Neural Physiology Flashcards
Nervous System Organization
Receptor > Sensory NS > CNS > Motor NS > Effector
action potential
a neural impulse; a brief electrical charge that travels down an axon
- produce electrical signal from ion mvmnt
- strong enough signals get action potentials
- (-50-55mmVol gets an action potential)
electrical signals
changes in a cell’s membrane potential
- when produced by cells called action potential
- transfer info to diff parts of body
- due to ion conc differences across PM and membrane permeability
resting potential of the membrane
the difference btwn the charges of the inside (-) and outside (+) of the membrane = -90mmVol
- change in this causes action potential (at -50mVol)
- lots of Na and Cl outside = (+)
- lots of K inside = (-)
depolarization
The process during the action potential when Na is rushing into the cell causing the interior to become more positive
- charge is less (-) and more (+) (closer to being equal)
- caused by hypopolarization (“less polar”)
repolarization
Return of the cell to resting state, caused closing of Na gates and opening of K gates
- more negative
Na/K exchange pump
- 3 Na ( moves inside) and 2 K (moves outside) move in opposite directions via antiport
- this movement starts repolarization since more Na leaks out than K leaks in
-Na/K pump fires up to push Na back outside and K inside to prevent repolarization (done w active transport (ATP payment))
membrane permeability
- K is attracted to the inside’s (-) and wants to move in to be with the neg. charged protein colloids
- Na also likes being inside with the (-)
- K moves in due to non-gated channels and Brownian mvmnt
- Na has a gated channel normally closed
- proteins do not leave cell as often too big to diffuse (also are (-) charged)
Non gated (leakage) channels
always open
- proteins repel the also (-) Cl out of the cell
- K moves out and follows conc gradient (more inside than outside) (despite attracted to the colloids)
- more K and Cl leakage channels than Na because leaks more often and causes depolarization
Gated ion channels
ion channels that open or close in response to stimuli
- voltage gated
- ligand gated
Ligand gated ion channel
Open/close in response to ligand/neurotransmitter binding to receptor protein (usually glycoprotein)
voltage gated ion channel
- open/close in response to voltage changes in cell membrane
- at rest more (-) inside > outside
- Ca (+) loves the (-) of proteins and will cover the gates; need slight depolarization to remove Ca
-ex: Na and K both have voltage gated channels
Touch receptors
respond to mechanical stimulation of the skin
Temperature receptors
respond to temperature changes in the skin
potential difference
unequal charge distributes btwn immediate inside and immediate outside of PM
-70 to -90mVol
establishing membrane potential
- at equilibrium there is little mvmnt of ions across PM
- K can leak out if Na leaks in (K’s job is to counteract Na)
- If K does not leak inside it leads to action potential since the inside is more (-)
- Cl, Ca and Na not important as they have few leakage channels
- if just rely on leakage channels then Na and K would be equal; instead we use Na/K pump
- 3 Na out and 2 K in per ATP used (outside (+))
K: change resting potential
- too much K outside = depolarization/hypopolarization
- too little K outside = hyperpolarization (steeper conc gradient)
- non gated K channels: help with maintaining membrane potential
- gated K channels: initiate repolarization after action potential
Na: change resting potential
- Na’s job is to get inside membrane and depolarize ASAP
- Initiates Action Potential
- Na has strong conc gradient
- Na has few leakage channels
Ca: change resting potential
- Ca2+ is attracted to voltage-gated channels and can block those gates
- lifts off when depolarization has occurred
- Decrease Ca2+ = Na gates open and depolarization
- Increase Ca2+ = Na gates closed, membrane repolarized/hyperpolarized
Local Potentials
changes in membrane potential of a neuron (not enough for the while membrane action potential)
- caused by: ligands binding to receptors, charge change in PM, mechanical stimulation, temp change, spontaneous change.
