Dorsolateral Nucleus Motoneurons Research Articles

Connexin36 in gap junctions forming electrical synapses between motoneurons in sexually dimorphic motor nuclei in spinal cord of rat and mouse

Pools of motoneurons in the lumbar spinal cord innervate the sexually dimorphic perineal musculature, and are themselves sexually dimorphic, showing differences in number and size between male and female rodents. In two of these pools, the dorsomedial nucleus (DMN) and the dorsolateral nucleus (DLN), dimorphic motoneurons are intermixed with non-dimorphic neurons innervating anal and external urethral sphincter muscles. As motoneurons in these nuclei are reportedly linked by gap junctions, we examined immunofluorescence labeling for the gap junction-forming protein connexin36 (Cx36) in male and female mice and rats. Fluorescent Cx36-labeled puncta occurred in distinctly greater amounts in the DMN and DLN of male rodents than in other spinal cord regions. These puncta were localized to motoneuron somata, proximal dendrites, and neuronal appositions, and were distributed either as isolated or large patches of puncta. In both rats and mice, Cx36-labeled puncta were associated with nearly all (> 94%) DMN and DLN motoneurons. The density of Cx36-labeled puncta increased dramatically from postnatal days 9 to 15, unlike the developmental decreases in these puncta observed in other central nervous system regions. In females, Cx36 labeling of puncta in the DLN was similar to that in males, but was sparse in the DMN. In enhanced green fluorescent protein (EGFP)-Cx36 transgenic mice, motoneurons in the DMN and DLN were intensely labeled for the EGFP reporter in males, but less so in females. The results indicate the presence of Cx36-containing gap junctions in the sexually dimorphic DMN and DLN of both male and female rodents, suggesting coupling of not only sexually dimorphic but also non-dimorphic motoneurons in these nuclei.

Sex difference in Onuf's nucleus homologue in the Asian musk shrew

Perineal muscles essential for copulatory functioning are innervated by Onuf's nucleus in humans and the spinal nucleus of the bulbocavernosus (SNB) and dorsolateral nucleus (DLN) in rats. These structures sexually differentiate as a result of developmental androgen exposure in most species examined. The homologous structure in the Asian musk shrew ( Suncus murinus) is a single cluster in the lateral DLN/Onuf's position in the ventral horn of the spinal cord; these motoneurons innervate both the bulbocavernosus and ischiocavernosus muscles of the musk shrew. We found the expected sex difference in motoneuron number in the shrew DLN, but not in two neighboring motoneuron clusters, the retrodorsolateral nucleus (RDLN) and ventrolateral nucleus (VLN). Male musk shrews also have significantly larger soma areas in the VLN and DLN than females, and male DLN motoneurons have significantly larger nuclei than female. The sex difference in DLN motoneuron number was evident both in raw counts and after accounting for split nuclei error.

Patterns of dye coupling in lumbar motor nuclei of the rat.

Gap junctions exist on motoneurons of the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN), both sexually dimorphic motor nuclei in the lumbar spinal cord of the rat. In addition, messenger RNA for gap junction proteins is expressed in motoneurons of the retrodorsolateral nucleus (RDLN), a nondimorphic spinal motor nucleus that innervates a muscle of the foot. Gap junctions on SNB and DLN motoneurons are androgen sensitive; the number and size of gap junctions decrease following castration, a change that can be reversed with exogenous testosterone replacement. In contrast, RDLN gap junction mRNA levels remain constant throughout hormone manipulation. In this study, dye coupling was used to examine patterns of gap junction-mediated connectivity in these three lumbar spinal motor nuclei. Injection of dye into single motoneurons resulted in spatially extensive labeling of neighboring cells in all three nuclei; significantly more coupling was observed in the sexually dimorphic nuclei than in the RDLN. Dye-coupled clusters of cells included motoneurons and interneurons; coupling was bilateral in the SNB. Treatment with oleamide, a gap junction blocker, completely attenuated labeling. In all nuclei, androgen manipulation did not alter the number, identity, or distribution of coupled cells. Thus, sexually dimorphic nuclei in the spinal cord exhibit greater dye coupling than do nondimorphic populations, and the patterns of connectivity are insensitive to androgen despite modification of their number and size.

