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Basic Neurophysiology 2
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Mind Map on Basic Neurophysiology 2, created by tanitia.dooley on 14/04/2013.
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tanitia.dooley
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Basic Neurophysiology 2
cell types of the CNS
Neurons
10%, extensively branched, 50% of CNS volume
3 basic parts: dendrites & cell body, Axon, Axon terminals
dendrites receive signals from other neurone. Cell body contains the nucleus & controls growth & repair
axon-single process extending from cell body/collaterals-side branches from the axon-transmit & recieve signals from other neurone
terminals-connect with other neurons
Axon length varies: >1nm in projection neurons connecting to muscles/glands & very short in interneurons forming local circuits in spinal cord
Glial cells
90%, branch less extensively, 50% of CNS volume
contribute to brain function by playing supportive roles in support, nutrition, insulation & repair
astrocytes-fill spaces between neurone, store glycogen,regulate [K+] in extracellular fluid
Oligodendroglia (CNS), Schwann cells (PNS)-wrap myelin sheaths around axon
Microglia-small phagocytic immune cells, repair & inflammation
Neuronal Communication
presynaptic neuron conducts information towards the synapse, synapse junction between 2 neurone, postsynaptic neurone-conducts info away from synapse
2 types
electrical
local currents from APs flow through gap junctions between neurone-connexins form pore so ions etc that convey electrical signals can pass through
Bi-directional currents
No synaptic delay
Reflex patheays for rapid transmission
Embryonic tissue, inspiration (coordinating breathing) & saccadic eye movements (moving eyes side to side)
chemical
most common synapse in mammalian cells
unidirectional transmission of signal pre- to post-
axodendritic-post onto pre synapse/axosomatic-attatches to cell body/axoaxonic-neuron forms synapse with another pre-synaptic neurone
Otto Loewi & 'Vagusstof'-removed neurons,added fluid with chemical-heart rate slowed when no neurone present-found the chemical to be Ach
synaptic cleft-extracellular space between the terminal bouton & the post synaptic neuron mem.No direct transfer of current (via neurotransmitter)
synaptic vesicles dock at the active zone of the presynaptic neurone. APs arrive & depolarises the mem, Ca2+ channels open,Ca2+ flows in=vesicles fuse
chemicals released into cleft & bind receptors on the postsynaptic men (QUANTAL RELEASE).
chemicals actively re-uptaken back into vesicles in the presynaptic,degrade or diffuse
synaptic delay-time from AP arriving at synapse to AP in postsynaptic (~0.5ms)
EPSP-neurontransmitter binding to receptor on post causes the mem to DEPOLARISE (Na+ influx exceeds K+ efflux) CNS:glutamate
single EPSP not sufficient to generate AP. Graded potential-summation required to reach threshold
1000's synapses can simultaneously fire a single neurone, activate different channels & receptors in postsyn. Integration of all EPSPs & IPSPs
= NEURAL COMPUTATION (all or nothing decision-AP fired or not)
spatial summation-signals from pres to one post at the same time, allows threshold to be met & AP fired
Temporal- single pre sends multiple signals in succession-mem potential doesnt have time to return to normal so when second fired=increase & so on...
shunting inhibition-if inhibitory synapse activated at same time as excitatory, the depolarising current leaks out before it reaches the soma
IPSP-neurotransmitter binding causes HYPERPOLARISATION (Cl- influx or K+ efflux) CNS:GABA
Facilitation & fatigue-with repeated presyn stimulation,post response is amplified (EPSP/IPSP) OR decreased.
Facilitation=increase- beneficial-learning or detrimental-chronic pain (signal bigger after continual stimuli=greater pain)
Fatigue-depletion of neurotransmitter stores at presynaptoc terminal-cant produce response as great as in the past
Muscle types (autonomic NS)
smooth muscle (GI tract, blood vessels, uterus)
striated muscle
skeletal (movement, attatched to bone-motor neurone)
each muscle is enclosed in a sheath of connective tissue. Within each muscle are hundreds of muscle fibres
each muscle fibre innervated by a single axon from the CNS. Multiple fibres innervated by branches of one nerve-coordinated contraction of many fibres
somatic motor neurons-nerves that innervate skeletal muscle fibres
cell bodies in spinal cord or brainstem, long branched dendrites which recieve many synaptic connections
myelinated axons & largest diameter-fast conduction. Axon terminates in NMJ-motor endplate
NMJ
presynaptic nerve, postsynaptic mem of muscle-plasma mem of muscle cell highly folded with many Ach receptors in folds
Ach channels-'all or none'-single channel secured in a portion of mem-either open or closed so always generated same current
but random duration of opening for single channel (mean=1ms)
curent can depend on other factors: no. of open channels, Ach conc, channel conductance & mem potential
1. AP triggered in motor neuron 2.depolarisation of motor terminal mem
3.depolarisation opens Ca2+, flows in-interferrs with docking process between snaar proteins & vesicles=vesicles fuse with mem=release Ach in cleft
4.Ach binds to ligand-gated nicotinic Ach receptors=depolarisation of muscle cell mem which causes voltage gated channels to open
rapid removal of Ach=diffusion away from receptor/breakdown by acetylcholinesterase,reuptake of choline into presynaptic via Na+ co-transporter
& recycling into vesicles via ATP driven H+ counter-transport
Ach is released in bursts /guanta. Single quantum causes only a slight depolarization, called a miniature end-plate potential (MEPP)
100-200quanta released simultaneously by a nerve impulse, cause multiple MEPPs=summate to produce an EPP=massive depolarisation (-20mv)=
voltage gated Na+ channels open
EPP's different from post synaptic potentials (IPSPs, EPSPs)
drugs & toxins that block NMJ transmission
Fugu-sushi delicacy (pufferfish)-tetrodotoxin-block voltage-gated Na+ channels so no AP in nerve-rapid decending paralysis & cardiovascular collapse
Black widow spider venom-binds receptors on presynaptic mems=increases Ca2+ influx-excessive vesicle release rapidly depletes stores=no neurotransmiss
Cobra bite-a-bungarotoxin binds Ach receptor-prevents receptor activation=paralysis of respiratory muscle
Curare-arrow tip poison-south american indians use to paralyse prey-Ach receptor antagonist
Organophosphates-compounds used in insecticides-block breakdown of Ach by acetylcholinesterases-were used in medicated shampoo-linked to brain damage
botulinum toxin-from bacterium clostridium botulinum-interferes with vesicle docking at synapse-blocks neurotransmitter release=no contraction (BOTOX)
Myasthenia Gravis-autoimmune-body produces Abs to Ach receptors=reduced mepps,smoothed endplate folds,loss of receptors,hypersensitivity to blockers
respond to drugs that inhibit cholinesterase's & prolong action of Ach
Cardiac (heart, change in heart rate , contracting is autonomous)
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