neurophysiology Flashcards
what are the concentration differences across the membrane generated by?
-low permeability of cell membranes
-ion channels
-sodium-potassium pumps
-the differences in K+ and Na+ which are critical to generating the resting potential and action potential
how are ion channels formed?
-by proteins that spawn the cell membrane to form a water filled pore
-they can be ion selective e.g K+,Na+,Cl- channels
when do ions move?
-ions move though the channels when they are open and don’t move when closed
what are leaky channels?
ion channels that are always open
e.g there are leaky K+ channels that set the resting potential of the cell
what do some channels only open in response to?
-some channels only open in response to a stimulus e.g neurotransmitters, pain and light
when do voltage-gated Na+ and K+ channels open?
-open in response to a change in the membrane potential and are responsible for the action potential
what do voltage gated Ca2+ channels do?
trigger the release of neurotransmitters at synapses
what do ligan gated ion channels do?
are responsible for synaptic transmission
what does the sodium-potassium pump do?
ransports Na+ out of cells against the conc gradient-it is produced by the mitochondria and requires energy from ATP
-K+ is exchanged and enters the cell
-it generates the Na+ and K+ conc gradients that are generated across the cell membrane,these gradients are only possible because the cell membrane is not very permeable to ions otherwise it requires massive amounts of energy if the ions were freely permeable
what does the sodium-potassium pump use ATP for?
to maintain the ion concentration gradients, the pump does not generate the RMP or the action potential but I does generate the cones gradients needed for neuronal activity
what is the importance of the sodium-potassium pump?
-the neurone needs to work hard to maintain the K= inside
-the brain needs a constant supply of energy (glucose) and oxygen to fuel the pumps
how do K+ ions set the RMP?
-the conc of potassium ions is much greater inside the cell than the outside,the potassium ions move out of the cell down its concentration through leaky potassium channels-the leak is very small however
-K+ is positively charged and its movement out of the cell leaves the inside of the cell more negative-this generates the RMP
how can the RMP be altered?
-there can be either depolarisation and hyyperpolarisation
what is depolarisation?
being closer to the action potential threshold=more excitable
what is hyperpolarisation?
being further from the action potential threshold=less excitable
what can an increase/decrease in extracellular K+ cause?
-increases can cause renal failure
-decrease can lead to a need for long term use of diuertics
why is the CNS protected against K+ fluctuations?
because of the BBB
what action potentials do excitable cells generate?
nerve and skeletal muscles and cardiac muscles which are much longer (300ms) due to differences in ion channels, the cardiac muscles have a large Ca2+ influx that causes muscle contraction
what are the different phases of an action potential?
-Resting membrane potential
-Threshold potential
-Depolarization-rising phases of the action potential
-Repolarisation-the falling or recovery phase of the action potential
-Hyperpolarization-the membrane potential goes more negative than the resting potential
-Absolute refractory period
-Relative refractory period
how do sodium-potassium channels generate action potentials?
-opening of voltage-gated Na+ channels at the threshold depolarizes the cell membrane to generate the rising phase of the AP
-opening of voltage gated K+channels depolarizes the cell membrane to generate the falling or recovery phase of the AP
-opening of voltage gated K+ channels repolarises the cell membrane to generate the falling or recovery phase of the AP
-both potassium and sodium ion channels being closed brings the cell back to the resting membrane potential
-the neuron is then ready to generate another AP
what are voltage gated channels responsible for?
AP depolarisation and repolarisation
what is the first stage of activity for AP depolarisation?
closed
-the channel is closed
-there is no movement of Na+
what is the second stage of activity for AP depolarisation?
open
-the stimulus depolarizes the cell membrane
-The channels open
-Sodium enters the cell,down the concentration gradient
-Depolarization
what is the third stage of activity for AP depolarisation?
inactivated
-At the peak of the AP the channel becomes activated
Sodium stops entering the cell
-The channel does not open in response to a new stimulus
-This gives rise to the absolute refractory period
how are voltage gated K+ channels responsible for AP repolarization?
-Voltage gated K+ channels close at rest
-K+ channels open in response to depolarization during the AP
-K+ leaves the cell down its concentration gradient
-There is a repolarization phase of the AP
-K+ channels remain briefly open after the AP this causes hyperpolarization (undershoot) and it gives rise to the relative refractory period
-There is then a closure of the K+ channels and this resets the membrane potential
what is the absolute refractory period?
-the period immediately after the action potential where the membrane is unresponsive and can’t generate another AP
-the sodium channels ae inactivated
what is the relative refractory period?
-period following the absolute refractory period, the membrane can generate an AP but requires a stronger stimulus
what happens in the relative refractory period?
-sodium channels are reactivated
-potassium channels remain open
-K+ efflux (the flowing out) hyperpolarizes the neuron
-this makes the cell membrane less excitable
-but an AP can be generated with a greater stimulus to overcome the hyperpolarization and take the cell to the threshold and open the voltage gated Na+ channels
what can sodium and potassium channel blocker cause?
-channelopathy,the disruption of the function of ion channels or the proteins that produce them e.g Na+ channelpothy which leads to generalised epilepsy with febrile seizures and hyperkalemic periodic paralysis
what is puffer fish?
where tetrodotoxin (TTX) blocks Na+ channels by clogging permeable pores and this prevents Na+ from entering the neuron
Batrachotxin also binds irreversibly to Na+ channels
describe calcium channel blockers…
cardiac muscles have a large Ca2+ component which causes muscle contraction
-verapamil is a blocker which is used to control tachycardia (increase heart rate)
what are the basic principles of synaptic signalling?
-input (presynaptic)
-action potential generated at the axon hillock
-action potentials propagated from node to node
-neurotransmission at the synapse
-output (postsynaptic)
the electrical properties of neurotransmission image and integration of synaptic inputs image
what does the integration of excitatory and inhibitory inputs determine(summation of EPSPs) ?
-neuronal output (an action potential)
