W2- Neuronal conduction and synaptic transmission Flashcards
membrane potential
difference in electrical charge between inside and outside of cell
how do you record membrane potential of neuron?
one microelectrode inside neuron and another outside
neuron is at rest- not receiving signals
what is the resting membrane potential of a neuron?
-70 mV- potential inside is 70mV less than outside
polarised
membrane potential that is not zero
Describe distribution of Na+ and K+ in resting neurons
more Na+ outside than inside the cell
more K+ inside than outside the cell
what causes the pressure on Na+ ions to enter resting neurons?
electrostatic pressure from the positive ions being attracted to negative charge inside neuron
random motion of Na+ ions wanting to move down concentration gradient
why do Na+ not enter resting neuron?
sodium ion channels are closed
why do K+ stay inside neuron?
potassium ion channels are open and a few K+ will leave but most stay due to electrostatic pressure from negative charge inside neuron
how does the resting potential stay constant despite some movement of K+ and Na+?
the leaking of Na+ and K+ ions is made up for by sodium-potassium pumps which transport three Na+ ions out of the neuron and two K+ into the neuron
postsynamptic potentials (PSPs)
potential which causes the postsynaptic cell’s membrane potential to move away from resting state
depolarise
decrease resting membrane potential
hyperpolarise
increase the resting membrane potential
excitatory postsynamptic potentials (EPSPs)
postsynaptic depolarisation
increases likelihood of neuron firing
inhibitory postsynaptic potentials (IPSPs)
postsynaptic hyperpolarisations
decrease likelihood of neuron firing
graded potential
all post-synpatic potentials
means amplitude of PSP is proportional to intensity of signal which elicited it
what are two main characteristics of PSP transmission?
it is rapid- essentially instantaneous
decremental- the amplitude of the PSP decreases as it travels through the neuron
what determines whether a neuron fires?
the balance between excitatory and inhibitory signals reaching its axon
if EPSPs and IPSPs are such that sum of depolarisations and hyperpolarisations allow neuron to be depolarised to threshold of excitement- AP is generated
where are axon potential generated?
axon initial segment- adjacent to axon hillock
threshold of excitation
-65mV
level of depolarisation needed to generate action potential
action potential
not graded- all-or-non response
a massive momentary reversal of the membrane potential from -70 to +50mV
lasts 1 millisecond
what are the two ways summation of PSPs occurs?
over space
over time
temporal summation
the integration of neural signals which occur at different times at the same synapse
this occurs when previous PSP has not dissipated yet so subsequent PSP is superimposed on lingering PSP
two simultaneous EPSPs or IPSPs can sum to produce greater PSP
or simultaneous IPSP and EPSP can cancel each other out
voltage-gated ion channels
ion channels that open or close in response to changes in membrane potential
what happens to ion concentrations when threshold of excitation is reached?
voltage-gated sodium channels in axon membrane open wide
Na+ ions enter neuron- membrane potential reversed to +50mV
this rapid voltage change triggers opening of voltage-gated potassium channels
K+ ions are driven out of the cells- due to concentration gradient and positive charge inside neuron
transition from rising phase to repolarisation phase when sodium channels close
repolarisation achieved by efflux of K+
potassium channels close, starting hyperpolarisation phase- since slow closing of ion channels allowed too many K+ ions out
which ions are involved in AP?
those right next to the membrane
absolute refractory period
a period of 1-2 milliseconds after AP initiation when another AP is not able to be elicited in the same neuron
relative refractory period
period after absolute refractory period where same neuron can only be fired again with high-than-normal amount of stimulation
how do refractory period cause APs to travel in only one direction?
the AP cannot reverse direction because the portion of the axon it has already travelled through become refractory
how are refractory periods responsible for rate of neural firing being related to stimulation intensity?
the stimulation intensity affects the rate of neural firing as a max of 1000 times per second is reached when stimulation is high enough for the neuron to fire again as soon as absolute refractory period is over and low stimulation can result in the neuron only firing when both refractory periods are over. Intermediate rates occur between these two
how does AP conduction along axon differ from PSP conduction?
