postsynaptic membranes. Questions also arise regarding how the growth of the axons is regulated, what makes them stop growing when they reach their target cells, and what brings about the changes in the ultrastructural organization of the cytoskeleton that results in metamorphosis of the growth cone (axon tip) into the normal nerve terminal. Much research during the past decade has attempted to answer these and other questions relating to the process of synaptogen-esis. Today, we have some insight into the mechanism, but we do not know all the details of the mysterious method whereby neurons establish their synaptic interconnections.

Many suggestions have been put forward to explain neuronal specificity in synaptogenesis. Sperry first proposed a chemoaffinity hypothesis that postulates that the specificity of neuronal connections is conferred by specific interactions between molecular addresses in the presynaptic membrane and the complementary molecules residing in the postsynaptic target membrane. This hypothesis is based on studies of presynaptic retinal neurons and the postsynaptic target neurons in the tectum. Hoffman and Edelman discovered a sialic acid-rich neuronal glycoprotein, termed N-CAM (neural cell adhesion molecule), that mediates intercellular adhesion in the absence ofCa2+. This glycoprotein might be a part of the molecular address (mentioned previously) on neuronal membranes that is recognized by specific receptor sites on target neurons, and it may be important in the development of the nervous system by maintaining the topographical relationships between individual neurons and/or their axons in a set of neurons.

During the formation of a synapse, a complex series of ultrastructural changes occur, notably in the synapsing axon and its tip. The net result is that the axon stops growing in length and its tip (the growth cone) takes the shape of a typical nerve terminal.

3. Orchestration at the Synapse

Another important aspect of synaptogenesis is the molecular and structural reorganization in the post-synaptic membrane upon formation of a synapse with a prospective presynaptic nerve terminal. It is conceivable that the receptor proteins in the postsynaptic membrane must be aligned exactly opposite to the sites in the presynaptic membrane where the transmitters are released. Such alignment is maintained as long as the membrane participates in synaptic activity. Indeed, during early periods of development when synapses have not yet formed, the transmitter receptor proteins are distributed throughout the membrane surface of the postsynaptic cell. Also, during nerve degeneration, the receptor proteins disperse and the whole orchestration at the synapse breaks down. On the other hand, during synapse formation as well as during nerve regeneration, the receptor proteins aggregate themselves again to form clusters at the point of synaptic junctions. Thus, some signal mechanism must exist that regulates the behavior of the postsynaptic membrane during synaptogenesis and synaptic degeneration.

Aspergers Answers Revealed

Aspergers Answers Revealed

Learn How to Help, Understand amp Cope with your Aspergers Child from a UK Chartered Educational Psychologist. Before beginning any practice relating to Aspergers it is highly recommended that you first obtain the consent and advice of a qualified health,education or social care professional.

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