Basic Neurophysiology 2

cell types of the CNS
1. Neurons
  1. 10%, extensively branched, 50% of CNS volume
  2. 3 basic parts: dendrites & cell body, Axon, Axon terminals
    1. dendrites receive signals from other neurone. Cell body contains the nucleus & controls growth & repair
    2. axon-single process extending from cell body/collaterals-side branches from the axon-transmit & recieve signals from other neurone
      1. terminals-connect with other neurons
  3. Axon length varies: >1nm in projection neurons connecting to muscles/glands & very short in interneurons forming local circuits in spinal cord
2. Glial cells
  1. 90%, branch less extensively, 50% of CNS volume
    1. contribute to brain function by playing supportive roles in support, nutrition, insulation & repair
  2. astrocytes-fill spaces between neurone, store glycogen,regulate [K+] in extracellular fluid
  3. Oligodendroglia (CNS), Schwann cells (PNS)-wrap myelin sheaths around axon
  4. Microglia-small phagocytic immune cells, repair & inflammation
Neuronal Communication
1. presynaptic neuron conducts information towards the synapse, synapse junction between 2 neurone, postsynaptic neurone-conducts info away from synapse
2. 2 types
  1. electrical
    1. local currents from APs flow through gap junctions between neurone-connexins form pore so ions etc that convey electrical signals can pass through
    2. Bi-directional currents
    3. No synaptic delay
    4. Reflex patheays for rapid transmission
    5. Embryonic tissue, inspiration (coordinating breathing) & saccadic eye movements (moving eyes side to side)
  2. chemical
    1. most common synapse in mammalian cells
    2. unidirectional transmission of signal pre- to post-
      1. axodendritic-post onto pre synapse/axosomatic-attatches to cell body/axoaxonic-neuron forms synapse with another pre-synaptic neurone
    3. Otto Loewi & 'Vagusstof'-removed neurons,added fluid with chemical-heart rate slowed when no neurone present-found the chemical to be Ach
    4. synaptic cleft-extracellular space between the terminal bouton & the post synaptic neuron mem.No direct transfer of current (via neurotransmitter)
      1. 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
    5. synaptic delay-time from AP arriving at synapse to AP in postsynaptic (~0.5ms)
      1. EPSP-neurontransmitter binding to receptor on post causes the mem to DEPOLARISE (Na+ influx exceeds K+ efflux) CNS:glutamate
      2. 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
    6. IPSP-neurotransmitter binding causes HYPERPOLARISATION (Cl- influx or K+ efflux) CNS:GABA
    7. Facilitation & fatigue-with repeated presyn stimulation,post response is amplified (EPSP/IPSP) OR decreased.
      1. 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)
1. smooth muscle (GI tract, blood vessels, uterus)
2. striated muscle
  1. skeletal (movement, attatched to bone-motor neurone)
    1. each muscle is enclosed in a sheath of connective tissue. Within each muscle are hundreds of muscle fibres
      1. 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
    2. NMJ
      1. 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
      2. 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)
      3. 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
  2. Cardiac (heart, change in heart rate , contracting is autonomous)

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