NEURONES

Cards (32)

  • what is the state of the neurone when it is not stimulated/resting?
    membrane polarised- outside positively charged vs inside negatively charged
  • movement of Na+ & K+:
    • resting potential maintained by Sodium and potassium pumps and potassium ion channels
    • Na+ & K+ pumps actively transport to move 3 Na+ out of neurone for 2 K+ in - ATP recq
    • K+ channel allows for faciliated diffusio of K+ out of neurone- down conc grad
  • Movement of Sodium ions and Potassium ions:
    1. Na+ pump moves 3 Na+ out of neurone- membrane not permeable to Sodium, thus Na+ cannot diffuse back in - creates electrochemical gradient- + outside
    2. Na+&K+ pump moves 2 K+ into cell
    3. when cell at rest- most K+ channel open- membrane permeable to K+ - some diffuse out
  • what is an action potential?
    the process in which the cell membrane becomes depolarised
  • A.P: i
    STIMULUS:
    • excites neurone cell membrane- Na2+ voltage gated channel open
    • membrane more permeable to Na2+, Na2+ diffuse into neurone down Na2+ electrochemical gradient
    • inside membrane less negative
  • A.P: ii
    DEPOLARISATION:
    • if potential difference reaches threshold (-55mv) more Na2+ channels open=more Na2+ diffuse into neurone
  • A.P: iii
    REPOLARISATION:
    • at potential difference (+30mv) Na2+ channels close & K+ channels open- membrane permeable to K+
    • K+ moves out of neurone - returns membrane to resting potential
  • A.P: iv
    HYPERPOLARISATION:
    • K+ channels slow to close- slight overshoot- too many K+ diffuse out of neurone
    • potential difference more negative resting potential
  • A.P: v
    RESTING POTENTIAL:
    • ion channels reset
    • Na2+ K+ pump returns membrane to resting potential- sodium diffuses out, Potassium in
  • A.P: vi
    REFRACTORY PERIOD:
    • ion channels recovering- neurone membrane cannot be excited
    • Sodium ions closed during REPOLARISATION
    • Potassium ions closed during HYPERPOLARISATION
    • acts as time delay- action potential doesnt overlay & unidrectional
  • waves of Depolarisation:
    • some Na2+ enter neurone by diffusing in sideways- causes Na2+ channel to open in next region
    • wave of depolarisation travels along neurone - wave moves away from parts of Neurone cell membrane that is in refractory period
  • All or Nothing principle:
    • once threshold reached (-55mV) - A.P fires same change in voltage- no matter size of stimulus
    • if threshold is not reached- A.P not fired
    • bigger stimulus will not cause a greater A.P but will cause A.P to fire more frequently
  • Speed of CONDUCTION:
    • myelination
    • saltatory conduction
    • axon diameter
    • temperature
  • S.O.C - Myelination:
    • neurones, e,g Motor neurones are myelinate- have myelin sheath
    • Myelin Sheath is an electrical insulator
    • in peripheral nervous system- sheath made of Schwann Cells
    • Between Schwann cells- tiny patches of bare membrane - Nodes of Ranvier
    • Nodes of Ranvier- where most Sodium ion channels are concentrated
  • S.O.C - Saltatory Conduction:
    • in myelinated neurone- depolarisation occurs at N.O.R (Sodium ions can pass through membrane)
    • Cyptoplasm conducts enough electrical charge to depolarise next node - impulse jumps from node to node
    • in non- myelinated- impulse travels along the whole axon membrane - depolarisation across whole membrane - slower
  • S.O.C - Axon Diameter:
    • Action potential quicker along axon with bigger diameter- less resistance to flow of ions than in cyptoplasm of smaller axon
    • wave of depolarisation reaches parts of neurone cell membrane quicker with less resistance
  • S.O.C - Temperature:
    • speed of conduction increases as temperature increases- ions diffuse faster
    • speed increases only until 40*c - after which protein denatures e.g channels
  • synapse: junction between neurones or between neurone and effector cell
  • tiny gaps between cells at synapes- Synaptic Cleft
  • pre-synaptic neurone swelling - synaptic knob- containing synaptic vesicles filled with neurotransmitters
  • effect of A.P on neurone:
    1. A.P reaches end of neurone - causes N.T to be released into synaptic cleft
    2. diffuse across to post synaptic membrane and bind to specific receptors
    3. when N.T binded to receptors, trigger A.P in neurone- cause muscle contraction, Hormone secretion
    • receptors only on post synaptic membrane- synapse ensures unidirectional
    • N.T removed from cleft - response not repeated - taken back into pre-synaptic neurone or broken down by enzyme
  • Acetylcholine: a neurotransmitter which binds to cholinergic receptors on Cholinergic Synapses
  • Cholinergic Synapse-
    1. Arrival of Action Potential
    2. Fusion of Vesicles
    3. Diffusion of Acetylcholine
  • Cholinergic Synapse: Arrival of Action Potential
    • Action potential arrives at synaptic knob
    • Action potential stimulates voltage-gates calcium ion channels to open
    • Calcium ions diffuse into synaptic knob (later pumped out by active transport)
  • Cholinergic Synapse: Fusion of Vesicles
    • influx of calcium ions into synaptic knob causes synaptic vesicles to fuse with pre-synaptic membrane
    • Vesicles releases Acetylcholine into synapse cleft by exocytosis
  • Cholinergic Synapse: Diffusion of Acetylcholine
    • Acetylcholine diffuses acros synaptic cleft and binds to cholinergic receptors on post-synaptic membrane- causes sodium ion channels to open
    • influx of sodium ions into post-synaptic membrane causes depolarisation
    • Action Potential on post-synaptic membrane generated if threshold reached
    • Acetylcholine then removed from synaptic cleft - response stopped
    • ACh broken down by ACETYLCHOLINESTERASE - products reabsorbed by pre-synoptic neuroneuted to make ACh
  • Excitatory & inhibitory neurotransmitters:
    • Excitatory- depolarise (increase positivity) post-synaptic membrane if threshold is reached - Acetylcholine in CNS
    • Inhibitory- hyperpolarise (increase negative potential difference) post-synaptic membrane preventing firing of A.P - ACh in Heart cause potassium ion channels to open
  • Summation at Synapses:
    • if stimulus is weak- small amount N.T released from neurone into synaptic cleft
    • not enough to excite post-synaptic membrane to threshold level for A.P
    • Summation is where the effect of N.T released from many neurones is added together , or one neurone stimulated a lot in a short amount of time
    • synapse accurately process information - tuning response
  • Spatial Summation:
    • 2 or more pre-synaptic neurones release their N.T at same time onto same post-synaptic neurone
    • small amount small amount of N.T released from each neurone can amount to reach threshold level in post synaptic neurone to trigger A.P
    • if Inhibitory - total effect of N.T might not be A.P
  • Temporal summation:
    • two or more nerve impulses arrive in quick succession from same pre-synaptic neurone - A.P more likely, N.T more in synaptic cleft
  • Neuromuscular junction : specialised cholinergic synapse between a motor neuron and muscle cell
  • Neuromuscular junction:
    • use ACh- bind to nicotinic cholingeric receptors
    • Post-synaptic membrane lots of folds forming clefts- stores AChE
    • Post-synaptic membrane more receptors than other receptors
    • ACh always excitatory where M.N fires A.P -> triggers response in muscle cell