Development of androgen receptor and p75 NTR mRNAs and peptides in the lumbar spinal cord of the gerbil

Development of sex differences in the spinal cord appears to be largely under the control of androgen and although neurotrophins may also have a role. Spinal cords of male and female neonatal gerbils (postnatal days 1, 5, 7, 10, 23) and adult gerbils (postnatal day 150) were examined to determine the relative temporal expression of androgen receptor (AR) and the low-affinity neurotrophin receptor (p75) mRNAs within the spinal nucleus of the bulbocavernosus (SNB) and dorsolateral nucleus (DLN). Furthermore, prepubertal male gerbils were placed into one of six gonadal hormone treatment groups at weaning: Either sham castrate, castrated with gonadal hormone replacement, or castrated without gonadal hormone replacement. Ten weeks later gerbils were aldehyde-perfused, spinal cords removed and processed for presence of AR and p75 immunoreactivity (ir) in motoneurons of the SNB and DLN. During neonatal development, there were significant increases in androgen receptor mRNA within the SNB and DLN. In the SNB, the increase in androgen receptor mRNA preceded the increase in p75 mRNA. Peripubertally, significantly more SNB than DLN motoneurons contained AR- and p75-ir. These data demonstrate that AR expression occurs along the same developmental time frame as the development of the SNB and DLN and the organizational effects of androgens on their development continues through puberty in the male gerbil.

Androgen Receptor (AR) Immunoreactivity in Rat Pudendal Motoneurons: Implications for Accessory Proteins

Pudendal motoneurons in male rats are located in two sexually dimorphic motoneuronal pools: the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN). SNB motoneurons innervate sexually dimorphic muscles bulbocavernosus (BC) and levator ani (LA) and the sexually monomorphic external anal sphincter (EAS) muscle. DLN motoneurons innervate either the sexually dimorphic ischiocavernosus (IC) muscle or the sexually monomorphic external urethral sphincter (EUS) muscle. Previous observations indicate that the size of BC, LA, and IC motoneurons in males is sensitive to adult androgen manipulations, whereas the size of EAS and EUS motoneurons is not, raising the question of whether this difference in androgen sensitivity among pudendal motoneurons reflects a difference in androgen receptor (AR) expression. AR immunocytochemistry using the PG-21 antiserum was carried out on spinal cord tissue from normal adult male rats in which specific pudendal motoneuronal subpopulations were identified with retrograde markers. Over 90% of BC, LA, and IC motoneurons displayed AR immunoreactivity in their nuclei. Among motoneurons in the SNB, significantly fewer EAS motoneurons had AR-positive nuclei, which may contribute to the reported failure of EAS motoneurons to morphologically respond to changes in androgen levels. However, within the DLN, despite the fact that IC but not EUS motoneurons are reported to respond to androgen with an increase in soma size, IC and EUS motoneurons had the same proportion of AR-positive nuclei. These results indicate that androgen receptors, while necessary, are not sufficient to confer androgen sensitivity to cells.

Ontogeny of androgen receptor immunoreactivity in lumbar motoneurons and in the sexually dimorphic levator ani muscle of male rats

We documented the ontogeny of androgen receptor (AR) immunoreactivity for rat lumbar motoneurons of the sexually dimorphic motor pools, the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN), and for the sexually monomorphic retrodorsolateral nucleus (RDLN). We also assessed the ontogeny of AR immunoreactivity in the rat sexually dimorphic levator ani (LA), which is a target muscle for SNB motoneurons. Lumbar spinal cords and LA muscles from gonadally intact males at ages postnatal days (P)7, P10, and P14 and as adults were incubated with the rabbit antiserum PG-21. Half of the prepubertal males (P7–P14) received 200 μg of testosterone propionate (TP) 2 hours prior to death to enhance immunodetection of ARs. We found that SNB motoneurons developed AR immunoreactivity first and achieved adult levels by P10. In contrast, the number of RDLN motoneurons with AR-immunopositive nuclei during development remained well below the adult number. Development of AR immunoreactivity in the DLN shared characteristics with both the SNB and the RDLN. AR immunoreactivity developed in some DLN motoneurons by P10, although the percentage of labelled motoneurons remained below that in adulthood. Acute TP treatment significantly increased the number of SNB motoneurons with AR-positive nuclei at P7. The LA showed a robust pattern of AR immunostaining from P7 to adulthood. Immunostaining was present only in nuclei and constituted only a subpopulation of the nuclei present in muscle. The present results confirm and extend previous results based on steroid autoradiography and steroid binding assays regarding regional and developmental differences in the expression of ARs. J. Comp. Neurol. 379:88-98, 1997. © 1997 Wiley-Liss, Inc.

