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5.1.3 Neuronal Communication, Produced by Schwann cells: grow around the…

- - - - 2 main features of sensory receptors (1) Specific to a single type of stimulus
        (2) Role as Transducer - convert stimulus into nerve impulse
    - - Mechanoreceptor → Stim: Pressure + movement → E.g. Pacinian corpuscle (detects pressure) IN deep SKIN (sense organ), abundant in fingers + soles + joints
        
        Pacinian corpuscle (SENSORY RECEPTOR)
        
        HOW P.C CONVERTS MECHANICAL PRESSURE → NERVE IMPULSE?
        
        @ Resting state, stretch-mediated [Na+] channels in the sensory neurone's membrane are too narrow for Na+ to pass. The neurone of P.C has resting potential
        
        When pressure is applied to P.C it changes shape = sensory neurone's membrane stretches
        
        S.N's Membrane stretches = [Na+] channels widen = Na+ diffuse into neurone
        
        Influx of positive [Na+] changes the potential of membrane - becomes depolarised. This results in a generator potential
        
        The generator potential creates an action potential (nerve impulse) that passes along the sensory neurone
        The action potential will be transmitted along neurones to the CNS
        
        INSIDE the P.C
      - Chemoreceptor → Stim: Chemicals → E.g. Olfactory receptor IN NOSE (sense organ)
      - Thermoreceptor → Stim: Heat → E.g. End-bulbs of Krause IN TONGUE (sense organ)
      - Photoreceptor → Stim: Light → E.g. Cone cells (detect diff light wavelengths) IN EYES (sense organ)
- - - - 🔴 NEUROTRANSMITTERS: chemicals which are used to transmit impulse from one neurone to the next
        
        2 TYPES OF NEUROTRANSMITTERS:
        
        1. EXCITATORY: result in DEPOLARISATION of POSTsynaptic neurone → IF DEPOLARISATION meets threshold →A.P generated in POSTsynaptic membrane
        
        E.G. ACh, Noradrenaline are all for inhibitory synapses
        
        2. INHIBTORY: result in HYPERPOLARISATION of POSTsynaptic membrane → prevents A.P generation → E.G. GABA found in some synapses in brain
        
        How?
        
        PresN releases an A.P which causes Ntr to be released
        
        Ntr binds and causes [Cl-] receptor/channels OPEN → [Cl-] enters via facilitated diffusion
        
        [Cl-] causes K+ channels to OPEN → K+ move out of PostsN into Synaptic cleft
        HYPERPOLARISATION occurs
        
        no new A.P occurs
    - - Axon's membrane
        
        RESTING POTENTIAL (-70mV) [3 steps]
        
        NO impulse transmitted
        
        Outside of axon membrane = MORE +ve charged >>> -ve inside axon
        
        Axon membrane = polarised because potential difference of -70mV
        
        (1) SODIUM-POTASSIUM PUMP (An intrinsic carrier protein) actively transports every 3 Na+ ion OUT of the axon = 2 K+ ion actively transported INTO the axon
        
        (2) More Na+ ions outside membrane> inside & More K+ inside cytoplasm> outside membrane.
        THEREFORE:
        
        Na+ ions diffuse back into axon down electrochemical gradient
        
        K+ ions diffuse out of the axon
        
        (3) However MOST gated Na+ ion channels closed - preventing movement Na+ ions
        BUT.. many K+ ion channels open = allowing K+ ions to diffuse out of the axon
        So.. More +ve charged ions outside axon >> inside, creating resting potential of (-70mV inside axon)
        
        ACTION POTENTIAL (+40mV) [6 steps]
        
        Occurs when voltage-gated ion channels (protein channels) in the axon membrane change shape (channel open/close) AS A RESULT of change of voltage across its membrane
        
        (1) Neurone @ resting potential = no transmission of impulse
        
        SOME K+ ion channels open (mainly NON-voltage-gated)
        
        ALL Na+ voltage-gated CLOSED
        
        (2) When the membrane potential reaches approximately –55 mV (threshold potential), voltage-gated sodium channels open, leading to depolarisation.
        Now DEPOLARISATION occurs:
        
        Stimulus' energy trigger ~ some Na+ voltage-gated channel to open = membrane more permeable to Na+ ion to diffuse down the electrochemical gradient
        
        SO now, inside the neurone less negative
        
        (3) E.G of Positive feedback: Change in charge → MORE Na+ ion channels OPEN = allowing MORE Na+ ions to diffuse into axon P.D reaches ~+40mV
        
        (4) Now need REPOLARISATION:
        
        Na+ V.G channels close = K+ V.G channels OPEN! = more permeable to K+
        
        K+ ions diffuse out of the axon down electrochemical gradient → the axon becomes more negative inside < outside
        
        1 more item...
        
        PROPAGATION OF ACTION POTENTIALS
        
        @ Resting potential → More Na+ outside (overall more positive) & More K+ inside axon (overall less positive) ∴ axon membrane is polarised (-ve)
        
        Stimulus causes sudden influx of Na+ & reversal of charge on axon membrane. ∴ Action potential + membrane is depolarised
        
        Influx of Na+ causes → New region: More V.G Na+ channels to open further along the axon so depolarisation occurs
        &
        Old region: Behind the V.G Na+ close & V.G K+ open → K+ leave axon down echmclgra
        
        So, action potential is propagated along the axon
        & Old region: K+ leaves until the region returns to original charged state (1.) so repolarised!
        
