8. Nervous System: Neuron Physiology

neuron plasma membrane

creates barrier separating ICF from ECF

• ICF + ECF contain (+) and (-) ions/proteins

  • both overall electrically neutral

    • unequal distribution of specific ions build up close to PM due to ion channels + ion pumps

      • establishes resting membrane potential

      • establishes electrochemical gradients

• polarized → RMP = -70mV

neuron integral proteins

• ion channels

  • leak channels

  • voltage-gated channels (VGCs)

  • ligand-gated channels (LGCs)

• membrane pumps

  • Na+/K+ pump

resting membrane potential (RMP)

measure of electrical charge difference across PM (in volts)

• neurons → -70mV

  • inside of cell negative compared to outside

• established by unequal distribution of specific ions that build close to PM due to ion channels + ion pumps

  • K+ leak channels → numerous + always open

    • K+ exit cell down electrochemical gradient

    • contributes greatly

  • (-) proteins → cannot leave

  • Na+ leak channels → few

    • Na+ ions enter cell

    • balanced by redistribution via Na+/K+ pump

resting membrane potential (RMP)

graded potential

temporary, local change in RMP

• caused by LGCs opening on PM of dendrite

  • select ions move in/out of cell down electrochemical gradient

• can be

  • depolarizing = more +

  • hyperpolarizing = more -

• vary in amplitude → depend on stimulus strength

  • strength influenced by

    • # of open ion channels

    • duration that channel is open

depolarizing graded potential

occurs when membrane potential becomes more positive = less polarized

• influx of (+) charged ions

• inhibition of efflux of (+) charged ions

• increase likelihood threshold value will be reached = -55mV

  • AP can occur

hyperpolarizing graded potentials

occurs when membrane potential becomes more negative = more polarized

• influx of (-) charged ions

• efflux of (+) charged ions

summation

multiple graded potentials adding together

• can have depolarizing OR hyperpolarizing effect

threshold

-55mV in neurons

• summated graded potentials depolarize enough to reach this level → VGNCs open

  • Na+ influx = AP initiated → propagated along axon

• subthreshold stimulus

  • stimulus too weak to bring membrane potential to required level

action potential (AP)

sequence of rapidly occurring events in which membrane potential reverses, then returns to resting state

• electrical signal propagated along axon length

• shape is always same

  • amplitude of graph determined by VG ion channels

• frequency can altered

resting state

MP = -70mV

• all VGNCs + VGKCs closed

depolarization

MP = -55mV

• (+) from graded potential depolarized MP

• VGNCs open in response to depolarization @ -55mV = Na+ influx

• 
  

repolarization

MP = +30mV

• VGNC close

• VGKC open = K+ efflux

hyperpolarization

MP = -80 to -90mV

• VGKCs still open

  • take longer to close → responsible for prolonged hyperpolarization

return to resting state

MP = -70mV

• VGKCs close

• K+ leak channels + Na+/K+ pump working in background constantly → redistributes ions = restores RMP

• VGNCs need time to rest to original configuration

• 
  

refractory period

period of time after AP is generated when threshold stimulus CANNOT generate second AP

• divided into:

  • absolute

  • relative

absolute refractory period

period of time where second AP cannot be fired no matter strength of duration of stimulus

• during depolarization + early repolarization

• VGNCs need time to return to original configuration

• no subsequent APs can fire

relative refractory period

period of time where second AP can only be fired w/ specific stimulus

• during late repolarization

• VGNCs have returned to original configuration

• some VGKCs still open

• requires SUPRATHRESHOLD stimulus to fire subsequent AP

voltage-gated Na+ channels (VGNCs)

• -70mV (RMP) = closed + can open

• -50mV to +30mV = open (activated)

• +30mV to -70mV = closed + cannot open (inactivated)

all-or-nothing principle

initiation of AP only occurs if threshold stimulus is reached

• increasing stimulus past amount required to attain threshold increases AP frequency

  • BUT frequency limited by absolute refractory principle

continuous conduction

occurs in unmyelinated axons

• AP initiation → VGNCs open = local current w/ intracellular ion flow

• local current depolarizes adjacent PM region to threshold → more VGNCs in new region open

• refractory period prevents backward conduction

  • K+ efflux repolarizes membrane

saltatory conduction

occurs in myelinated axons

• VG ion channels only @ nodes of Ranvier

• intracellular local current swiftly moves through insulated areas of axon

  • electrical activity “leaps” from node to node

    • greatly increases speed of AP propagation

neural synapse action

1. AP depolarizes axon terminal

2. voltage-gated Ca2+ channels = Ca2+ enters cell

3. calcium entry = exocytosis of synaptic vesicle contents

4. NTs diffuse across synaptic cleft → bind w/ receptors on postsynaptic cell

5. NT binding = response in postsynaptic cell

6. opening of ligand-gated channels = influx of ions → intracellular electrical environment changed

   1. can be excitatory or inhibitory

excitatory post-synaptic potential (EPSP)

ligand binding to post-synaptic receptor causes depolarization

• eg. acetylcholine (ACh)

  • released by pre-synaptic neuron

  • binds to post-synaptic ligand-gated Na+ channels

  • Na+ influx

  • depolarizing graded potential → closer to threshold

inhibitory post-synaptic potential (IPSP)

ligand binding to post-synaptic receptor causes hyperpolarization

• eg. gamma-aminobutyric acid (GABA)

  • released by pre-synaptic neuron

  • binds to post-synaptic ligand-gated Cl- channels

  • Cl- influx

  • hyperpolarizing graded potential → further from threshold

neurotransmitter regulation

NTs removed from synaptic cleft to regulate its action (effect)

1. reuptake by pre-synaptic neuron

   1. NT components actively transported back into pre-synaptic neuron

2. enzymatic degradation

   1. enzymes in synaptic cleft break down NTs

3. diffusion

   1. NTs diffuse away from synaptic cleft

depression treatment

depression = serotonin deficiency

• drugs prevent serotonin reuptake = prolong serotonin action

botox (botulinum toxin)

inhibits release of NTs from somatic motor neurons, ex. ACh

• no NTs to bind onto myocyte = no post-synaptic AP initiated in myocyte = temporary muscle paralysis

  • neuromuscular junction → where motor neurons + myocytes contact

    • myocytes electrically excitable

      • APs in myocytes = contraction