Ontogeny of androgen receptor immunoreactivity in lumbar motoneurons and in the sexually dimorphic levator ani muscle of male rats

We documented the ontogeny of androgen receptor (AR) immunoreactivity for rat lumbar motoneurons of the sexually dimorphic motor pools, the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN), and for the sexually monomorphic retrodorsolateral nucleus (RDLN). We also assessed the ontogeny of AR immunoreactivity in the rat sexually dimorphic levator ani (LA), which is a target muscle for SNB motoneurons. Lumbar spinal cords and LA muscles from gonadally intact males at ages postnatal days (P)7, P10, and P14 and as adults were incubated with the rabbit antiserum PG-21. Half of the prepubertal males (P7-P14) received 200 micrograms of testosterone propionate (TP) 2 hours prior to death to enhance immunodetection of ARs. We found that SNB motoneurons developed AR immunoreactivity at first and achieved adult levels by P10. In contrast, the number of RDLN motoneurons with AR-immunopositive nuclei during development remained well below the adult number. Development of AR immunoreactivity in the DLN shared characteristics with both the SNB and the RDLN. AR immunoreactivity developed in some DLN motoneurons by P10, although the percentage of labelled motoneurons remained below that in adulthood. Acute TP treatment significantly increased the number of SNB motoneurons with AR-positive nuclei at P7. The LA showed a robust pattern of AR immunostaining from P7 to adulthood. Immunostaining was present only in nuclei and constituted only a subpopulation of the nuclei present in muscle. The present results confirm and extend previous results based on steroid autoradiography and steroid binding assays regarding regional and developmental differences in the expression of ARs.

Short- and long-term effects of ciliary neurotrophic factor on androgen-sensitive motoneurons in the lumbar spinal cord.

Motoneuron death in the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN) of the lumbar spinal cord is androgen regulated. As a result, many more SNB and DLN motoneurons die in perinatal female rats than in males, whereas treatment of newborn females with androgen results in a permanent sparing of the motoneurons and their target muscles. We previously observed that a neurotrophic molecule, ciliary neurotrophic factor (CNTF), also arrests the death of SNB motoneurons and their target musculature, at least in the short term. The present study compares the short- and long-term consequences of perinatal CNTF treatment on motoneuron number in the SNB, the DLN, and the retrodorsolateral nucleus (RDLN), a motor pool in the lower lumbar cord that does not exhibit hormone-regulated cell death. Female pups were treated with CNTF or vehicle alone from embryonic day 22 through postnatal day 6 (P6). Motoneuron number in the each nucleus was then determined immediately after treatment on P7, or 10 weeks later (P77). CNTF treatment significantly elevated motoneuron number in the SNB and DLN on P7; the volume of SNB target muscles on P7 was also greater in the CNTF-treated group. These effects were transient, however, as motoneuron number and ratings of muscle size were not different in CNTF-and vehicle-treated females on P77. Perinatal CNTF treatment did not alter cell number in the RDLN at either age. The finding that effects of CNTF on SNB and DLN motoneuron number are short lived contrasts with the permanent effects of early androgen treatment, and has implications for molecular models of the actions of androgen and neurotrophic factors on the developing spinal cord.

