Exam 2: Ch 6 Book Flashcards
2 ways signals move from point to point along the plasma memb.
graded potentials
action potentials
receptor potential
physical stimulus received and changes the membrane potential
graded potential in proportion with the stimulus
decremental transmission
sensory receptors lack voltage gated ion channels that produce APs so signal decays over distance
membrane at spike initiating zone of a sensory neuron contains
many voltage gated ion channels
if graded potential reaching this zone is still strong enough, AP generated
transfer of info between neurons is usually accomplished though
chemical signals carried by neurotransmitters
causes change in membrane potential of post-syn neuon
amount of nt released and thus the amplitude of the response from post-syn neuron depends on
number and frequency of AP arriving in terminals of pre-syn neuron
post-syn potential
change in membrane potential of post-syn neuon
graded signal (if large enough can initiate an AP in posy-syn neuron toward next neuron)
cable properties
electrical properties that affect conduction of a signal over distance
why would signal along longitude of an axon decay with distance
cytoplasm has resistance to flow of electrical signals
resistance of plasma membrane to electrical signals is high
charges leak out of the cell across plasma memb.
a perfectly insulated wire moves electrical signal without _______
decrement
membrane capacitance on signal decay
slows passive transmission of signal along axon
length constant
depends on resistance of membrane, cytoplasm, external solution
spread of electric current along interior of an axon in enhanced by
high membrane resistance
low cytoplasm resistance
in length constant equation what does each variable represent
Rm = resistance of a unit length of membrane
R1 = summed longitudinal internal and external resistance (Ri + Ro)
nonspiking neurons
very small neurons incapable of producing APs
graded signals conducted electrotonically to axon terminals without aid of APs
signals strong enough to release nt
where are nonspiking neurons found
retina
CNS
how does AP current move down an axon
Na current moves through activated patch of membrane, and depol adjacent patch
repolarized patch is refractory so AP travels in 1 direction
adjacent patch reaches threshold, current flows, and depol next patch
stim AP in middle of an axon
current moves in both directions but can’t get a backwards AP b/c membrane is in refractory state
propagation of an AP depends on 2 factors
passive cable properties that permit electrotonic spread of local current to adjacent patches of inactive memb.
electrical excitability of Na channels in axon memb.
why don’t neighboring axons excite each other when conducting current
high resistance of inactive membrane
small amount of current flowing is not enough to bring neighboring axon to threshold
speed of AP equation
v(p) = Δd / Δt
v(p) = velocity of propagation
Δ distance
Δ time
what does conduction velocity primarily depend on
how fast the membrane ahead of the active region is brought to threshold by local currents
higher length constant means farther the local currents can flow before they’re too weak to elicit threshold
how is length constant increased in squid, arthropods, annelids
increase in axonal diameter
reduces cytoplasmic resistance
why not in humans: takes up too much space
what do vertebrate do to increase length constant
myelinate axons
test speed of propagation
frog nerve muscle prep stimulated at 2 locations 3 cm apart
measure latency (time) to peak muscle twitch
muscle contraction moves a lever that scratches a piece of paper
myelin
glial cells wrapped around segments of axons to produce layers of insuating fatty membranes
2 effects of myelin on cable properties of neurons
increase transmembrane resistance
decrease effective membrane capacitance (thick)
greatly increase length constant
nodes of Ranvier
short unmyelinated gaps exposed to extracellular fluid
myelin is laid down by two kinds of glial cells
schwann cells : PNS
oligodendrocytes: CNS
saltatory conduction
occurs in myelinated axons
APs produced in small areas of membrane exposed at nodes of ranvier (Na moves in, tons of Na + K channels)
APs jump from node to node
is saltatory conduction fast?
