Embryonic development of a peripheral nervous system: Nerve tract associated cells and pioneer neurons in the antenna of the grasshopper Schistocerca gregaria

2007 ◽  
Vol 36 (3) ◽  
pp. 336-350 ◽  
Author(s):  
G.S. Boyan ◽  
J.L.D. Williams
Development ◽  
1991 ◽  
Vol 112 (1) ◽  
pp. 241-253 ◽  
Author(s):  
T. Meier ◽  
F. Chabaud ◽  
H. Reichert

To determine the generality of developmental mechanisms involved in the construction of the insect nervous system, the embryonic development of the peripheral nervous system in the grasshopper Schistocerca gregaria was characterized at the level of identified neurons and nerve branches and then compared to that previously described from the fly Drosophila melanogaster. For this, immunocytochemistry using a neuron-specific antibody was carried out on staged grasshopper embryos. Our results show that initially a simple peripheral nerve scaffolding is established in each segment of the animal. This scaffolding consists of a pair of intersegmental nerves that are formed by identified afferent and efferent pioneer neurons and a pair of segmental nerves that are formed by afferent pioneers situated in limb buds. Subsequently, identified sets of sensory neurons differentiate in a stereotyped spatiotemporal pattern in dorsal, lateral and ventral clusters in each segment and project their axons onto these nerves. Although segment-specific differences exist, serial homologs of the developing nerves and sensory neurons can be identified. A comparison of these results with those obtained from Drosophila shows that virtually the same pattern of peripheral nerves and sensory structures is formed in both species. This indicates that the construction of the peripheral nervous system in extremely divergent modern insects relies on conserved developmental mechanisms that evolved in ancestral insects over 300 million years ago.


2018 ◽  
Vol 34 (1) ◽  
pp. 495-521 ◽  
Author(s):  
Michele Curcio ◽  
Frank Bradke

After an injury in the adult mammalian central nervous system (CNS), lesioned axons fail to regenerate. This failure to regenerate contrasts with axons’ remarkable potential to grow during embryonic development and after an injury in the peripheral nervous system (PNS). Several intracellular mechanisms—including cytoskeletal dynamics, axonal transport and trafficking, signaling and transcription of regenerative programs, and epigenetic modifications—control axon regeneration. In this review, we describe how manipulation of intrinsic mechanisms elicits a regenerative response in different organisms and how strategies are implemented to form the basis of a future regenerative treatment after CNS injury.


Science ◽  
2019 ◽  
Vol 365 (6456) ◽  
pp. eaaw8231 ◽  
Author(s):  
Tracey A. C. S. Suter ◽  
Alexander Jaworski

The central and peripheral nervous system (CNS and PNS, respectively) are composed of distinct neuronal and glial cell types with specialized functional properties. However, a small number of select cells traverse the CNS-PNS boundary and connect these two major subdivisions of the nervous system. This pattern of segregation and selective connectivity is established during embryonic development, when neurons and glia migrate to their destinations and axons project to their targets. Here, we provide an overview of the cellular and molecular mechanisms that control cell migration and axon guidance at the vertebrate CNS-PNS border. We highlight recent advances on how cell bodies and axons are instructed to either cross or respect this boundary, and present open questions concerning the development and plasticity of the CNS-PNS interface.


Author(s):  
Eduardo E. Benarroch ◽  
Jeremy K. Cutsforth-Gregory ◽  
Kelly D. Flemming

The study of neuroscience begins with a survey of the embryonic development of the nervous system because it provides a framework and background for understanding the anatomy and function of the nervous system in the adult. The eventual location and connectivity of the structures in the brain, spinal cord, and peripheral nervous system reflect the orderly development of the nervous system.


Development ◽  
1998 ◽  
Vol 125 (10) ◽  
pp. 1845-1856 ◽  
Author(s):  
C.A. Dye ◽  
J.K. Lee ◽  
R.C. Atkinson ◽  
R. Brewster ◽  
P.L. Han ◽  
...  

Notch signaling is required in many invertebrate and vertebrate cells to promote proper cell fate determination. Mutations in sanpodo cause many different neuronal peripheral nervous system precursor cells to generate two identical daughter neurons, instead of a neuron and sibling cell. This phenotype is similar to that observed when Notch function is lost late in embryonic development and opposite to the numb loss-of-function phenotype. Genetic interaction studies show that sanpodo is epistatic to numb. sanpodo encodes a homolog of tropomodulin, an actin/tropomyosin-associated protein. Loss of sanpodo leads to an aberrant F-actin distribution and causes differentiation defects of actin-containing sensory structures. Our data suggest that an actin-based process is involved in Notch signaling.


Author(s):  
S.S. Spicer ◽  
B.A. Schulte

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.


2000 ◽  
Vol 5 (2) ◽  
pp. 3-3
Author(s):  
Christopher R. Brigham ◽  
James B. Talmage

Abstract Lesions of the peripheral nervous system (PNS), whether due to injury or illness, commonly result in residual symptoms and signs and, hence, permanent impairment. The AMA Guides to the Evaluation of Permanent Impairment (AMA Guides) describes procedures for rating upper extremity neural deficits in Chapter 3, The Musculoskeletal System, section 3.1k; Chapter 4, The Nervous System, section 4.4 provides additional information and an example. The AMA Guides also divides PNS deficits into sensory and motor and includes pain within the former. The impairment estimates take into account typical manifestations such as limited motion, atrophy, and reflex, trophic, and vasomotor deficits. Lesions of the peripheral nervous system may result in diminished sensation (anesthesia or hypesthesia), abnormal sensation (dysesthesia or paresthesia), or increased sensation (hyperesthesia). Lesions of motor nerves can result in weakness or paralysis of the muscles innervated. Spinal nerve deficits are identified by sensory loss or pain in the dermatome or weakness in the myotome supplied. The steps in estimating brachial plexus impairment are similar to those for spinal and peripheral nerves. Evaluators should take care not to rate the same impairment twice, eg, rating weakness resulting from a peripheral nerve injury and the joss of joint motion due to that weakness.


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