lecture 12.docx

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Department
Cell and Systems Biology
Course
CSB332H1
Professor
Francis Bambico
Semester
Winter

Description
 Spinal cord injury and possible methods  Depends on where the injury is  Complete recovery has not be seen in severe injury to the CNS – there are some that show promises  Depends on intrinsic and extrinsic factor and substances around the damage  31 spinal nerves projecting from spinal cord; nerves are a cluster of axons  Each of these nerves consist of several layers  Entire nerve is covered by epineurium  Under epineurium are diff clusters of axons called fascicles which are covered by perineurium  Under perneurium are the individual axons which are covered by endoneurium (a tube)  Within endoneurium is where you’ll find the myelin sheaths  Common, less severe nerve injuries  Cyclists: handle bar palsy – compress ulnar nerve on the wrist  Soccer players: when they hit the ball with their head -> the stretch could injure the brachial plexus but recovery is possible; from hours to days  Carpal tunnel syndrome or repetitive movement injuries – strain or compress nerves such as medial nerve when you’re on the computer all the time  Several grades of injuries; there are less severe and more severe  common: neuropraxia – nerve compression or disruption of blood vessels; are reversible o does not result in regeneration o complete recovery in several mins to months  more severe: axonotmesis – actual severing or physical damage to the axons; o can result from lacerations/crushing o if the endoneurial and perineurial covering are intact – recovery is possible  most severe: neurotmesis – recovery is possible but extremely difficult o contusions, lacerations, severe stretch, toxicity o axon and CT are severed or displaced/loose in addition to axon being damaged o or entire nerve ripped off  symptoms: o severity increase as the severity of the damage increase o pain o fibrillation – contraction of the muscle fibre o normally, fibrillation and fasciculation are benign – don’t know what causes it but sometimes it means severe nerve damage when accompanied by other symptoms such as o loss of function, paralysis  when an axon is cut or severed, several events take place immediately after it’s severed  this order of events is called wallerian degeneration  immediately after the lesion, distal region of the neuron degenerates and detoriate  in response, macrophages from the blood stream infiltrate the region of the damage and clear out the debris and phagocytose the remnants of the neurons  this is adaptive because the clearing of the debris is necessary for the eventual regeneration  after phagocytosis, proximal region also degenerates but a stump is usually left  the cell body may still survive from the axotomy but there are some things that occur in the cell body including the shrinking of the cell body  chromatolysis occurs – the nissl bodies (RER) dissolve so loss of colour;  RER are usually purplish/violet colour  after denervation, they lose the purple colours  nucleus is dislocated  the Schwann cells begin to dedifferentiate – switch to embryonic form of Schwann cells  these sequence of events are called wallerian degeneration; happens in both PNS and CNS   Presynaptic input  Postsynaptic cell body shrinks -> presynaptic axons retract because of the absence of neurotropic factors that usually comes from postsynaptic neuron  These factors are usually taken up by dynein  If the growth factors  When you severe an axon, you block the transmission of the growth factors -> slow deterioration of the cell body   Postsynaptic region when an axon is severed  Increases ACh receptors  If we look into the NMJ, the postsynaptic target of the nerves are the muscle fibres  You would think the sensitivity of the muscle fibre is decreased BUT the sensitivity increases  increase in the number of receptors  the number of nicotinic receptors dramatically increase; can label the receptors with a radio active antagonist or agonists -> alpha-bungarotoxin (from snakes)  this has a high affinity for nicotinic receptors  using this technique, they found an increase in the number of acetycholine receptor   Nicotinic receptors are conc in the folds of the motor end plate  Upon axonotomy, many other nicotinic receptors start to emerge and cover a large expanse of the myofibre region, away from motor end plate region  But they are the embryonic form of the receptor, no adult form  Adult form has epsilon instead of gamma subunit found in embryonic form  Experimentally axotomize a motor neuron and at the same time, electrically stimulate the region of the injury, you can reduce the super sensitivity  Increase in nicotinic receptors was reversed by the electrical stimulation  This is the principle behind physiotherapy: stimulate and rehabilitate the muscle affected by the injury can hasten the recovery; exert systematic/orderly movements to naturally stimu
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