yes, velocity of signal transmission enhanced
diseases of demyelination
multiple sclerosis: myelin sheath reduced in CNS
compromises sensory perception and control of coordinated movement
electrical synapse
pre-syn neuron electrically connected to post-syn neuron by gap junctions
rare
chemical synapse
APs in pre-syn neuron cause release of nt that diffuse across synaptic cleft
synaptic cleft
narrow gap separating membranes of pre and post syn neurons
neuromuscular junctions (NMJ)
synapses connecting motor neurons and the skeletal muscle fibers they control
some functions of nt
inc/dec # of ion channels inserted into membrane of post-syn cell
alter excitability of post-sun neuron by changing rate at which ion channels open or close
modify sensitivity of channels to activating signals
rectifying junctions
junctions where ionic current flows more readily in one direction than the other
fast/direct chemical synaptic transmission
found at the NMJ and CNS
AP reaches axon terminals and vesicles release nt that diffuses across cleft and binds receptors in post-syn membrane (opens ligand gated ion channels)
synaptic vesicles
membrane bound vesicles containing nt
release nt by exocytosis
nt binding post-syn receptors has what effect
allows brief ionic current to flow through membrane of post-syn cell
slow/indirect chrmical synaptic transmission
affect post-syn cell by activating receptors that alter levels of signal molecules that modify ion channels
multiple steps make it slower
fast chem synapses structure
small molecules
release nt at active zones in pre-syn memb.
slow chem synapses structure
larger peptide molecules
release nt at many sites in pre-syn terminal
what causes release of nt into cleft other than AP
AP stimulates release of Ca2+ from voltage gated Ca channels
this initiates exocytosis
study of frog motor end plate (NMJ)
muscle membrane has junctional folds under depression (where pre-syn axon branches are to inc surface area)
active zones above folds release nt ACh and vesicles recycled
ACh causes post-syn Na and K ion channels to open
breakdown of ACh in cleft
performed by AChE
acetylcholinesterase
endplate potentials (epps)
post-syn potentials in muscle fibers
degrade with distance
study of synaptic transmission at frog NMJ
muscle fiber has a resting pot
impale fiber with microelectrode at a point several mm from endplate to record resting pot and APs
curare
blow dart poison
applied to frog nerve-muscle preparations
at some concentration APs fail and muscle does not contract
APs in motor neuron unaffected though and muscle can generate AP if current directly injected
curare mechanism of action
interfere with synaptic transmission at NMJ
blocks some post-syn receptors and reduces size of epps
how is curare useful
reduce size of epp below threshold so no AP, but can still record epps
postsynaptic current (psc)
change in rate of ion flow across post-syn mem
what drives psc
nt binding receptors to change amount of ionic current crossing membrane
direction and intensity of psc controlled by size of conductance and electrochemical driving force
ions responsible for ps at NMJ
influx of Na partly canceled normally by smaller efflux of K
both move through post-syn ACh channels (less selective than voltage gated ion channels)
are psc shorter lived than postsynaptic potentials (psp)?
yes, ACh only opens channels momentarily
why does a psp last longer than psc
time depends on duration of psc and time constant of membrane
reversal potential (Erev)
resting potential at which there is no change in voltage in post-syn cell
no net driving force on ions so no net charge movement
for 1 ion its the nernst potential
excitatory postsynaptic potential (epsp)
any change in membrane potential of post-syn membrane that increases probability of an AP being generated in post-syn cell
inhibitory postsynaptic potential (ipsp)
any change in membrane potential of post-syn membrane that reduces probability of AP being generated in post-syn cell
if reversal potential of post-syn current is more pos than threshold the synapse is…
excitatory
if reversal potential is more negative than threshold the synape is…
inhibitory
inhibitory post-syn currents are typically carried through what channels
permeable to K and Cl-
ACh is excitatory in…. and inhibitory in….