Motoneuron development after deafferentation: II. Dorsal rhizotomy does doe block estrogen-supported growth in the dorsolateral nucleus (DLN)

The lumbar spinal cord of the rat contains two sexually dimorphic motor nuclei, the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN). Postnatally, SNB and DLN motoneurons grow substantially and reach their adult morphology by 7 weeks of age. The masculinization of SNB and DLN motoneuron dendrites depends upon steroid hormones. After early castration, the growth of SNB and DLN dendrites is markedly attenuated, but testosterone replacement restores this growth. In the SNB, initial dendritic growth is also supported in castrates treated with estrogen. By using castration and hormone replacement techniques, we examined the development of DLN motoneuron morphology in estrogen-treated castrated rats to determine if estrogen also supports the growth of DLN motoneurons. In addition, given that dorsal root ganglia may be a site of estrogen action, we tested the hypothesis that estrogen acts at primary afferents to support DLN dendritic growth. Thus, we attempted to block the potential trophic effect of estrogen by performing unilateral dorsal rhizotomies in estrogen-treated castrates. DLN motoneuron morphology was analyzed at 4 and 7 weeks of age by using cholera toxin horseradish peroxidase (BHRP) histochemistry. As found for SNB motoneurons, estrogen treatment transiently supported development. DLN motoneurons in estrogen-treated castrates developed normally through 4 weeks of age, but by 7 weeks, DLN motoneuron morphology in estrogen-treated castrates was no longer different from that in oil-treated castrates. Moreover, deafferentation via unilateral dorsal rhizotomy did not inhibit estrogen's ability to masculinize the early development of DLN motoneurons. Thus, the trophic effect of estrogen did not appear to act via the dorsal root ganglia to support the early postnatal development of DLN motoneurons.

Motoneuron development after deafferentation. I. Dorsal rhizotomy does not alter growth in the spinal nucleus of the bulbocavernosus (SNB)

The spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN) are sexually dimorphic motor nuclei in the rat lumbar spinal cord. During postnatal development, SNB and DLN motoneurons grow substantially in measures of soma size, dendritic length, and radial dendritic extent. SNB motoneurons exhibit a biphasic pattern of dendritic growth, where there is an initial period of exuberant growth followed by a period of retraction to mature lengths by 7 weeks. In this experiment, we examined whether primary afferent input to the SNB nucleus was necessary for the normal postnatal growth of SNB motoneurons. We partially deafferented the SNB via unilateral dorsal rhizotomy of lumbosacral dorsal roots in male rats at 1 week of age. Using cholera toxin horseradish peroxidase (BHRP) to visualize SNB motoneurons, we examined SNB motoneuron morphology at 4 and 7 weeks of age. SNB motoneurons in rhizotomized males developed normally; measures of dendritic length in rhizotomized males were typically exuberant at 4 weeks of age, and declined significantly to mature lengths by 7 weeks of age. In addition, dorsal rhizotomy did not alter the development of SNB motoneuron soma size or radial dendritic extent. These results are discussed in reference to sensorimotor connections in the SNB, the extent of the deafferentation, and dendrodendritic interactions.

Hormone-sensitive periods for the control of motoneuron number and soma size in the dorsolateral nucleus of the rat spinal cord

The dorsolateral nucleus (DLN) of the rat lumbosacral spinal cord is sexually dimorphic, with males having more and larger DLN motoneurons than do females. The development of this dimorphism depends on the presence of perinatal androgens. The present study sought to determine the periods in development during which the DLN is sensitive to the masculinizing effects of the androgen testosterone propionate (TP). The size and number of DLN motoneurons in neonatally ovariectomized female rats that were exposed to TP during either the late prenatal, early postnatal, or late postnatal period were compared to control males and females. Both late prenatal and early postnatal TP injections significantly increased DLN number by 48% and 50%, respectively, but the sensitive period for TP masculinization of soma size seems to be primarily postnatal, because prenatal TP injections had little or no effect on that measure. The sensitive period for TP masculinization of DLN neuron number is similar to that of the sexually dimorphic spinal nucleus of the bulbocavernosus (SNB). However, the sensitive period for TP masculinization of DLN soma size appears to begin later than for the SNB.