- must be strong and/or frequent stimulus to make action potential (can add on to each other)
all-or-none principle
the law that the neuron action potentials either fires at 100% or not at all
5 action potential steps
1: resting membrane potential - voltage gated Na and K channels are closed
2: depolarization - Na gates open as activation gates open. All Na gates open and diffuse in, causing K to diffuse out at a slower rate than Na
3: repolarization - Na gates close because inactivation gates open. Now K keeps diffusing out to repolarize cell
4: after potential - Na gates close, activation gates close, inactivation gates open; Na gates return to rest
5: resting membrane potential is reestablished once K gates close
refractory period
a period of inactivity after a neuron has fired; incapable of repeating action potential
-absolute: no size of stimulus can produce another action potential
- relative: if stimulus is stronger than the threshold an action potential may occur
threshold stimulus
cause strong local potential to make action potential
subthreshold stimulus
not cause strong enough local potential to make action potential
maximal stimulus
just strong enough to make action potential
submaximal stimulus
all stimuli btwn threshold and max stimulus strength
supramaximal stimulus
any stimulus stronger than max stimulus strength
action potential propagation
- Unmyelinated axon
- threshold at trigger zone cause action potential
- Action potential moves one segment at a time
Because of the absolute refractory period it cant go backwards
saltatory conduction
the jumping of action potentials from node to node
nerve fiber types
*Type A: large-diameter, myelinated. Conduct at 15-120 m/s. Motor neurons supplying skeletal and most sensory neurons
*Type B: medium-diameter, lightly myelinated. Conduct at 3-15 m/s. Part of ANS
*Type C: small-diameter, unmyelinated. Conduct at 2 m/s or less. Part of ANS
synapse
A junction where information is transmitted from one neuron to the next
-presynaptic: neuron that does the sending
-postsynaptic: neuron receiving neurotransmitter
electrical synapses
Synapses that transmit information via the direct flow of electrical current at gap junctions
- cardiac and smooth muscle tissues
- action potential in one cause action potential in another, as if whole tissue firing
chemical synapses
Specialized for release and reception of chemical neurotransmitters
- presynaptic terminal releases (synaptic vesicles); synaptic cleft is btwn terminal and receiver; postsynaptic membrane receives and binds to neurotransmitter (via diffusion)
neurotransmitter removal
- Acetylcholinesterase has a high turnover rate into acetic acid and choline
- Norepinephrine: recycled within presynaptic neuron or diffuses away from synapse
receptor molecules and neurotransmitters
Neurotransmitter only “fits” in one receptor.
Not all cells have receptors.
Neurotransmitters are excitatory in some cells and inhibitory in others.
Some neurotransmitters (norepinephrine) attach to the presynaptic terminal as well as postsynaptic and then inhibit the release of more neurotransmitter
excitatory post synaptic potenital (EPSP)
depolarization , response stimulus; may reach threshold to make action potential
inhibitory post synaptic potential (IPSP)
hyperpolarization, response inhibitory; decrease action potential by move membrane from threshold
general senses
distributed all over body; travel to brain (primary receptor)
- somatic (about body/env): touch, pressure, temp
- visceral (about int organs): pain, pressure
special senses
smell, taste, sight, hear, balance
- receptor > neurotransmitter > brain
- secondary receptor
Cerebellar Comparator Function
- motor cortex send AP to lower motor neurons in spinal cord
- AP from motor cortex to cerebellum, inform of intended action
- lower motor neurons send AP to muscles to contract
- proprioceptive signals from muscles/joints to cerebellum
- cerebellum compare motor cortex info and proprioceptive signal info
- AP from cerebellum > spinal cord> lower motor neurons
- AP from cerebellum to motor cortex to make action
brain waves and sleep
*EEGS = record electrical activity in brain
*alpha = resting state w eyes closed
*beta = intense mental activity
