Characteristics of dorsal root potentials recorded from the isolated spinal cord of the neonate rat

Summary Dorsal root potentials (DRP) and dorsal root reflexes (DRR) have been recorded from the isolated cord of the neonate rat. A single stimulus to the adjacent rostral or adjacent caudal dorsal root or dorsal columns evoked a DRP, the peak amplitude of which was reached in 110–115 msec and which decayed exponentially over most of its time course (time constant 800–850 msec). The same stimuli evoked field potentials in the dorsal horn comprising fast negative, slow negative and slow positive potentials. DRP had a lower threshold than DRR and reached a maximal amplitude at stimulus voltages sub-maximal for DRR. Increasing the intensity of stimulation shortened the latency of DRP and prolonged its time course. DRR and DRP were depressed by a prior conditioning stimulus (CS) and by the addition of Mg⁺⁺ ions to the bathing solution. A CS was more effective in producing depression of responses evoked more rostrally than more caudally.     

Effect of vasopressin and oxytocin on the dorsal root potentials of the isolated perfused spinal cord in rat pups

The effect of vasopressin and oxytocin on the dorsal root potentials were studied in isolated spinal cord of 12-16 days old rats. It was shown that both neuropeptides evoked reversible depression of the dorsal root potential induced by stimulation of the neighbouring dorsal root. Application of vasopressin or oxytocin caused the reversible dose-dependent depolarization in the dorsal root. The depolarization was preserved in Ca2+-free manganese-containing solution. Functional significance of presynaptic effects of hypothalamic neuropeptides is discussed.     

Regeneration of dorsal root fibers into the adult rat spinal cord

Regeneration of dorsal root nerve fibers into the spinal cord of adult rat was studied with the electron microscope after crushing the roots. Regenerated dorsal root myelinated fibers were observed in the substantia gelatinosa and posterior funiculi around the tenth week after lesion. Cytoplasmic processes of oligodendrocytes were often found close to the young myelinated nerve fibers. The astrocytic response subsided as regeneration progressed. Clusters of small, circular profile of cellular processess were found in the neuropil about the sixth week and are considered to be regenerated unmyelinated axons. At this period, groups of segments of cellular processes containing clear vesicles were also encountered in the substantia gelatinosa and resembled growth cones described in peripheral regenerating nerves.     

Spontaneous dorsal root potentials arise from interneuronal activity in the isolated frog spinal cord

Spontaneous dorsal root potentials (sDRPs) were recorded from the dorsal roots of the isolated frog spinal cord using sucrose gap techniques. sDRPs were always negative (depolarizing) in sign and ranged in size from about 100 μV to 6.0 mV. The largest sDRPs were 25–40% of the amplitude of DRPs evoked by stimulation of adjacent dorsal roots. Hypoxia or accumulation of extracellular K⁺ ions did not appear responsible for the generation of this spontaneous activity since exposing the cord to unoxygenated Ringer's solution decreased sDRPs and K⁺-sensitive microelectrodes indicated that only small changes in extracellular K⁺ (approximately 0.15 mM) were produced coincidently with the largest sDRPs.Chemically-mediated synaptic transmission was found to be necessary for the production of sDRPs because the addition of Mn²⁺ or Mg²⁺ ions or tetrodotoxin to the Ringer's solution or reduction of its Na⁺ concentration blocked sDRPs, whereas application of 4-aminopyridine enhanced them.It did not seem that a direct action of GABA on afferent fiber terminals was responsible for the generation of spontaneous potentials since an increase in sDRPs was seen after: application of the GABA antagonists, bicuculline and picrotoxin; exposure to the glutamic acid decarboxylase inhibitor, semicarbazide (which significantly reduced the concentration of GABA in the cord); and lowering of the external Cl⁻ concentration. Similarly taurine is probably not significant since the taurine antagonist, TAG, increased the amount of spontaneous activity.On the other hand, (−)-baclofen, which is thought to reduce excitatory amino acid release,d,l-α-aminoadipic acid, α,-diaminopimelic acid, and 2-amino-4-phosphonobutyric acid, which are believed to be selective postsynaptic excitatory amino acid antagonists, and [d-Pro²-d-Phe⁷-d-Trp⁹]-substance P, a postsynaptic blocker of the action of substance P, markedly and reversibly reduced sDRPs.Experiments were performed on isolated cords without supraspinal or afferent input; therefore sDRPs must be generated by intraspinal structures. It would seem that interneurons are responsible because addition of mephenesin or pentobarbital — compounds which inhibit polysynaptic reflex transmission involving interneurons — reduced the production of sDRPs.sDRPs may result from the action of excitatory transmitters such asl-glutamate,l-aspartate, or substance P released by interneuronal firing in the spinal cord. Moreover, because sDRPs were increased by application of yohimbine, corynanthine and propanolol and reduced by haloperidol, such interneurons may be under descending control of adrenergic and dopaminergic fibers.     