Hormonally mediated plasticity of motoneuron morphology in the adult rat spinal cord: A cholera toxin‐HRP study

The dorsolateral nucleus (DLN) and the spinal nucleus of the bulbocavernosus (SNB) of the rat lumbar spinal cord are sexually dimorphic groups of motoneurons that innervate striated perineal muscles involved in male copulatory behavior. Androgens control the development of these motoneurons and their target muscles, and continue to influence the system in adulthood. Given that several features of SNB motoneuron morphology have been shown to be androgen sensitive in adult male rats, we examined the effects of androgen manipulations on the morphology of motoneurons in the DLN in adult rats. Adult male rats were castrated and implanted with testosterone-filled or blank implants, or were subjected to a sham-castration procedure. Six weeks after treatment, motoneurons in the DLN were retrogradely labeled with cholera toxin-horseradish peroxidase (HRP) after injection into the ischiocavernosus (IC) muscle and their morphology assessed. Measures of the radial extent and coverage of the dendritic arbor of DLN motoneurons projecting to the IC (DLN-IC motoneurons) were similar across the groups, indicating comparable degrees of HRP transport. However, DLN-IC motoneurons in castrates with blank implants possessed both shorter dendritic lengths and smaller somas than those of castrates treated with testosterone. Castrates with testosterone implants had DLN-IC motoneurons that were significantly larger than those of sham castrates in dendritic length and soma area. These results suggest that motoneurons in the DLN, like those in the SNB, possess a significant degree of structural plasticity in adulthood which is influenced by androgens.

Morphology of rat spinal motoneurons with normal and hormonally altered specificity

Potential determinants of motoneuronal morphology were examined by using a sexually dimorphic, steroid-sensitive neuromuscular system in the rat spinal cord. In males, the spinal nucleus of the bulbocavernosus (SNB) innervates the perineal muscles bulbocavernosus (BC) and levator ani (LA), and the dorsolateral nucleus (DLN) innervates the ischiocavernosus muscle (IC). Adult females normally lack these motoneurons and the peripheral targets. Prenatal exposure of females to the androgen dihydrotestosterone propionate (DHTP) partially masculinizes this neuromuscular system and alters moto-neuron-to-muscle specificity, resulting in retained SNB target muscles anomalously innervated by motoneurons in the DLN. Because the morphology of SNB and DLN motoneurons normally differs significantly, the influence of spinal cord location and peripheral target on motoneuron morphology can be directly compared. Injection of cholera toxin conjugated to horseradish peroxidase (CTHRP) into the LA of DHTP-treated females labeled motoneurons predominantly in the SNB. These (SNB-LA) motoneurons in DHTP females were identical in all morphological measures to those of normal males. CTHRP injection into the BC of DHTP females labeled motoneurons in both the SNB and the DLN. SNB-BC motoneurons in DHTP females resembled those of normal males in process number and orientation, but were significantly smaller in dendritic length per motoneuron and in soma size. The DLN motoneurons anomalously projecting to the BC in DHTP females differed significantly from SNB-BC motoneurons in soma size and number and orientation of primary processes. However, these motoneurons were identical in all respects to DLN-IC motoneurons in DHTP females; DLN-IC motoneurons were similar to those of normal males in the orientation of their dendritic arbor, but were significantly smaller in dendritic length, soma size, and number of primary processes. These comparisons make it clear that DHTP selectively affects motoneuronal specificity and morphology in specific motoneuron classes. Further, motoneuronal morphology in the SNB/DLN system appears to be influenced more by spinal cord location than by peripheral target.

Gap junctions between lateral spinal motoneurons in the rat

Ultrastructural examination reveals gap junctional plaques between motoneurons in the dorsolateral nucleus (DLN), an androgen-sensitive motor nucleus in the lumbar spinal cord of rats. This nucleus contains motoneurons innervating the ischiocavernosus muscle and urethral sphincter. Gap junctional plaques were found along the somatic and proximal dendritic membranes of DLN motoneurons, and between membranes of bundled dendrites in the neuropil of this nucleus. Castration and androgen treatment had no significant effect on the size or frequency of gap junctions.

Hormonal control of neuron number in sexually dimorphic spinal nuclei of the rat: I. Testosterone-regulated death in the dorsolateral nucleus.

