Nerve and Muscle

• Types of information transmitted in the nervous system

  • Somatic
  • Autonomic
• Somatic

  Stuff we are aware of/have control over
• Somatic nervous system functions

  • Voluntary muscle control
  • Sensory information
• Somatic efferent (motor)


  Voluntary muscle control
• Somatic afferent (sensory)


  Sensory information
• Autonomic


  Stuff we aren't aware of/can't control
• Autonomic nervous system functions

  • Involuntary muscle control
  • Sensory information
  • Regulation of essential life processes
• Autonomic efferent (motor)


  Involuntary muscle control
• Autonomic afferent


  Sensory information that we aren't aware of (e.g. heart rate, breathing)
• Somatic nervous system

  1. Upper motor neuron (CNS)

  2. Lower motor neuron (PNS)
• Upper motor neuron

  • Cell body in brain
  • Axon in spinal cord
• Lower motor neuron

  • Cell body in spinal cord
  • Axon in spinal nerve
• Divisions of the autonomic nervous system

  • Sympathetic
  • Parasympathetic
• Sympathetic division

  • Effectors are skeletal muscle fibres
  • Neurotransmitter is acetylcholine
• Parasympathetic division

  • Effectors are smooth muscle, cardiac muscle, glands, adipose tissue
• ganglia/effector organs

  short axon
• ion channels

  Channels that allow passive diffusion of a substance down its electrochemical gradient
• How are ion channels gated?

  They need a stimulus (key) to open the door, which is the neurotransmitter that will bind and open it. It unbinds to close.
• How do chemically-gated ion channels work?

  Chemical neurotransmitter will bind to the ion channel and open it, causing ions to flow until it unbinds and the channel closes.
• How do voltage gated ion channels work?


  The membrane will depolarise to the threshold voltage, where it will open and allow ion flow until the threshold changes and the channel inactivates.
• How do mechanically gated ion channels work?


  When the membrane is deformed the channel changes shape to allow ion flow, when the membrane returns to original shape it will close.
• Local potential

  Change in membrane potential voltage (electrical charge) at a localised area in the dendrite or cell body, caused by movement of K/Na.
• EPSP

  Excitatory Post-Synaptic Potential. Pre-synaptic neuron releases excitatory neurotransmitter (Ach/NE) that will bind open channels, Na enters post-synaptic cell, causing depolarisation.
• IPSP

  Inhibitory Post-Synaptic Potential. Pre-synaptic neuron releases inhibitory neurotransmitter (GABA) that will open chemically gated K channels, K enters post-synaptic cell, causing hyperpolarisation.
• How do EPSP and IPSP differ?

  EPSP uses Ach/NE, IPSP uses GABA, EPSP controls Na and IPSP controls K, EPSP causes depolarisation, IPSP causes hyperpolarisation.
• Spatial summation


  Summed input from multiple pre-synaptic neurons.
• Temporal summation


  Summed input from repeated firing of one pre-synaptic neuron.
• Difference between spatial and temporal summation


  Spatial summation comes from multiple neurons, temporal is only 1 repeatedly.
• How is summation related to threshold potential and action potential generation?


  At the axon hillock the inputs will add together until they reach 60mV, which will then open the voltage gated channels. The influx of Na+ causes the rapid depolarisation phase of the action potential.
• Action potential generation


  1. Inputs summate at axon hillock

  2. Reach -60mV threshold

  3. Open voltage-gated Na+ channels

  4. Rapid depolarisation phase
• Action potential propagation in unmyelinated vs myelinated axons

  Unmyelinated: action potential develops as membrane depolarises, propagates to next segment, previous segment repolarises

  Myelinated: initial segment absolute refractory, local current depolarises nodes, action potential propagates faster without needing to open gates
• Myelination


  • Allows current to flow freely down axons without needing to open gates
• Types of refractory period

  • Absolute
  • Relative
• Components of a chemical synapse

  • Presynaptic axon terminal
  • Synaptic cleft
  • Voltage-gated Ca2+ channels
  • Neurotransmitter-containing vesicles
  • Enzymes
  • Postsynaptic cell
• Chemical synaptic transmission

  1. Depolarisation of axon terminal

  2. Ca2+ influx

  3. Neurotransmitter release

  4. Neurotransmitter binding to postsynaptic receptors

  5. EPSP/IPSP formation

  6. Neurotransmitter unbinding and degradation
• Neuron-to-neuron vs muscle-to-neuron transmission

  Neuron-to-neuron: Cholinergic synapses, Ach neurotransmitter, less summation required

  Muscle-to-neuron: More synapses, more summation required
• Chemical vs electrical synapse

  Electrical: Flow straight through gap junctions

  Chemical: Use neurotransmitters to bind to postsynaptic receptors
• How an action potential propagates along an unmyelinated vs myelinated axon

  1. In unmyelinated axons, the action potential develops as the membrane depolarises. The axon is broken into segments and the action potential will move down the axon, bringing each segment to threshold. Then passing through and the previous segment is left to repolarise (relative refractory period). This continues flowing only in a forward direction because of the absolute and relative refractory period.

  2. In myelinated axons, the initial segment (absolute refractory period) is the same, but the local current produces a graded depolarisation that brings the axolemma at node 1 to threshold - developing the action potential. As this happens, the initial segment begins repolarisation (relative refractory period). This continues down the axon as it flows freely (faster because it doesn't need to depolarise the entire membrane)
• Absolute refractory period


  Period where the axon cannot be stimulated to produce another action potential
• Relative refractory period


  Period where a stronger than normal stimulus is required to produce another action potential