Changes in galanin immunoreactivity in rat lumbosacral spinal cord and dorsal root ganglia after spinal cord injury

Alterations in the expression of the neuropeptide galanin were examined in micturition reflex pathways 6 weeks after complete spinal cord transection (T8). In control animals, galanin expression was present in specific regions of the gray matter in the rostral lumbar and caudal lumbosacral spinal cord, including: (1) the dorsal commissure; (2) the superficial dorsal horn; (3) the regions of the intermediolateral cell column (L1-L2) and the sacral parasympathetic nucleus (L6-S1); and (4) the lateral collateral pathway in lumbosacral spinal segments. Densitometry analysis demonstrated significant increases (P < or = 0.001) in galanin immunoreactivity (IR) in these regions of the S1 spinal cord after spinal cord injury (SCI). Changes in galanin-IR were not observed at the L4-L6 segments except for an increase in galanin-IR in the dorsal commissure in the L4 segment. In contrast, decreases in galanin-IR were observed in the L1 segment. The number of galanin-IR cells increased (P < or = 0.001) in the L1 and S1 dorsal root ganglia (DRG) after SCI. In all DRG examined (L1, L2, L6, and S1), the percentage of bladder afferent cells expressing galanin-IR significantly increased (4-19-fold) after chronic SCI. In contrast, galanin expression in nerve fibers in the urinary bladder detrusor and urothelium was decreased or eliminated after SCI. Expression of the neurotrophic factors nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) was altered in the spinal cord after SCI. A significant increase in BDNF expression was present in spinal cord segments after SCI. In contrast, NGF expression was only increased in the spinal segments adjacent and rostral to the transection site (T7-T8), whereas spinal segments (T13-L1; L6-S1), distal to the transection site exhibited decreased NGF expression. Changes in galanin expression in micturition pathways after SCI may be mediated by changing neurotrophic factor expression, particularly BDNF. These changes may contribute to urinary bladder dysfunction after SCI.     

The role of GABA and serotonin in the mediation of raphe-evoked spinal cord dorsal root potentials

The possible involvement of bulbospinal serotonergic systems in the mediation of analgesia has created a need for a better understanding of the influence this system has on neuronal mechanisms in the spinal cord. Therefore, these studies were designed to examine the effects of caudal raphe stimulation on primary afferent depolarization and to determine the role of serotonin (5-HT) and GABA in the mediation of these stimulation-produced effects. Stimulation of the raphe evoked two electrotonically conducted dorsal root potentials (DRP-1 and DRP-2) and two compound action potentials (VRP-1 and VRP-2) which were recorded from the dorsal and ventral roots, respectively. Length constant measurements indicated that DRP-1 was generated in group II and DRP-2 in group I primary afferent fibers. Histological determination of stimulation sites revealed that short-latency potentials (DRP-1 and VRP-1) were evoked from many sites within the caudal brain stem, while the long-latency potentials (DRP-2 and VRP-2) were evoked primarily from sites within the caudal raphe nuclei. The role of serotonin in mediating these evoked potentials was assessed by administering various antagonists of serotonin (cinanserin, methysergide and D-lysergic acid diethylamide). These agents consistently attenuated the long-latency potentials (DRP-2 and VRP-2) but increased the magnitude of DRP-1. The possibility of a GABAergic neuron in the descending systems projecting to primary afferent terminals was studied. Depletion of GABA by semicarbazide blocked DRP-1, but had only a modest effect of DRP-2. However, the putative GABA antagonist, bicuculline, inhibited both DRP-1, and DRP-2. These results suggest that a GABA interneuron is not involved in the bulbospinal serotonergic depolarization of primary afferent terminals. This system appears to constitute a presynaptic filter of afferent input, with the capacity to inhibit different fiber groups.     