Adult male rats have substantially more motoneurons than do females in two motor nuclei in the lumbar spinal cord: the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN). Previous studies of the development of the SNB revealed that the sex difference in SNB motoneuron number is established through a differential motoneuron death which is under the control of androgens. In this study the development of the sexually dimorphic DLN was examined to test the hypothesis that early androgen action also determines the sex difference in DLN motoneuron number by regulating normally occurring motoneuron death. Because SNB motoneurons may migrate from the DLN, quantitative examination of DLN development was necessary in order to understand more completely the cellular mechanisms contributing to the establishment of dimorphic motoneuron number. At 5 days before birth, the number of motoneurons in the DLN is significantly higher than in adulthood in both sexes, and no sex difference is present. There is a decrease in motoneuron numbers prenatally in both sexes, which is consistent with the emigration of presumptive SNB motoneurons. Motoneuron number declines differentially through the first week of postnatal life and by postnatal day 10 motoneuron numbers are in the adult range and the sex difference is fully expressed. Females lose significantly more DLN motoneurons than males through a differential death as revealed by the higher incidence of degenerating cell profiles. Females treated with testosterone propionate have a male-typical motoneuron loss and incidence of degenerating cells. These results indicate that steroid hormones establish the sex difference in DLN motoneuron number by regulating normally occurring cell death.

Hormonal control of neuron number in sexually dimorphic spinal nuclei of the rat: III. Differential effects of the androgen dihydrotestosterone.

The spinal cord of the rat contains two sexually dimorphic nuclei: the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN). These nuclei and the perineal muscles they innervate are present in males but reduced or absent in females. The sex difference in motoneuron number in these nuclei is due to an androgen-regulated motoneuron death. Developing females treated with the androgen testosterone propionate (TP) have a fully masculine number of SNB and DLN motoneurons and retain the perineal muscles they would normally have lost. Paradoxically, females treated prenatally with the androgen dihydrotestosterone propionate (DHTP) also retain the perineal musculature but as adults lack the SNB motoneurons which would normally innervate them. The SNB target muscles retained by DHTP females are anomalously innervated by motoneurons in the DLN. Counts of motoneurons and degenerating cells in the developing SNB of DHTP-treated females showed that their feminine number is the result of a failure of DHTP to prevent the death of SNB motoneurons. Furthermore, the peak number of SNB motoneurons was below that of normal females, suggesting that DHTP treatment may also have inhibited motoneuronal migration. However, DHTP treatment fully masculinized both motoneuron number and degenerating cell counts in the DLN of these females, and it is this masculinized DLN that gives rise to the anomalous projection. Taken together, these results suggest that the effects of different androgens during development are specific and complex, involving the regulation of motoneuron death, migration, and specification of peripheral projections.

Electrophysiological properties of neurons in the A1 area projecting to the paraventricular nucleus of the hypothalamus in rats

The lumbar spinal cord of the rat contains two sexually dimorphic motor nuclei, the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN). Postnatally, SNB and DLN motoneurons grow substantially and reach their adult morphology by 7 weeks of age. The masculinization of SNB and DLN motoneuron dendrites depends upon steroid hormones. After early castration, the growth of SNB and DLN dendrites is markedly attenuated, but testosterone replacement restores this growth. In the SNB, initial dendritic growth is also supported in castrates treated with estrogen. By using castration and hormone replacement techniques, we examined the development of DLN motoneuron morphology in estrogen-treated castrated rats to determine if estrogen also supports the growth of DLN motoneurons. In addition, given that dorsal root ganglia may be a site of estrogen action, we tested the hypothesis that estrogen acts at primary afferents to support DLN dendritic growth. Thus, we attempted to block the potential trophic effect of estrogen by performing unilateral dorsal rhizotomies in estrogen-treated castrates. DLN motoneuron morphology was analyzed at 4 and 7 weeks of age by using cholera toxin horseradish peroxidase (BHRP) histochemistry. As found for SNB motoneurons, estrogen treatment transiently supported development. DLN motoneurons in estrogen-treated castrates developed normally through 4 weeks of age, but by 7 weeks, DLN motoneuron morphology in estrogen-treated castrates was no longer different from that in oil-treated castrates. Moreover, deafferentation via unilateral dorsal rhizotomy did not inhibit estrogen's ability to masculinize the early development of DLN motoneurons. Thus, the trophic effect of estrogen did not appear to act via the dorsal root ganglia to support the early postnatal development of DLN motoneurons.