3-Neurophysiology Primer

double-layered structure, forms fundamental framework of all cell membranes

functions:

• selective barrier

• controls entry and exit of substances in and out of cell

it has both a resistance and capacitance

Voltage(U) = R • Current(I)

C = ε0 • ε •A •d-1

ε0 = dielectricity constant of vacuum

ε = dielectricity constant of the membrane

A = membrane area

d = membrane thickness

= major drain of energy in organism (also called -ATPase)

pumps for each ATP:

• 3 sodium-ions to outside

• 2 potassium-ions to inside of cells

—> maintains major chemical gradients in cell

transmembrane proteins -> form hydrophilic pore across membrane

How?

—> charged amino-acids in center of large 3-dimensional protein forms a charged (hydrophilic) tunnel —> allows ions to pass

non-selective

—> let all types of cations pass

selective

• entrance of channel carries charges that repel ‘wrong’ charges

• center of pore has diameter —> restrict passage

not permanently open, but gated

change in 3-dimensional form of protein

—> opens/closes channel

• Ligand-gated (e.g neurotransmitter)

• Mechanically gated

• Voltage-gated (changes in electrical field)

From ion distributions to resting potentials

system with 2 chambers, seperated by semipereable membrane

• freely diffusable salt put into one of chambers —> ions diffuse through membrane to equalize concentrations

  —> electrochemical equilibrium

• non-diffusable salt anion added —> push out other anions (Cl-) and keep cations (K+) on its side

  —> unequal distribution (but both sides electrically neutral, bc equal number of pos and neg)

• K+ out of cell —> decreased chemical gradient (driving force for K⁺ diffusion)

  (high concentration inside → low concentration outside)

• the more K+ out of cell —> charge imbalance

  • inside more negative (remaining non-diffusable anions)

  • outside more positive

  generates voltage across membrane

• at given equilibrium point: chemical and voltage gradient cancel each other out —> balanced

  this equilibrium described as Nernst equation

computes resulting voltage for given chemical gradients

[K+]a = Ion concentration outside cell (extracellular)

[K+]i = Ion concentration inside cell (intracellular)

For Anions, inner and outer concentrations switched!!

m-gate (activation gate) = opens quickly due membrane depolarization —> sodium in cell

h-gate (inactivation gate) = closes after 1 millisecond —> stop sodium ion flow

1. Resting state

   both gates closed —> no sodium ions flow through channel

2. Voltage threshold exceeded (Open)

   membrane depolarization opens m-gate —> Na+ ions flow in cell

3. Timed closure (inactivated)

   h-gate closes after brief delay (1 ms) —> stop Na+ ion flow

4. Refractory period

   h-gate remains closed, m-gate resets to closed state

1. Resting State (Vm near resting potential)

2. Threshold Crossing (small depolarization —> open sodium channel)

3. Depolarization (sodium influx raises Vm)

4. Repolarization (sodium channels close, potassium channel open —> K+ flow out —> lower Vm)

5. Afterpotential / Hyperpolarization (membrane shortly negative —> turn to equilibrium)

absolute RP

too few sodium channels regenerated —> no positive feedback loop —> cell is non-excitable, irrespective of depolarization

relative RP

# of sodium channels high enough to sustain positive reinforcement

but: cell needs to be depolarized stronger —> smaller action potential

passive/electronic conductance

not regenerative and decreases with time and distance

—> conduction = fast (not rely on opening/closing channels)

actively regenerated potential (by voltage-gated channels of neuron)

conduction = slow (signal needs to be regenerated at each membrane area)

both types propagated differentially in neurons

• consists of pre- and postsynaptic structures

• Transmitter between both is acetylcholine

• at postsynaptic membrane: receptors for acetylcholine —> open after binding Ach —> sodium can pass (->depolarization)

opening of channels for sodium/calcium —> depolarization (excitatory postsynaptic potential, EPSP)

opening of channels for potassium/chloride —> hyperpolarization (inhibitory postsynaptic potential, IPSP)

effect depends on

• transmitter

• receptor for transmitter

• ion gradients at postsynaptic membrane

cause Dynamic changes of synapses

positioned at dendrite of neuron

receive input from single synapse (excitatory)

function: memory formation and learning

postsynaptic to 1-2 axonal terminals

both chemical and electrical compartments

Ca flows through activated channels in head

—> concentration change triggers molecular cascades

• form local chemical and electrical compartments (e.g. spines)

• may have voltage-gated channels

• may have action potentials that use sodium/calcium

• can be dynamically changed by activity

• may boost / hinder electronic conductance

• quickyl change physical/electronic form

• not just passive receiving cell structures