorsal thalamus, with axons that project to dorsal thalamic nuclei, where they regulate the thalamocortical output (e.g., Ohara et al, 1983;Jones, 1985).…”

Section: Discussionsupporting

confidence: 84%

“…Neurons in the central nervous system (CNS) of adult mammals cannot normally regenerate their axons following injury, but it is now well established that axotomised CNS neurons can regenerate axons for long distances through segments of peripheral nerve implanted into the brain or spinal cord or attached to the retinal stump of severed optic nerves (David and Aguayo, 1981;Benfey et al, 1985;Aguayo, 1985;Berry et al, 1986). Not all populations of CNS neurons show the same propensity for axonal regeneration.…”

Section: Indexing Terms: Axotomy; Cns Regeneration; Nerve Graft; Cellmentioning

confidence: 99%

“…The most thoroughly studied example of this phenomenon, however, relates to the thalamus. When peripheral nerve grafts are implanted into the dorsal thalamus of adult rats, only very small numbers of neurons in the dorsal thalamic nuclei into which the graft is placed contribute regenerating axons to the graft; instead, the great majority of the axons that regenerate into such grafts arise from neurons in one particular nucleus, closely as-sociated with, but not a part of the dorsal thalamus, the thalamic reticular nucleus (TRN) (Benfey et al, 1985;Morrow et al, 1993;Vaudano et al, 1995Vaudano et al, , 1998.…”

Section: Indexing Terms: Axotomy; Cns Regeneration; Nerve Graft; Cellmentioning

confidence: 99%

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The cell recognition molecule CHL1 is strongly upregulated by injured and regenerating thalamic neurons

et al. 2000

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Close homologue of L1 (CHL1) is a cell recognition molecule known to promote axonal growth in vitro. We have investigated the expression of CHL1 mRNA by regenerating central nervous system (CNS) neurons, by using in situ hybridisation 3 days to 10 weeks following the implantation of living and freeze-killed peripheral nerve autografts into the thalamus of adult rats. At all survival times after implantation of living grafts, neurons of the thalamic reticular nucleus (TRN), close to the graft tip and up to 1 mm away from it, displayed strong signal for CHL1 mRNA, even though TRN neurons show very low levels of CHL1 mRNA expression in unoperated animals. When the cell bodies of regenerating neurons were identified by retrograde labelling from the distal portion of the grafts, 4-6 weeks after operation, most of the labelled cells were found in the TRN and could be shown to haveupregulated CHL1 mRNA. In addition, some neurons in dorsal thalamic nuclei near the graft tip transiently upregulated CHL1 mRNA during the first 3 weeks after graft implantation, and glial cells showing CHL1 mRNA expression were present at the brain/graft interface 3 days to 2 weeks after operation. Freeze-killed grafts, into which axons do not regenerate, caused a transient upregulation of CHL1 in very few TRN neurons near the graft tip and in glial cells at the brain/graft interface but did not produce prolonged CHL1 mRNA expression. CHL1 can therefore be added to the list of molecules (including GAP-43, L1, and c-jun) strongly expressed by CNS neurons that regenerate their axons into nerve grafts, but not by those neurons that fail to regenerate their axons.

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Section: Discussionsupporting

confidence: 84%

Section: Indexing Terms: Axotomy; Cns Regeneration; Nerve Graft; Cellmentioning

confidence: 99%

Section: Indexing Terms: Axotomy; Cns Regeneration; Nerve Graft; Cellmentioning

confidence: 99%

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The cell recognition molecule CHL1 is strongly upregulated by injured and regenerating thalamic neurons

et al. 2000

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“…These ob servations confirm and extend recent findings of axonal re generation into peripheral nerve grafts [1][2][3][4][5][6]9. II.…”

Section: Discussionsupporting

confidence: 80%

Peptidergic Neurosecretory Axons Regenerate into Sciatic Nerve Autografts in the Rat Hypothalamus

Hd¹,

Lf²,

Bellin³

1986

Neuroendocrinology

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Pieces of intact or degenerated sciatic nerves autografted into contact with transected neurosecretory axons within the hypothalamus were invaded by neurophysin-positive axons. With increasing time after grafting, increasing numbers of axons were present in both types of grafts, but grafts of degenerated sciatic nerves always contained more axons. At the fine-structural level typical neurosecretory as well as nonneurosecretory axons were usually associated with basal lamina-enclosed neurolemmocyte processes; occasional axons occurred among collagen fibrils or within basal lamina scaffolds. Profiles with the fine structural characteristics of axon terminals were present by 20 days after transplantation.