Differential expression of annexins I-VI in the rat dorsal root ganglia and spinal cord

The annexins are a family of Ca²⁻-dependent phospholipid-binding proteins. In the present study, the spatial expression patterns of annexins I-VI were evaluated in the rat dorsal root ganglia (DRG) and spinal cord (SC) by using indirect immunofluorescence. Annexin I is expressed in small sensory neurons of the DRG, by most neurons of the SC, and by ependymal cells lining the central canal. Annexin II is expressed by most sensory neurons of the DRG but is primarily expressed in the SC by glial cells. Annexin III is expressed by most sensory neurons, regardless of size, by endothelial cells lining the blood vessels, and by the perineurium. In the SC, annexin III is primarily expressed by astrocytes. In the DRG and the SC, annexin IV is primarily expressed by glial cells and at lower levels by neurons. In the DRG, annexin V is expressed in relatively high concentrations in small sensory neurons in contrast to the SC, where it is expressed mainly by ependymal cells and by small-diameter axons located in the superficial laminae of the dorsal horn areas. Annexin VI is differentially expressed by sensory neurons of the DRG, being more concentrated in small neurons. In the SC, annexin VI has the most striking distribution. It is concentrated subjacent to the plasma membrane of motor neurons and their processes. The differential localization pattern of annexins in cells of the SC and DRG could reflect their individual biological roles in Ca²⁻-signal transduction within the central nervous system. © 1996 Wiley-Liss, Inc.     

Immunohistochemical localization of calretinin in the dorsal root ganglion and spinal cord of the rat

Calretinin (CR). a recently identified calcium-binding protein, is present in nervous tissue, including sensory pathways, where it may play an important role in regulation of cellular activity. Using immunocytochemistry, we examined the cellular localization of CR in dorsal root ganglia (DRG) and spinal cord of normal rats and after multiple unilateral dorsal root ganglionectomies. In DRG, CR-immunoreactive cell bodies and axons were a small subpopulation (10%) of medium- to large-sized neurons. In the spinal cord, CR-like immunoreactivity (LI) in neurons and fibers was found in all laminae except motoneurons. Dense fiber networks were also found in Clarke's column. The densest staining of both cell bodies and fibers was in the superficial laminae, especially lamina II, and in the lateral spinal and lateral cervical nuclei. CR-immunoreactive fibers were also observed in the fasciculi cuneatus and gracilis. Fasciculus gracilis exhibited the greatest number of labeled axons at the lumbosacral levels, but few labeled axons were found at the rostral thoracic and cervical levels. In contrast, the corticospinal tract at the base of the dorsal column was devoid of CR-immunoreactive fibers. Unilateral multiple lumbar ganglionectomies resulted in a loss of CR-LI in the dorsal columns ipsilateral to the surgery. In the spinal gray matter ipsilateral to the ganglionectomies, CR-LI was reduced in Clarke's column and slightly enhanced in the medial third of lamina II. Our observations demonstrate a unique distribution pattern of CR-LI compared to other calcium-binding proteins in the spinal cord, and suggest a role for CR in nociceptive and proprioceptive pathways.     

Effects of amino acid antagonists on spontaneous dorsal root activity and evoked dorsal horn field potentials in an isolated preparation of rat spinal cord

Fast and slow dorsal horn field potentials and spontaneous dorsal root activity were recorded from 19-23-day-old rat isolated spinal cord preparations. The effects of GABA, glycine, and glutamate antagonists were tested on these recordings. CNQX, an AMPA/kainate antagonist, reduced all 3 components of the dorsal horn field potential whereas MK801, an NMDA ion channel antagonist, reduced the fast S2 component and the slow wave. Both reduced spontaneous dorsal root activity. NMDA antagonists, D-AP5, 7-chlorokynurenic acid and arcaine, and the metabotropic glutamate antagonists L-AP3 and ethylglutamic acid, while having little effect on the fast components of the field potential, all reduced the slow component. The GABA antagonist, bicuculline, and the glycine antagonist, strychnine, while having no effect on the fast S1 and slow components of the field potential, reduced both the fast S2 component of the field potential and spontaneous dorsal root activity. These results suggest that non-NMDA glutamate receptors are involved in low and high threshold transmission to dorsal horn neurones while NMDA and metabotropic glutamate receptors are primarily involved in high threshold transmission and both GABA and glycine have roles in the transmission or modulation of sensory information within the dorsal horn of the cord.     