nondecremental
conducted more slowly
this is because initial AP travels along axon as graded potential (rapid and decremental) and if it is sufficiently large upon reaching next voltage-gated sodium channel, gates open and Na+ rush in creating another AP. This continues along the axon until full AP is triggerd at axon terminal buttons
antidromic conduction
axonal conduction in opposite direction towards cell body
occurs with APs starting at axon initial segment- large graded potential spreads back to cell body and dendrites- thought to play role in synaptic plasticity
orthodromic conduction
normal direction of axonal conduction towards terminal buttons
how does conduction occur for myelinated axons?
axons can only pass through axonal membrane at nodes of ranvier
this is where gated ion channels are concentrated
this causes signal to jump along axon at faster rate due to less delays created by more frequent AP generation
saltatory conduction
AP conduction from one node of Ranview to next along myelinated axon
what characteristics affect speed of AP conduction?
faster in large-diameter axons and myelinated axons
how does conduction occur in neurons without axons?
conduction in interneurons typically occurs only through graded potentials
axodendritic synapse
synapse of axon terminal button onto dendrite
often terminate on dendritic spine
axosomatic synapse
synapse of axon terminal button on somas
dendritic spine
nodules of many different shapes located on dendrite surface
tripartite synapse
synapse composed of two neurons and astroglial cell
communicate through synaptic transmission
dendrodendritic synapse
synapse of dendrite on dendrite
transmission can occur in both directions
axoaxonic synapse
synapse of axon on axon
mediate presynaptic facilitation and inhibition by specifically targetting effects of specific terminal button on postsynaptic neuron rather than affecting entire presynaptic neuron
directed synapses
sites of neurotransmitter release and reception are in close proximity
axomyelenic synapse
synpase of axon on myelin sheath of oligodendrocyte
form of neuron-glia communication
nondirected synapse
site of release far from site of reception
certain types include release of neurotransmitters from varicosities
neurotransmitter are widely dispersed
varicosities
bulges or swellings along axon and axon branches
string-of-beads synapses
neuropeptides
large neurotransmitters
short amino acid chains- 3-36 amino acids
synthesis of neuropeptides
synthesised in cytoplasm on ribosomes
packaged in vesicles by cell body’s Golgi complex
transported by microtubules to terminal buttons- rate of 40cm per day
vesicles congregate a bit further away from presynaptic membrane compared to small-molecules neurotransmitters
synthesis of small-molecule neurotransmitters
synthesised in cytoplasm of terminal button
packaged in synpatic vessels by button’s Golgi complex
vesicles stored in clusters next to presynaptic membrane- in areas rich in voltage-gated calcium channels
how many neurotransmitter types does each neuron produce?
presence of more than one neurotransmitter in the same neuron
can be one small one large, multiple small, or neurons may change over time to produce different types of neurotransmitters
exocytosis
process of neurotransmitter release from presynaptic neuron
process of neurotransmitter exocytosis
AP triggers opening of calcium channels and entry of Ca2+ into terminal button
triggers chain reaction resulting in fusing of synaptic vesicles with presynaptic membrane
vesiclse empty contents into synaptic cleft
release of small-molecule neurotransmitters vs neuropeptides
small-molecule release in pulses each time influx of Ca2+ is triggered by AP
neuropeptides release gradually in response to increasing Ca2+ concentrations- for example from increasing rate of neuron firing
extracellular vesicles
when vesicles doesn’t fuse with presynaptic membrane but is release into synaptic cleft as intact vesicle
carry larger molecules- proteins, RNA
carry molecules between neurons and glia
may induce persistent changes in gene expression- epigenetic mechanisms
receptor
proteins which contain binding sites for particular neurotransmitters
ligand
molecule which binds to another molecule eg neurotransmitters which bind to receptors
may have many different receptors they can bind to
receptor subtypes
types of receptors a nueotransmitter can bind to
different subtypes often in different brain areas and often result in different responses- allows neurotransmitter to relay different messages in different parts of brain