        Following repolarisation of axon → returns to resting potential ready for new stimulus
        
        🔴 REFRACTORY PERIOD: short period of time when the axon cannot be excited
        
        V.G Na+ channels CLOSED
        
        IMPORTANT:
        
        Prevents the propagation of an A.P backwards along the axon
        
        Ensures A.P are are unidirectional, do not overlap and occur as discrete impulses
        
        SIGNIFICANCE OF FREQUENCY OF IMPULSE TRANSMISSION
        
        Factors affect Speed of Conduction/A.P:
        
        Axon diameter - BIGGER Axon = Faster impulse transmission → less resistance to flow of ions in cytoplasm
        
        Temp - HIGHER Temp = faster nerve impulse → ions diffuse faster @ higher temp ~4) degrees or proteins will denature like (Na/K pump)
        
        Nerve impulses are ALL-OR-NOTHING RESPONSES
        
        IF ONLY threshold is reached → A.P generated
        
        DIFF SIZE STIMULI = SAME SIZE A.P
        
        Bigger stimulus = MORE frequent A.P generated in a given time
  - - - 🔴 Motor neurone: transmit impulses from a relay/sensory neurone → effector.
        Has 1 long axon and many short dendrites
      - 🔴 Relay neurone: transmit impulses between neurones. Has many short axons and dendrons
      - 🔴 Sensory neurone: Have 1 dendron (carries impulse to the cell body) and 1 axon (carries impulse away from the cell body)
- - - - Synaptic cleft: gap which separates one neurone's axon and next neurone's dendrite
      - PREsynaptic neurone: neurone along which impulse has arrived
      - Synaptic vesicles: containing neurotransmitters. → Vesicles fuse with PREsynaptic membrane and release neurotransmitters into Synaptic cleft
      - POSTsynaptic neurone: neurone that receives neurotransmitters
      - Synaptic knob: swollen end of PREsynaptic neurone
        
        CONTAINS many Mitochondria & Endoplasmic Reticulum → to enable production of neurotransmitters
      - Neurotransmitters Receptors: receptor molecules which the neurotransmitter BINDS to in the POSTsynaptic membrane
    - - Each stimulus from PREsynaptic neurone = release same amount neurotransmitters
        
        OR
        
        🔴 Summation: When the amount of neurotransmitter builds up to sufficiently reach the threshold to trigger an A.P
        
        Temporal summation:
        
        1 PREsN has several A.P in a short time period (quick succession) building up the release of neurotransmitters in the synapse until sufficient quantity to trigger A.P in POSTsN
        
        Spatial summation:
        
        MANY of PREsynaptic neurones connect to → 1 POSTsynaptic neurone
        ↳ Each PREsN releases neurotransmitters to reach high threshold level in the synapse to trigger an A.P in the 1 POSTsN
      - Transmission of impulse across synapses
        
        A.P reaches end of PREsynaptic neurone
        
        DEPOLARISATION of PREsynaptic neurone → Ca2+ channels to OPEN
        
        Ca2+ diffuse into PREsynaptic knob → synaptic vesicles (contain neurotransmitters) FUSE with PREsynaptic m.
        
        Neurotransmitters diffuse across synaptic cleft
        
        Neurotransmitters BIND to specific N. Receptor molecule on POSTsynaptic membrane → Na+ channels to OPEN & diffuse into POSTsynaptic neurone
        
        Triggers an A.P & Impulse is propagated along POSTsynaptic neurone
        IMPORTANT: Once Neurotransmitter triggers A.P, it should be removed so: stimulus not maintained & another stimuli can arrive at to affect the synapse. Any left in synaptic cleft is removed preventing → E.G Acetylcholine broken down by enzymes & released from N. Receptors → Products taken to PREsynaptic knob!
        
        E.G. Transmission across Cholinergic synapses using Acetylcholine
        
        Arrival of A.P at PREsynaptic neurone → Ca2+ channels OPEN for Ca2+ to enter synaptic knob
        
        Influx of Ca2+ into PREsynaptic neurone → Vesicles fusing with PREsynaptic membrane → releasing Acetylcholine into synaptic cleft
        
        Acetylcholine fuse with receptor site on Na+ channel in membrane of POSTsynaptic neurone → Na+ channel OPEN so Na+ diffuse down into echmclgra
        
        Influence of Na+ generates a new A.P in the POSTsynaptic neurone
        
        Enzy. Acetylcholinesterase HYDROLYSES Acetylcholine → Choline + Ethanoic acid diffusing back across synaptic cleft into PREsynaptic neurone = recycling. && Breakdown of Acetylcholine prevents continuous generation of new A.P in POSTsynaptic neurone
        
        ATP released by Mitochondria to recombine ethanoic acid + choline & stored in vesicles. Na+ channels CLOSE = Absence Acetylcholine at receptor sites
        
        Cholinergic synapse
        
        common @ CNS of vertebrates & neuromuscular junction (where motor neurone and muscle cell (effector) meet)