Neurophysiology Fundamentals Flashcards
Is the cell membrane a good conductor of electrical signals?
No!
It is a double-lipid structure, charged particles (e.g. ions) can’t pass through it
Therefore, ion channels are needed instead
Two types of ion channel
Voltage-gated: activated through electrical changes
Ligand-gated: activated by the binding of a neurotransmitter
How is the resting membrane potential reached?
At rest, K+-channels are open, which allow K+ ions to diffuse out of the cell, according to the gradient. Cl- ions have no way of leaving the cell. This leads to an increasing intracellular negative charge, which pulls the K+ ions against the gradient. The electrochemical equilibrium is obtained when there is a balance between the gradient pull and the electric pull. For K+ ions in the neurons, the equilibrium potential is -65 Mv.
Neuron with nothing to say
(Inside of cell is) negatively charged: working hard to stay silent
Neuron with something to say
(Inside of cell is) positively charged: hard work stops and (Na+) ions flood in
Hyperpolarization vs Depolarization
Incoming signals, mostly through neurotransmitter binding that have an effect on the membrane potential.
Hyperpolarization = more negative
Depolarization = more positive
Hyperpolarization is inhibitory (IPSP) as moves membrane potential further from the action potential threshold (-50Mv), and depolarization is excitatory (EPSP) as it moves the membrane potential closer to the threshold.
Explain whats going on
When threshold is reached at -50Mv, voltage-gated Na+-channels open, causing an influx of Na+, creating self-reinforcing sharp increase in membrane positivity up to a peak of approx. +60 mV.
voltage-gated Na+-channels self-inactivate, ending the surge, and voltage-gated K+-channels briefly open, causing an “undershoot” below resting membrane potential
RMP is _____ driven; AP is _____ driven [Which ions?]
RMP is potassium-driven (K+); AP is sodium-driven (Na+)
Passive axonal conductance
Axonal conductance = how the action potential goes from postsynaptic dendrites down to the cell body and further on to the axon terminals.
Fluctuations in membrane potential, e.g. from action potentials, travel a brief distance
along the membrane and dissipate
The process is fast but leaky, just like my ass.
Active axonal conductance
Nearby voltage-gated Na+-channels are activated from an action potential, restarting the whole action potential cycle in adjacent parts of the membrane.
This process is energy-costly and slow
Describe the pic
Increasing the distance between clusters of ion channels and thoroughly insulating
the intermediate segment with myelin (inert membrane from oligodendrocytes)
combines robust active and fast passive conductance.
Lightning fast pew pew
Short term synaptic plasticity.
Explain synaptic facilitation, synaptic depression, synaptic augmentation/potentiation
synaptic facilitation: rapid successions of action potentials lead to accumulation of
Ca2+ in synaptic terminal, causing release of larger transmitter quantities after each
action potential
synaptic depression: in persisting high-frequency stimulation, transmitter releases
surpasses synthesis rate, decreasing quantities released after each action potential
synaptic potentiation/augmentation: lesser understood processes (e.g. calciumdependent enzymatic activations) that lead to a somewhat delayed release of higher neurotransmitter amounts (as compared to baseline) after high-frequency activations