*theta = children / frustrated adults
*delta = deep sleep/infancy/severe neurological damage
retina
sensory retina: photoreceptor, bipolar, ganglionic neuron layers
- light pass thru all 3 layers, hit retina, rebound
pigmented retina: single layer of cells filled w melanin
- increase visual acuity by isolate photoreceptors; decrease light shattering
rods
- rhodopsin change shape when hit by light into opsin and retinal (vitamin A)
- when not stimulated, rods hyperpolarize
- light cause depolarization of rods > depolarize bipolar cells and ganglionic cells
Rhodopsin Cycle
11 cis(bent) to all-trans (straight) > excite alpha in G protein > enzyme to phosphorylate > phosphorylate protein channel to close (already depolarized, become hyperpolarize)
-Change in retinal shape cause action potential to happen
-Retinal is a protein to change shape to excite G protein
rod cell hyperpolarization
- Glutamate continuously being released by bipolar cell
Always in a depolarized state (more -ve from RMP) - Does this to inhibit the release of glutamate which inhibits the release of a neurotransmitter
Cones
color vision; bipolar receptor cells
- numerous in fovea centralis and macula luctea
- red, blue, and green iodopsin
- black absorbs; white reflects
dark and light configuration
-dark configuration? 11-cis-retinal
-Light configuration? All-trans-retinal
-Use ATP to turn A-T-R (dark) into 11-C-R (light)
inner layers of retina
-Rods and cones synapse w bipolar cells synpase w ganglion cells in all areas except fovea
-All cones in fovea interact directly w ganglion = more clear or less sensitive to light
-Spatial summation (rods only): one bipolar cell might interact w numerous rods; one ganglion cell might interact w many bipolar cells > leads to great sensitivity (cones do not have, are 1:1)
neuronal pathways for eye
-Nasal retina (near nasal bone) - travel along same side (optic nerve to optic chiasm to superior colliculi to thalamus to visual cortex)
-Temporal retina (near temporal bone) - crosses over
-Info cross to other side of brain even if one eye crosses over
-L and R visual field; not all crosses over only temporal
The ear Compartents
- mechanical sense system
External Ear (hearing)
Middle Ear (hearing)
Inner Ear (hearing and balance)
sensitivity of hearing
-Outer hair cells hear
-Inner hair cells tune frequency
-Tune actin fiber attached to gate (more tense or loose)
-Efferent action potentials inhibit other action potentials (stiffen and not allow other action potentials to come in, focus on one clear and pure sound)
-Increase hearing sensitivity (3): Stiffen membrane to stop more sounds coming in or tune actin filament to control gate sensitivity or inhibit action potentials
Olfaction
- seven primary odors
- dendrites of olfactory neurons have enlarged ends (olfactory vesicles)
- cilia in mucous; odorants dissolve in mucus; depolarize and make action potentials
odorant binding to olfactory hairs
ATP is dephosphorylated by adenylate cyclase enzyme (g-protein)
- Cyclic AMP, phosphorylates the ion channel
- Sodium and or calcium initiates the action potential
Olfactory neuron pathway
olfactory neurons > olfactory epithelium > cribiform plate > olfactory bulbs, synapse w mitral tufts > olfactory cortex of prefrontal (not thalamus)
-Lateral olfactory area: conscious perception of smell
-Medial olfactory area: visceral and emotional reactions to odors
-Intermediate olfactory area: effect modification of incoming information.
taste
- texture and temp and olfaction affect taste
- rapid at CNS and taste bud level
- every taste has a different action pot.
major tastants: Salt (Sodium)
Leakage channels for sodium create Na+ action potentials
major tastants: Sugar
- adeneylate cyclase - turns ATP into cAMP
- Causing the K+ channels to close and leading to depolarization
- cAMP turns into Kinase
major tastants: Umami
Receptor proteins - for glutamate and has attached G-protein inside
Adenylate cyclase - enzyme that turns ATP into cAMP
Ligand gated Ca2+ channels - opened by cAMP and lets calcium to enter the cell
major tastants: Bitter
- Receptor protein - bitter tastants bind to and attach to G-protein
- Phospholipase - enzyme that turns PIP into IP
- releases Ca2+