Expression and localization of insulin receptor in rat dorsal root ganglion and spinal cord

The expression and localization of the insulin receptor (IR) was examined in rat dorsal root ganglia (DRG) and spinal cord using Western blotting, in situ hybridization and immunocytochemistry. Western blotting showed that the molecular weight of the IR beta subunit was higher in PNS than that found in CNS. Both IR mRNA and protein expressions were highest in small-sized sensory DRG neurons and myelinated sensory root fibers expressed higher levels of IR protein than myelinated anterior root fibers. In the spinal cord, IR immunoreactive neurons were present in lateral lamina V and in lamina X, suggesting the presence of IR in nociceptive pathways. Electronmicroscopy of DRGs revealed a polarized localization of the IR in abaxonal Schwann cell membranes, outer mesaxons in close vicinity to tight junctions of both myelinating and non-myelinating Schwann cells and to plasma membranes of sensory neurons. From these findings, we speculate that insulin may play a role in sensory fibers involved in nociceptive function often perturbed in diabetic neuropathy. The high expression of IR localizing to tight junctions of dorsal root mesaxons of DRGs may suggest a regulatory role on barrier functions compensating for the lack of a blood-nerve barrier in dorsal root ganglia. This is consistent with the colocalization of IR with tight junctions of the paranodal barrier and endoneurial endothelial cells in peripheral nerve.     

Nogo-A在成年大鼠脊髓和背根节的分布

目的研究Nogo—A在成年正常大鼠脊髓和背根节的分布。方法免疫组织化学方法(ABC法)和免疫荧光双标记法。结果正常成年大鼠的脊髓灰质分布有大量的Nogo—A免疫阳性的寡突胶质细胞、运动神经元和中间神经元，免疫阳性反应产物主要分布于细胞的胞体和部分突起中。Nogo—A广泛分布于穿行于脊髓白质的纤维包裹的髓鞘和轴突上。在脊髓前根、后根和坐骨神经的运动和感觉的有髓和无髓纤维也可观察到Nogo—A的表达。而背根神经节的神经元也大量表达Nogo—A，其强度由弱至强不等，广泛分布于大、中、小各类感觉神经元的胞质及突起中。结论Nogo—A在成年大鼠脊髓，背根神经节和外周神经纤维的广泛存在提示其在正常状态下的神经功能中可能起重要作用。     

GABAB receptor protein and mRNA distribution in rat spinal cord and dorsal root ganglia

The presence of metabotropic receptors for GABA, GABAB, on primary afferent terminals in mammalian spinal cord has been previously reported. In this study we provide further evidence to support this in the rat and show that the GABAB receptor subunits GABAB1 and GABAB2 mRNA and the corresponding subunit proteins are present in the spinal cord and dorsal root ganglion. We also show that the predominant GABAB1 receptor subunit mRNA present in the afferent fibre cell body appears to be the 1a form. In frozen sections of lumbar spinal cord and dorsal root ganglia (DRG) GABAB receptors were labelled with [3H]CGP 62349 or the sections postfixed with paraformaldehyde and subjected to in situ hybridization using oligonucleotides designed to selectively hybridize with the mRNA for GABAB(1a), GABAB(1b) or GABAB2. For immunocytochemistry (ICC), sections were obtained from rats anaesthetized and perfused-fixed with paraformaldehyde. The distribution of binding sites for [3H]CGP 62349 mirrored that previously observed with [3H]GABA at GABAB sites. The density of binding sites was high in the dorsal horn but much lower in the ventral regions. By contrast, the density of mRNA (pan) was more evenly distributed across the laminae of the spinal cord. The density of mRNA detected with the pan probe was high in the DRG and distributed over the neuron cell bodies. This would accord with GABAB receptor protein being formed in the sensory neurons and transported to the primary afferent terminals. Of the GABAB1 mRNA in the DRG, approximately 90% was of the GABAB(1a) form and approximately 10% in the GABAB(1b) form. This would suggest that GABAB(1a) mRNA may be responsible for encoding presynaptic GABAB receptors on primary afferent terminals in a manner similar to that we have previously observed in the cerebellar cortex. GABAB2 mRNA was also evenly distributed across the spinal cord laminae at densities equivalent to those of GABAB1 in the dorsal horn. GABAB2 mRNA was also detected to the same degree within the DRG. Immunocytochemical analysis revealed that GABAB(1a), GABAB(1b) and GABAB2 were all present in the spinal cord. GABAB(1a) labelling appeared to be more dense than GABAB(1b) and within the superficial dorsal horn GABAB(1a) was present in the neuropil whereas GABAB(1b) was associated with cell bodies in this region. Both 1a and 1b immunoreactivity was expressed in motor neurons in lamina IX. GABAB2 immunoreactivity was expressed throughout the spinal cord and was evident within the neuropil of the superficial laminae.     

