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Sunday, July 13, 2008

Day 168 Part 2

^^

Continuous Conduction.

At rest potential, -70mV, there is a high concentration of Na+ ions outside and high concentration of K+ ions inside the neurone. when the neurone is stimulated, local Na+ voltage-gated channels open and Na+ rush into the neurone. This causes depolarisation of the membrane to the Threshold Potential, -50mV. At or above the threshold potential, all the local Na+ voltage gated channels open and further influr of Na+ results in an action potential.

Depolarisation spreads to the portion of the membrane just ahead of the action potential. Depolarisation causes the membrane potential to reach the threshold level. All the Na+ ions channels will open and further influx of Na+ ions results in an action potential. Behind the action potential, the Na+ ions channels close and the K+ ion channels will open. K+ ions begin to move out of the neurone and the membrane is repolarised. Hyperpolarisation takes place when too much K+ ion leaves the neurone and the channel din close in time. thus causing the membrane potentail to go below -70 mV. the K= ion channels are closed and the resting potential is reestablished via Na+ and K+ pump.

Druing the restoration of resting potential right after the refractory period, the Na+ K+ pumps pump 3 Na+ ions out for every 2 K+ ions taken in. this restores the unequal distribution of Na+ and K+ ions in the intracellular and extracellular fluids at resting potentail and therefore allows another nerve impulse to be transmitted.

Once an action potential ioccurs at one end of the neurone, it will reach the other end of the neurone. note that an action potential does not actually tavel but is regenerated anew at each postion along the neurone.

Saltatory Conduction (along myelinated neurone).

Na+ and K+ cannot flow through the myelin sheath therefore depolarisation cant occur in axons covered with myelin sheath.instead, Na+ ions generated by the action potential at a node of Ranvier diffuses with the axoplasm, to cause a depolarisation and a new action potential at the next node of Ranvier.

The action potential theus jumps from one node of Ranvier to another along the axon. therefore the voltage gated ion channels are concentrated in the nodes of Ranvier.

!@#@#$@#%#$%^!@#$@$@$#@#!@!~!

Chemical Synapse.

A synapse is the point which an axon of one neurone comes into close contact with the dendrites of another neurone. however due to the present of a synaptic cleft, the electrical signal cant pass through. thus it have to be converted to chemical signals in the presynaptic membrane and reconverted in to electrical signals in the postsynaptic membrane.

the syanptic knob is the expansion od the terminal axon of a presynaptic neurone. its cytoplaasm contains many mitochondira and synaptic vesicles.

the synaptic vesicles contains neurotransmitters such as acetylcholine and noradrenaline.

Transimisson across a cholinergic synapse. (this is the SHIT!)

Arrival of action potential at the synaptic knob depolarises presynaptic membrane. Depolarisation results in an increase in the membrane premeablilty of Ca2+. Voltage gated calcium channels opens and Ca2+ influx into the cytoplasm of the presynaptic neurone. this influx of Ca2+ causes the synaptic vesicles to fuse with presynaptic membrane(how the hell did it cause the thing to go fuse?? like "HEY U vesicle. its time to fuse!") and discharge nerotransmitters by exocytosis in to the synaptic cleft. Acetylcholine disffuses across the synaptic cleft and binds to specific receptor sites on the postsynaptic membrane causing them to open chemically gated Na+ channels.

The receptor proteins on the cell surface membrane has a complementary shape to ACh so that ACh can temporarily bind with the receptors. Upon binding, this changes shape of the protein and tehrefore open the chemically gated Na+ channels.

Na+ ions rushes into the cytoplasm of the postsynaptic neurone resultiing in deolarisation of postsynaptic membrane. If the excitatory postsynaptic potential reaches threshold, an action potential is triggered in the postsynaptic neurone.

However, if the acetylcholine was to bound to the receptors, the Na+ ion channels will remain open and action potential will be fired continuously. therefore the acetylcholine bounded to the receptors are quickly broken down by the hydorltic enzyme, acetylcholinesterase.

choline is reabsorbed into the synaptic knob of th epresynaptic neurone and combined with the acetyl-coA to resynthesize acetylcholine. Acetylcholine is then repackaged into synaptic vesicles and ready for the next action potential. This removal of acetylcholine from the receptors ensures the effect of a nerotransmitter on a postsynaptic cell will be precise so that the next action potential arriving at the synapse will be transmitted. *note: that means action potential can only be triggered will everything is at still and a threshold potential occurs?*

At synapses using noradrenaline, noradrenaline is not hydrolyzed but its actively reabsorbed back into the presynaptic neurone for repackaging.

LOL!! great! i just typed out all the things i should know but i still dunno for the nervous control topical test tmr.

-.- how sweet~~

prelims in 45 days i guess...

and i got 45 days to finish up to 100 topics.

may the force be with me~~~

hmm.. i am still there!! yohu~ just that u cant see... * wave frantically*

see! i have become too insignificant already. ^^

covered by some guy who is shorter than me?!

!@#@#$#@%#$%^@$#!@#@#$@#!@#!

but his talent outshone me~ ^^

URGH~! finish bio then tok cock~

nono.. finish A level then talk. ^^

11:27 PM

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