The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Edit The neuromuscular junction NMJ is the most well-characterized synapse in that it provides a simple and accessible structure that allows for easy manipulation and observation. The synapse itself is composed of three cells: In a normally functioning synapse, when a signal causes the motoneuron to depolarize, the motoneuron releases the neurotransmitter acetylcholine ACh.
Acetylcholine travels across the synaptic cleft where it reaches acetylcholine receptors AChR on A study on synaptogenesis plasma membrane of the myotube.
As the AChRs open ion channels, the membrane depolarizes, causing muscle contraction. The entire synapse is sheathed within a myelin cover provided by the Schwann cell to insulate and encapsulate the junction. The individual myoblasts originate in the mesoderm and fuse to form a multi-nucleated myotube.
During or shortly after myotube formation, motoneurons from the neural tube form preliminary contacts with the myotube. The Schwann cells arise from the neural crest and are led by the axons to their destination. Upon reaching it, they form a loose, unmyelinated covering over the innervating axons.
The movement of the axons and subsequently the Schwann cells is guided by the growth cone, a filamentous projection of the axon that actively searches for neurotrophins released by the myotube. Although it may seem that the axons specifically target the midpoint of the myotube, several factors reveal that this is not a valid claim.
It appears that after the initial axonal contact, the newly formed myotube proceeds to grow symmetrically from that point of innervation. Coupled with the fact that AChR density is the result of axonal contact instead of the cause, the structural patterns of muscle fibers can be attributed to both myotactic growth as well as axonal innervation.
There is evidence that Schwann cells may facilitate these prliminary signals by increasing the amount of spontaneous neurotransmitter release through small molecule signals. This pioneer axon is of crucial importance because the new axons that follow have a high propensity for forming contacts with well-established synapses.
This increased acmount of AChR allows for more effective transmission of synaptic signals, which in turn leads to a more-developed synapse. This high concentration of AChR in the synapse is achieved through clustering of AChR, up-regulation of the AChR gene transcription in the post-synaptic nuclei, and down-regulation of the AChR gene in the non-synaptic nuclei.
The axon of the motoneuron releases agrin, a proteoglycan that initiates a cascade that eventually leads to AChR association. Agrin binds to a muscle-specific kinase MuSK receptor in the post-synaptic membrane, and this in turn leads to downstream activation of the cytoplasmic protein rapsyn.
Rapsyn contains domains that allow for AChR association and multimerization, and it is directly responsible for AChR clustering in the post-synaptic membrane: The axon also provides signals that regulate gene expression within the myonuclei directly beneath the synapse.
This signaling provides for localized up-regulation of transcription of AChR genes and consequent increase in local AChR concentration.
The two signaling molecules released by the axon are calcitonin gene-related peptide CGRP and neureglin, which trigger a series of kinases that eventually lead to transcriptional activation of the AChR genes. Reduced concentration of AChR in the extrasynaptic membrane in addition to increased concentration in the post-synaptic membrane helps ensure the fidelity of signals sent by the axon by localizing AChR to the synapse.
Because the synapse begins receiving inputs almost immediately after the motoneuron comes into contatct with the myotube, the axon quickly generates an action potential and releases ACh.Synaptogenesis in the Hippocampal CA1 Field following Traumatic Brain Injury S.W.
SCHEFF, D.A. PRICE, R.R. HICKS, S.A. BALDWIN, S. ROBINSON, ent study was designed to examine the time course of loss and replacement of synaptic contacts in. ideal model organism to study synaptic development and neural circuitry.
The organism has relatively simple nervous system, having neurons and its neurochemistry and genetics are reporter has been a key reagent to study synaptogenesis and its attheheels.coms(Nonet,;ShenandBargmann,; Frontiers in Synaptic .
Start studying Synaptogenesis. Learn vocabulary, terms, and more with flashcards, games, and other study tools.
Posts about Synaptogenesis written by Dana Smith. The brain is a plastic organ constantly changing and adapting, creating new connections with the inclusion of novel thoughts and memories, and losing others as we age and decay. Synaptogenesis. Synaptogenesis is a long developmental process involving synapse formation, synapse maintenance (stabilization), and activity-dependent synapse refinement and elimination, and is important for the establishment of the neuronal network and the precision of brain circuitry (Cohen-Cory, ).
Genetic Approach to the Study . Psychology Definition of SYNAPTOGENESIS: The formation of synapses between neurons as the axons and dendrites grow. Read also the experience-dependent process; experience-expectantPROCESS.