Plasticity in the spinal cord: the dorsal root connection

There is considerable evidence supporting a naturally occuring increase in the density of projections by intact systems induced by partial denervation of targets within the spinal cord. The phenomenon of sprouting in the spinal cord appears to be quite similar to the denervation evoked sprouting shown elsewhere in the CNS. Sprouting appears to be regulated rather than random since not all systems projecting to a denervated region may show demonstrable sprouting. In adults, the extent of sprouting is usually limited to the normal target zone of the intact systems and thus reasonably rigorous quantitative methods may be required to provide a clear demonstration of the increased projection. Greater plasticity, including regenerative like changes can be elicited in the undamaged processes of DRGs within the CNS by lesion to the peripheral process. Expansion of terminal fields into novel territories in adults has been demonstrated most convincingly in cases where additional manipulations are made, e.g. addition of peripheral nerve injury to the lesion paradigm. This suggests that the limitation on sprouting in adults can be overridden by increasing the metabolic drive of the sprouting neurons. In contrast there appear to be fewer limitations on sprouting in the neonate, since extensive sprouting into aberrant targets occurs if denervation occurs before development has ceased. Changing patterns of synaptic activity can also evoke quite dramatic modifications of the synthetic activity of neurons. Some of these changes appear to be long lasting and may lead to modifications in the activity of spinal neurons. Naturally occurring plasticity thus represents a major compensatory response to CNS lesions which needs to be taken into account in considering the consequences of CNS lesions, the extent of recovery of function and ways of improving the extent of recovery of function.     

Changes in cholinergic and opioid receptors in the rat spinal cord,dorsal root and sciatic nerve after ventral and dorsal root lesion

Summary Changes in the distribution of³H-quinuclidinylbenzilate (³ H-QNB),³ H-acetylcholine (³ H-ACh) and³ H-alpha-bungarotoxin (alpha-BTx) binding sites were studied with the use of quantitative in vitro autoradiography in the L4–L6 segments of rats 7 days after ventral L4–L6-rhizotomies and 24 hours after ligation of the dorsal roots L4–L6. The changes in the binding sites of these ligands and of³ H-etorphine binding sites were also studied in the dorsal roots of the rats operated with dorsal root ligation and in the sciatic nerves (around a ligature) in the rats operated with ventral rhizotomy. After ventral rhizotomy³ H-QNB binding sites in the ipsilateral motor neuron area were decreased by about 25% from 100±5 to 73±5 fmol/mg wet weight. After dorsal root ligation³ H-QNB binding sites in the ipsilateral posterior horn were reduced by about 30% from 91±5 to 64±7 fmol/mg wet weight. No significant changes in the binding of the other cholinergic ligands in the spinal cords were observed after the operations. In the dorsal root³ H-alpha-Btx and³ H-etorphine binding sites were higher on the distal side of the ligation (3.5±0.8 and 14±4 fmol/mg wet weight, respectively) than on the proximal side (0.7±0.5 and 2.4±1.2 fmol/mg wet weight, respectively).The same level of³ H-ACh (total, muscarinic and nicotinic) binding was observed on both sides of the ligation. In the sciatic nerve³ H-QNB and total, muscarinic and nicotinic ACh binding sites were higher on the proximal side of the ligation than on the distal side. Except for a small emergence of muscarinic-ACh binding distally to the ligation there were no changes in the number of binding sites in the sciatic nerve after the ventral rhizotomy.Muscarinic antagonist binding sites are probably located on the perikarya of the motor neurons and presynaptically on the primary afferents in the posterior horn and in the dorsal root. Cholinergic agonist binding sites in the spinal cord seem less sensitive to axonal damage than antagonist binding sites. Cholinergic and opioid receptors in peripheral nerves are transported in both anterograde and retrograde directions and their origin seems to be the dorsal root ganglion.     

Anatomical studies of dorsal column axons and dorsal root ganglion cells after spinal cord injury in the newborn rat

