Nerve Potentials Flashcards
what is a potential in terms of nerves and conduction
3 types of Potentials
potential = a difference in charge (mV) between the inside and outside of a cell membrane regulated through K+ and Na+ ions
Three Types
- Resting potential = no active neurotransmission
- graded = a small depolarization of a cell membrane
- active = depolariation reaching -55mV leading to actual neurotransmission to occur
why is a resting potential possible
how is it maintained
The Resting Pontential
- approx. -70 mV = resting potential of a neuron
- the charge difference between the outside and inside of the nerve cell
- this is a result of the differences in ion concentration in and out due to flow of ions across the membrane
Maintained
maintained via leaky channels, ion pumps and proteins
- there are leaky channels for BOTH K+ and Na+ : where the ions will move across their membrane via concentration gradeint (high to low) and by charge difference (away from its like charge)
- but there is no “free movement” as the membrane is not as permisable to Na+
- more K+ channels leaking K+ OUT than there are Na+ channels allowing Na+ in
- there are also K+/Na+/ATP pumps: which pump 3 K+ out for every 2 Na+ in using energy = against the natural gradient
- there is also negatively charged proteins inside the cell: further adding to the negative charge inside
net result: K+ flowing out, K+ being pumps out and negative protiens inside = 70 mV resting
Action Potential
- 4 phases
- how does it work
4 Phases of an AP
- resting state
- depolarization
- repolarization
- hyperpolarization
How it works
- cell begins at its resting potential of -70
- a stimulus triggers the peripheral receptor to start a receptor potential, a grade potential
- think of grade potentials as like mini AP’s need a few of them to create enought stimuli to FINALLY have the cells negative chargeiside lessen to the -55 mV threshold
- when threshold is reached: this triggers voltage-dependent Na+ channel to swing wide open and let all the Na+ in this immediately depolarizes the cell
- then the cell quickly repolarizes, hyperpolarizes and gets back to resting
How is an AP at a specific point on the neuron trigger a potentiation down the axone to continue to travel
Role of Mylein
- Na+ diffuses from the dendrites through the cell body to the axon hillock (the jummper start of the AP down the axon)
- the Na+ channels get stimualted to open up (when they get the threshold) and allow Na+ to flow inside
- these Na+ ions then diffuse down the axon where its negative (since + goes to -) = this triggers the reaching of the threshold for this areas of teh axon, and the Na+ channels swing open too
- and then it continues down the axon
Role of Mylein
- mylein= helps speed up the conduction through the axon via saltatory conduction
- electrical signal “jumps” to nodes of ranvier where there is higher concentration of Na+ channels to allow the signal to continue
- the mylein just acts as a buffer: the Na+ iside has to travel further to get to next Na+ channel to open = thus faster travel of teh signal over a distance
what happens when the AP reaches the axon terminal
- the synpatic vesicles filled with NT’s are waiting here: theres always some vesicles docked with NT’s ready to go (via endosomes to help create these vesicles)
- the signal from the axon triggers voltage gated calcium channels to open flooding the inside of the cell with calcium
- this causes a release of teh NT into the synpatic cleft via exocytosis to go bind to receptors on next neuron
Excitatory/Inhibitory Post-synpatic Potentials
when the NT is taken up what happens
- the NT is taken up via special receptors on teh dendrites of the next cell
- this triggers different pathways to occur depending on the NT released
if NT was Glutamate (depolarization = excitatory)
- this triggers voltage gated Na+ channels to swing open and allow Na+ to enter: depolarization cell an dpropagating excitatory signal
- EPSP occurs
If NT was GABA (inhibiatory)
- voltage gated K+ (outflow) or Cl- (influx) channels to open
- this causes an inhibition of the AP to continue on
- HYPERPOLARIZATION of the cell: no more passing the AP
how does the AP travel all the way from the dendrite to the axon wihtout getting lost
- the EPSP gets to the dendrtie: passively travels through the dendrite and teh cell body
- there will be mini small depolarizations which will ouccur through the journey
- but overtime the EPSP will decay further away = more decay
- thus, there needs to be MULTIPLE EPSP from MULTIPLE DENDRITES synapsing and passing this signal down to the axon
- once at the axon hillock: its like the speed zone: where all those EPSPs come together and summation of the AP occurs
membrane potential
neruon
cardiac
skletal cells
Neuron = –70
skeletal = - 70
cardiac = -90
smooth = - 60
average of all cells = - 50
not all cells are excitable
how does the size in diamete change the signal and resistance
bigger in diameter = less resistance; faster signal ; higher conduction velocity
the giant squid example
Brain wave v AP
whats the difference
Brain Wave
- rhythmic patterns of neural activity
- these reflect multiple synchronous firing of post-synaptic potentials suppation of the AP on the post-synaptic neruon
- measured by EEG
- gamma (biggest) , beta, alpha, theta, delta (tiniesy)
what are some conditions that impact neurotransmission
all neurologic lesion sinturrupt neurotransmission to a degree
- trauma or tumor: destroys a large area and disruppt incoming and outgoing signals from that location
- disease that impact electrolyte balances (liver disease, alcoholism, etc.)
- progressive polio, ALS and MS affect neuron bodies or axons
electrolyte imbalances
- too much too little K+, Ca+, Na+ affect neuro function
- dehydration too in adults and babies
Multiple Sclerosis
what is it
why does it happen
assocation with what
MS: an autoimmune impact that destorys the oligodendrocytes therefore impacting and destroying the mylein in the CNS only!!!!
- also breaks down the BBB ;allowing inflammatory processes to occur
- strong relationship with lack of Vit D/sunlight
- a progressive demyleination and plaque formation
- central SC and CNS(BS, cerebellum and pre-frontal) sensory first then motor tracts
MS
subtypes
flares
symptoms
treatments
Subtypes
- can range in severity of disease
- MC : relapsing/remitting
Flares: make it worse
- heat
- stress
- exersion
- infection
Symptoms (best seen on T2 MRI to see demyleination (white gone)
- parasthesias
- cramping
- spasticity
- visual and cogntion issues
- pain (common)
treament
- interferons, Monoclonal ab, steroids