excitatory: NMJ opening Na/K channels
inhibitory: parasympathetic neurons innervating the heart (K channels open longer reducing frequency of spontaneous depolarizations that drive heart beat)
presynaptic inhibition
inhibitory transmitter released from a terminal that ends on the pre-syn terminal of an excitatory axon
reduce amplitude of AP invading excitatory axon
postsynaptic inhibition
globally reduces excitability of post-syn cell
miniature endplate potentials
accidental release of nt from 1 vesicle resulting in a depol of .1mV
amount of transmitter released varies directly with…
amount of depol in presyn terminal
more = more
if low extracellular Ca, less postsyn response
function of Ca in nt release
concentration of Ca in NMJ must rise after an AP arrives in order to nt to be released
docking of vesicles at active zones
SNARE proteins located in vesicular membrane (v-SNARE) and in plasma memb of active site (t-SNARE)
v and t SNARES form a complex to dock vesicles
synaptotagmin
protein associated with memb of mature vesicles
interacts with proteins of SNARE docking complex to permit fast Ca dependent membrane fusion
cholinergic
neurons that release ACh
agonist
molecules that mimic that action of a nt b/c they are analogs
antagonists
structural analogs that block nt binding sites
synaptic desensitization
if nt remains in cleft too long, receptors become inactivated
adrenergic neurons
neurons that use norepi or epi as transmitters
can be excitatory or inhibitory
2 classes of ACh receptor
nicotinic (nAChR): NMJ; nicotine mimics action of ACh (fast direct mechanisms)
muscarinic (mAChR): toxin from mushrooms; target cells of parasympathetic ns (indirect mechanisms)
electric ray and nAChR
high densities of these receptors in electroplax organ help them stun prey with high intensity electrical discharges
structure of AChR
5 subunits
ligand must bind 2 alpha subunits to open channel
denervated muscle fiber
crushed axon
causes AChR to spread out
other nt-gated channels in neurons that are fast direct acting
GABA, glutamate
all have one subunit type that binds ligand
ionotrophic glutamate receptors (iGluR)
modifications in synaptic strength that underlie learning and memory
2 receptors named for sensitivity to specific agonists
kainate
AMPA
NMDA
AMPA and NMDA
appear to worth together in post-syn memb. in CNS
NMDA opening
both gly and glu must bind to open
AND depol must happen through AMPA channel –> NMDA (otherwise ion channel blocked by Mg)
AMPA selectivity
selective for Na ions
NMDA selectivity
allow Ca and Na to pass
Ca intracellular messenger
G-proteins
membrane linked molecules that play a role in signal transduction and are linked to slow synaptic receptors
how does G protein complex work
nt receptor protein (spans membrane) gets nt bound extracellularly and activates G protein on cytoplasmic face
G protein regulates activity of effector proteins which could be ion channels, enzymes (control [ ] 2nd messengers) or both
metabotrophi gluatamate receptors lack…
an ion channel
G-protein coupled that modify intracellular pathways
neuromodulation
pre-syn neuron can modify synaptic responses in post-syn neuron and other neurons in its vicinity
last from secs to mins
synaptic plasticity
changes in synaptic efficacy that are longer lasting or permanent
fast epsp
ACh binds nAChR
slow epsp
ACh binds mAChR
late slow epsp
GnRH like peptide
released from pre-syn neuron, but not directly onto post-syn neuron
enhances fast responses
density of inhibitory synapses contacting many neurons is highest near the…
axon hillock
synaptic summation
addition of several post-syn potentials in post-syn neuron
spatial summation
summed inputs coming from 2 or more different neurons
temporal summation
summed inputs from a series of high-frequency APs arriving at a single synaptic terminal
neuronal plasticity
modification of neuronal function as a result of experience
homosynaptic modulation
activity in terminal itself causes a change in release of nt
heterosynaptic modulation
changes in pre-syn function induced by action of a modulator substance released from another close axon terminal
synaptic facilitation
when the amplitude of a second stim (summation) is greater than adding the two stims together
due to lingering Ca in pre-syn terminal (more nt release)
tetanic stim (depression)
normal ca: reduced efficacy at NMJ b/c depleted vesicles
low Ca: no depression b/c no depletion
tetanic stim (potentiation)
normal ca: occurs after depression, lasts a long time
low ca: occurs immediately, short lived
heterosynaptic facilitation
amount of nt released increased by presense of modulator
alters number of Ca ions that enter pre-syn terminals following AP
long term potentiation (LTP)
neurons innervating hippocampus stimulated at high frequency
increase in amplitude of post-syn potentials long after stim ends
excitatory nt glutamate
AMPA/NMDA receptors contribute
long term depression (LTD)
repeated low frequency stimulation of hippocampus