The response of dorsal column axons was studied after neonatal spinal overhemisection injury (right hemicord and left doral funiculus). Rat pups (N = 11) received this spinal lesion at the C2 level within 30 hours after birth. The cauda equina was exposed 3 months later in one group of chronic operates (N = 5) and in a group of normal adults (N = 2), and all spinal roots from L5 caudally were cut bilaterally; 4 days later the spinal cord and medulla were processed for Fink-Heimer impregnation of degenerating axons and terminals. In a second group of chronic operates (N = 6) and normal adult controls (N = 4) the left sciatic nerve was injected with a cholera toxin-HRP conjugate (C-HRP), followed by a 2-3 day transganglionic transport period, and then the spinal cord and medulla were processed with tetramethylbenzidine histochemistry. Both control groups have a consistent dense projection in topographically adjacent regions of the dorsal funiculus and gracile nucleus. However, there is no sign of axonal growth around the lesion in either group of chronic experimental operates. Instead, there is a decreased density of projection within the dorsal funiculus near the lesion site. Many remaining C-HRP labeled axons in the experimental operates have abnormal, thick varicosities and swollen axonal endings (5-10 microns x 10-30 microns) within the dorsal funiculus through several spinal segments caudal to the lesion. Ultrastructural analysis of the dorsal funiculus in three other chronic experimental operates reveals the presence of numerous vesicle filled axonal profiles and reactive endings which appear similar to the C-HRP labeled structures. Transganglionic labeling after C-HRP sciatic nerve injections (N = 4) and retrograde labeling of L4, L5 dorsal root ganglion neurons after fast blue injections of the gracile nucleus (N = 6) both suggest that all dorsal column axons project to the gracile nucleus in the newborn rat. Dorsal root ganglion (DRG) cell survival following the neonatal overhemisection injury was also examined in the L4 and L5 DRG. DRG neurons that project to the gracile nucleus were prelabeled by injecting fast blue into this nucleus at birth two days prior to the cervical overhemisection spinal injury. Both normal littermates (N = 9) and spinally injured animals (N = 12) were examined after postinjection survival periods of 10 or 22 days.(ABSTRACT TRUNCATED AT 400 WORDS)     

Alpha-CGRP and beta-CGRP mRNAs are differentially regulated in the rat spinal cord and dorsal root ganglion

We found an increase in calcitonin gene-related peptide (CGRP)-like immunoreactivity in motoneurons of rat spinal cord after peripheral axotomy. By means of in situ hybridization histochemistry and Northern blotting, we further demonstrated that this increase was the result of increased levels of alpha-CGRP mRNA, not beta-CGRP mRNA. The increased level of alpha-CGRP mRNA was maintained for at least 5 weeks, and was present on both sides. In addition, alpha-CGRP and beta-CGRP mRNAs had different distributions from each other in the dorsal root ganglia and levels of both were decreased after axotomy. These results indicate that alpha-CGRP and beta-CGRP are regulated independently and have different roles in the motor and sensory systems of the spinal cord.     

Differentiation and migration of astrocytes in the spinal cord following dorsal root injury in the adult rat

Nerve fibre degeneration in the spinal cord is accompanied by astroglial proliferation. It is not known whether these cells proliferate in situ or are recruited from specific regions harbouring astroglial precursors. We found cells expressing nestin, characteristic of astroglial precursors, at the dorsal surface of the spinal cord on the operated side from 30 h after dorsal root injury. Nestin-expressing cells dispersed to deeper areas of the dorsal funiculus and dorsal horn on the operated side during the first few days after injury. Injection of bromodeoxyuridine (BrdU) 2 h before the end of the experiment, at 30 h after injury, revealed numerous BrdU-labelled, nestin-positive cells in the dorsal superficial region. In animals surviving 20 h after BrdU injection at 28 h postlesion, cells double-labelled with BrdU and nestin were also found in deeper areas. Labeling with BrdU 2 h before perfusion showed proliferation of microglia and radial astrocytes in the ventral and lateral funiculi on both sides of the spinal cord 30 h after injury. Nestin-positive cells coexpressed the calcium-binding protein Mts1, a marker for white matter astrocytes, in the dorsal funiculus, and were positive for glial fibrillary acidic protein (GFAP), but negative for Mts1 in the dorsal horn. One week after injury the level of nestin expression decreased and was undetectable after 3 months. Taken together, our data indicate that after dorsal root injury newly formed astrocytes in the degenerating white and grey matter first appear at the dorsal surface of the spinal cord from where some of them subsequently migrate ventrally, and differentiate into white- or grey-matter astrocytes.     

NGF mRNA is expressed in the dorsal root ganglia after spinal cord injury in the rat

Nerve growth factor (NGF) mRNA is expressed in a variety of cell types in the injured spinal cord and its protein implicated in both positive and negative neurological outcomes of cord injury. Here we demonstrate that NGF mRNA is also upregulated in dorsal root ganglion (DRG) neurons after spinal cord injury and that the percentage of sensory neurons expressing NGF mRNA correlates with proximity to the lesion epicenter. Our data suggest that, in DRG, NGF gene expression may be upregulated by damage to the central processes of sensory neurons.