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“…Neurons in the cerebellar cortex of adult rats do not regenerate their axons into peripheral nerve grafts placed into the subcortical white matter of the cerebellum, whereas neurons in the deep cerebellar nuclei may do so (Dooley and Aguayo, 1982;Vaudano et al, 1993). The best documented example of differential regenerative responses is provided by studies involving the insertion of peripheral nerve grafts into the thalamus: in most experiments, more than 90% of the neurons that regenerate axons into such grafts have cell bodies in one nucleus, the thalamic reticular nucleus (TRN); by comparison, only a few thalamic projection neurons, always with cell bodies situated close to the graft tip, regenerate axons into the same grafts (Benfey et al, 1985;Morrow et al, 1993). Neurons of the TRN regenerating their axons into peripheral nerve grafts markedly upregulate their expression of mRNAs for the growth-associated protein 43 (GAP-43; Vaudano et al, 1995), which is involved in axonal growth and/or pathfinding (Skene, 1989;; the cell recognition molecule L1 (Zhang et al, 1995), which is known to be involved in axonal elongation during development and regeneration (Schachner, 1994); and the immediate early gene c-jun (Vaudano et al, 1993), a transcription factor, elevated expression of which precedes and accompanies axonal regeneration in the peripheral nervous system (e.g., Jenkins et al, 1993).…”

mentioning

confidence: 99%

Differential effects of autologous peripheral nerve grafts to the corpus striatum of adult rats on the regeneration of axons of striatal and nigral neurons and on the expression of GAP-43 and the cell adhesion molecules N-CAM and L1

et al. 1998

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A segment of tibial nerve was autografted to the right corpus striatum of deeply anesthetized adult rats; the distal graft was left beneath the scalp. Horseradish peroxidase (HRP) conjugates were injected into the distal graft after 2-30 weeks, and the animals were killed 2-3 days later. Small numbers of neostriatal perikarya were HRP labeled at all survival times; most were large (ca. 20 microm in diameter), and many contained acetycholine esterase (AChE). Many more neurons were labelled in the substantia nigra pars compacta (SNpc) 4 weeks or more after grafting. When the graft encroached on the globus pallidus, numerous pallidal neurons, most of them AChE positive, were also labeled. Nigrostriatal neurons, a population of pallidal cholinergic neurons, and a subclass (or classes) of neostriatal neurons, including cholinergic interneurons, thus can be classified as central nervous system (CNS) neurons with a relatively strong regenerative response. In a second experimental series, animals were killed 1-4 weeks after grafting, and sections were probed for the expression of mRNAs encoding growth-associated protein 43 (GAP-43) and the cell adhesion molecules N-CAM and L1. Subpopulations of mostly large neurons scattered throughout the neostriatum gave moderate signals for GAP-43 and N-CAM mRNAs and a stronger signal for L1 mRNAs. Most SNpc neurons were strongly labeled with all three probes. Neostriatal grafts had no apparent effect on the expression of any of the mRNAs in the SNpc or on L1 and N-CAM mRNAs in the striatum. However, GAP-43 mRNA levels were increased in a few, mainly large neostriatal neurons around the graft tip, resembling the HRP-labeled cells. In contrast, previous work has shown upregulation (from an undetectable level) of GAP-43 and L1 mRNAs in neurons regenerating axons into grafts placed in the thalamus and cerebellum. Thus, GAP-43 and L1 mRNA expression, but not necessarily marked upregulation, may correlate with, and be intrinsic determinants of, the ability of CNS neurons to regenerate their axons.

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Axonal regeneration from GABAergic neurons in the adult rat thalamus

Cited by 79 publications

References 36 publications

The cell recognition molecule CHL1 is strongly upregulated by injured and regenerating thalamic neurons

The cell recognition molecule CHL1 is strongly upregulated by injured and regenerating thalamic neurons

Peptidergic Neurosecretory Axons Regenerate into Sciatic Nerve Autografts in the Rat Hypothalamus

Differential effects of autologous peripheral nerve grafts to the corpus striatum of adult rats on the regeneration of axons of striatal and nigral neurons and on the expression of GAP-43 and the cell adhesion molecules N-CAM and L1

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