ionotropic receptors
associated with ligand-activated ion channels
ligand binding causes ion channels to either open or close- induces immediate postsynaptic potential
EPSP/depolarisation if sodium channel opened
IPSI/hyperpolarisation if potassium or chloride channels opened- K+ ion go out and Cl- go in
metabotropic receptors
assoicated with signal proteins and G proteins
more prevalent
effects develop slower, last longer, more diffuse and varied
different kinds but each connected to serpentine signal protein outside protein whilst G protein is attached to serpentine signal protein inside neuron
G proteins
guanosine-triphosphate-sensitive proteins
process of metabotropic reception
neurotransmitter binding causes subunit of G protein to break away
next response depend on G protein type
subunit may move along inside surface of membrane and bind to ion channel- induce EPSP or IPSP
or synthesis of second messenger may be triggered- diffuse through cytoplasm and influence neuron activities
second messenger
synthesised as a result of metabotropic reception
neurotransmitters are first messengers
influene neuron activity
can influence genetic expression by binding to DNA in nucleus- long-last effects
may also be produced by ionotropic receptors
epigenetic effects on neurotransmitter reception
epigenetic mechanisms can alter receptors
may result in certain disorders
autoreceptors
type of metabotropic receptor
bind to neuron’s own neurotransmitter molecules
located on presynaptic membrane
monitor number of neurotransmitter molecules in synapse
small-molecular vs peptide neurotransmitter release and receptor binding patterns
small-molecule- tend to release into directed synapses and bind to both ionotropic and metabotropic receptors which act directly on ion channels. transmit rapid, brief, excitatory or inhibitory signals to adjacent cells
neuropeptides- release diffusely, almost all bind to metabotropic receptors which act on second messengers. transmit slow, diffuse, long-lasting signals
reputake
most common mechanism for deactivating release neurotransmitter by taking it back into terminal button via transporter mechanisms
enzymatic degradation
mechanism for deactivating neurotransmitters through breakdown of chemicals by enzymes
enzymes
proteins which stimulate or inhibit biochemical reactions without being affected by them
acetylcholinesterase
enzyme which breaks down acetylcholine, one of nfew neurotransmitter which is mainly deactivated by enzymatic degradation
astrocyte functions
release chemical transmitters
contain neurotransmitter receptors
conduct signals
influence synaptic transmission between neurons
gap junctions
narrow spaces between adjacent neurons bridged by fine tubular proteins channels containing cytoplasm
electrical signals and small molecules pass through these channels
responsible for existence of electrical synapses- more rapid transmission than chemical synapses
cerebral gap junctions
majority occur between cells of same type
eg gap junctions which link astrocyted together forming glial cell network
eg gap junctions between inhibitory interneurons of same type
function of synchronising activities of like cells in particular area
function of astrocytic organisation
role in synchronising activities of like cells in particular area
even distribution unlike neurons- one astrocyte per location and little overlap- potential for coordinating activity
seven general steps of neurotransmitter synthesis, release and action
synthesis of neurotransmitter
storage in vesicles
breakdown in cytoplasm of neurotransmitters which leak from vesicles
exocytosis
inhibitory feedback via autoreceptors
activation of postsynaptic receptors
deactivation
agonist
drugs which facilitate effect of neurotransmitter
may bind to postsynaptic receptor and activate them or increase effect of neurotransmitter on them
may increase synthesis of neurotransmitter- increase precursor amount, destroy degrading enzymes
increase neurotransmitter release from terminal buttons
bind to autoreceptors
block degradation or reuptake
antagonist
drugs which inhibit effect of neurotransmitter
block neurotransmitter synthesis- eg destroying synthesising enzymes
cause neurotransmitter molecules to leak from vesicle so they are destroyed
block release from terminal buttons
activate autoreceptors
receptor blocker
receptor blockers
antagonist drug which binds to receptor without activating it thus preventing neurotransmitter from binding and activating receptor
