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Autonomic nerves, apart from the preganglionic motor axons arising from the CNS, are formed by the neural crest. The autonomic nervous system includes the sympathetic and parasympathetic neurones in the peripheral ganglia and their accompanying glia, the enteric nervous system and glia, and the suprarenal medulla.

In the trunk at neurulation, neural crest cells migrate from the neural epithelium to lie transitorily on the fused neural tube. Thereafter crest cells migrate laterally and then ventrally to their respective destinations (Fig. 24.11). Within the head the neural crest cells migrate prior to neural fusion, producing a vast mesenchymal population as well as autonomic neurones.

The four major regions of neural crest cell distribution to the autonomic nervous system are cranial, vagal, trunk and lumbosacral. The cranial neural crest gives rise to the cranial parasympathetic ganglia, whereas the vagal neural crest gives rise to the thoracic parasympathetic ganglia. The trunk neural crest gives rise to the sympathetic ganglia, mainly the paravertebral ganglia, and suprarenomedullary cells. This category is often referred to as the sympathosuprarenal lineage.

Neurones of the enteric nervous system are described as arising from the vagal crest, i.e. neural crest derived from somite levels 1–7, and the sacral crest, caudal to the 28th somite. At all of these levels the crest cells also differentiate into glial-like support cells alongside the neurones (Fig. 24.19).


Fig. 24.19  The derivatives of neural crest cells in the trunk. The fate of crest cells arising at particular somite levels is shown.

Parasympathetic ganglia

Neural crest cells migrate from the region of the mesencephalon and rhombencephalon prior to neural tube closure. From rostral to caudal, three populations of neural crest have been noted: cranial neural crest, cardiac neural crest and vagal neural crest. The migration of the sacral neural crest and the formation of the caudal parasympathetic ganglia have attracted little research interest.

Neural crest cells from the caudal third of the mesencephalon and the rostral metencephalon migrate along or close to the ophthalmic branch of the trigeminal nerve and give rise to the ciliary ganglion. Cells migrating from the nucleus of the oculomotor nerve may also contribute to the ganglion; a few scattered cells are always demonstrable in postnatal life along the course of this nerve. Preotic myelencephalic neural crest cells give rise to the pterygopalatine ganglion, which may also receive contributions from the ganglia of the trigeminal and facial nerves. The otic and submandibular ganglia are also derived from myelencephalic neural crest and may receive contributions from the glossopharyngeal and facial cranial nerves respectively (see Fig. 12.4).

Neural crest from the region located between the otic placode and the caudal limit of somite 3 has been termed cardiac neural crest. Cells derived from these levels migrate through pharyngeal arches 3, 4, and 6 where they provide, inter alia, support for the embryonic aortic arch arteries, cells of the aorticopulmonary septum and truncus arteriosus. Some of these neural crest cells also differentiate into the neural anlage of the parasympathetic ganglia of the heart. Sensory innervation of the heart is from the inferior ganglion of the vagus, which is derived from the nodose placodes. Neural crest cells migrating from the level of somites 1–7 are collectively termed vagal neural crest; they migrate to the gut along with sacral neural crest.

Sympathetic ganglia

Neural crest cells migrate ventrally within the body segments, penetrate the underlying somites and continue to the region of the future paravertebral and prevertebral plexuses, where they form the sympathetic chain of ganglia and the major ganglia around the ventral visceral branches of the abdominal aorta (Figs 24.11 and 24.19). Neural crest cells are induced to differentiate into sympathetic neurones by the dorsal aorta through the actions of the signaling molecules, Bmp-4 and Bmp-7.

There is cell specific recognition of postganglionic neurones and the growth cones of sympathetic preganglionic neurones. They meet during their growth, and this may be important in guidance to their appropriate target. The position of postganglionic neurones, and the exit point from the spinal cord of preganglionic neurones, may influence the types of synaptic connections made, and the affinity for particular postganglionic neurones. When a postganglionic neuroblast is in place it extends axons and dendrites and synaptogenesis occurs. The earliest axonal outgrowths from the superior cervical ganglion occur at about stage 14: although the axon is the first cell process to appear, the position of the neurones does not apparently influence the appearance of the cell processes.

The local environment plays a major role in controlling the appropriate differentiation of the presumptive autonomic ganglion neurones. The identity of the factors responsible for subsequent adrenergic, cholinergic or peptidergic phenotype has yet to be elucidated: it has been proposed that fibronectin and basal lamina components initiate adrenergic phenotypic expression at the expense of melanocyte numbers. Cholinergic characteristics are acquired relatively early and the appropriate phenotypic expression may be promoted by cholinergic differentiation factor and ciliary neurotrophic factor.

Neuropeptides are expressed by autonomic neurones in vitro and may be stimulated by various target tissue factors in sympathetic and parasympathetic neurones. Some neuropeptides are expressed more intensely during early stages of ganglion formation.

Enteric nervous system

The enteric nervous system is different from the other components of the autonomic nervous system because it can mediate reflex activity independently of control by the brain and spinal cord. The number of enteric neurones that develop is believed to be of the same magnitude as the number of neurones in the spinal cord, whereas the number of preganglionic fibres that supply the intestine, and therefore modulate the enteric neurones, is much fewer.

The enteric nervous system is derived from the neural crest. The axial levels of crest origin are shown in Fig. 24.19. Premigratory neural crest cells are not prepatterned for specific axial levels, rather they attain their axial value as they leave the neuraxis. Once within the gut wall there is a regionally specific pattern of enteric ganglia formation which may be controlled by the local splanchnopleuric mesenchyme. Cranial neural crest from somite levels 1–7 contributes to the enteric nervous system, forming both neuroblasts and glial support cells.

The most caudal derivatives of neural crest cells, from the lumbosacral region, somites 28 onwards, form components of the pelvic plexus after migrating through the somites towards the level of the colon, rectum and cloaca. Initially the cells come to lie within the developing mesentery, then transiently between the layers of the differentiating muscularis externa, before finally forming a more substantial intramural plexus characteristic of the adult enteric nervous system.

Of the neural crest cells that colonize the bowel, some in the foregut may acquire the ability to migrate outwards and colonize the developing pancreas.

Hirschsprung’s disease appears to result from a failure of neural crest cells to colonize the gut wall appropriately. The condition is characterized by a dilated segment of colon proximally and lack of peristalsis in the segment distal to the dilatation. Infants with Hirschsprung’s disease show delay in the passage of meconium, constipation, vomiting and abdominal distension. In humans, Hirschsprung’s disease is often seen associated with other defects of neural crest development, e.g. Waardenburg type II syndrome, which includes deafness and facial clefts with megacolon.

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