Chapter 5: Synaptic Transmission Flashcards
Who named the synapse?
Charles Sherrington( 1897)
Synaptic transmission
information trnafer at the synpase
Two Hypothesizes of information transfering in two ways:
- electrical curernt flow
- chemcial informaiton transfer
Electrical synapes
transfer electrical change across the synapse
* ions pass from cell to cell
Chemical synapse
- chemcial transfer of information
- majority of the synapses in the brian
NT relased by presyantpc neruron carry info to postsynaptic
how are cells electrically coupled?
ions flow form one cells cytoplasm to another cell’s cytoplasam
How are Gap junctions invloved?
- common in non-nruronal cells
- channels made of two connexons
Key points of electrical synapses
- very fast transmission
- synpatic integration; several PSPs occuring togrether can cuases an AP.
Otto loewi
experminentally demonstrated chemical NT
explian the otto loewi:
- proved that chemical transmission is the mode of communication in neurons/ nerves
- called the chemical vasgusstuf; but now known as **acetylocholrine **
- shared the nobel proze with Sir Henry (1936)
chemical synapse
Two neurons don’t physically touch, why?
- synatpci cleft of 2-50mm
- presynaptic elemen, postsyantpic element
- temporal delay between presyantpic AP and postsynatpic repsosne
chemical synapse
release mechanisms
- synaptic vesicles
- secretory grandules
chemical synapse
synaptic vesicles
contain neutotransmitters
secreting grandules
dense-core vesciles
* contians neuropeptides
chemcial synapse
sides of synapse
proteins are dustered on both side of the synaptic cleft
pesyantpic and postsynaptic
chemical synapse
presynaptic
active zone(NT release site)
* voltage-gated ca+ channels
* IMPORTANT for effecient NT release
chemical synapse
Postsynaptic
- density ( NT receptors)
- IMPORTANT got manging postsynaptic response to NTs
CNS synapse
postsynatpi appearance differs by chemical transmision types
- gray type 1 and 2
Gray type 1
asymmerterical, excitable
gray type 2
symmeterical, inhibitory
synaptic arrangement
axodindretic, axosomatic, axoaxonic
neuromuscale junction
synapse controlling muscle movement
basic strps
- neurotransmitter synthesized
- neurotransmitter loaded into synaptic vessels
- vesicles fuse to presynaptic terminal
- neurotranmitter spills out into synaptic cleft
- neurotranmitter binds to postsynaptic receptor
- biochemcial/ electrical response in postsynaptoc cell
- neurotransmitter removed form syunaptic cleft
what activitate postsynpatic receptors?
chemical released by the presynaptic
amino acids and amines
synthesized in axon temrinal
amino acids and amine location
store in synaotic vesicles for release
peptides
synthesizes in soma, packaged into dense core vesicles and trnasmitted to axon terminal for rlease
Synthesis of NT
from metabloic precussors, amino acid, and amino acids joined by peptide bonds
storage of NT in AA and amine
in the axon temrinal; store: packaged into synaptic vesciles by tranpsort
storage and location of NT w/ peptide
location- soma
storage- secretory graduate, golgi for transportation
NT release process inside axon terminal steps
- action potential reaches terminal
- voltage - gated calcium channels open
- very rapid onset of vesicles fusion and 0.2 m/sec form calcium entry
how do synaptic vesicles respond so quiclkly
synaptic vesciles are ready and waiting to release transmitter at synapse upon influx of ca+
NT release
exocytosis, and endocytosis
excytosis
vesciles memebrane fuses w/ presyanptic plasma membrane, contents can access outside of the terminal, diffuse across synaptic cleft
endocytosis
recovering of vesicles ffrom teh plasma membrane
Neuropeptide release
- secretoty granules also release contents through exocytosis
- but usually aren’t at active zones
needs high frequency to retain Ap - release of peptide is slower
chemical neurotranmission
summary
- neurotransmitter synthesized( AA, amine, and pepetide)
- neurotransmiitered loaded into synatic vesicles
- . vesciles fuse to presyanmtpci terminal
- neurotransmiter spills out into syntic cleft
- neurotransmitter binds to postsynatic receptor
- biochemcial/ electrical response in postsynaptic cell
- neurotranmitter removed form synatpic cleft
NT receptor+ effecvtir: tramistter- gated ion channels
- fast receptor
- NT or drug binds= channels subunits shift to open ion channel( inotropic)
- channels may let ions in= causes postsynaptic potential
EPSP- excitatory Postsynaptic potential
caused by release of excitatory NT( Glu)
* membrane in postsynaptic neuron is deploraized by entry of Na and somethiunf ca2+
IPSP- inhibitory postsynaptic potential
- cuased by release of inhibitory NT: GABA, glycine
- membrane in postsynaptic neuron: hyperplorization
NT Receptors and effectot: G protein- coupled receptors
- slower, long lasting transmission
- works thorugh “effector proteins” the G protein
1. * metabtopic(need atp)
G-protein
- activate or inhibit secodn messengers effect enzyme
- stimulus or inhibit, channnel opening
Mechanism of Nt inactivation: recovery and degradtion
- diffusion away from synaptic cleft
- retupke by presynaptic neuron
* invloes proetins knwon as transporters
* nts repackages into recycled vesicles or degraded by enzymes
* nearby glail cells also help with cleareance - enzymatic degration
* eg. acetylocholine
Autoreceptors
- locations on presynatptic neuron
- often providea feed back signal to regualte on going neurotransmission
summation
integration- adding together individual EPSPS to pridce signifiacnt deploraiztion
Spitial summation
ESPSP generated at the same time in different spaces
* single peak, height based on how many inputs activated together
temperol summation of EPSP
EPSPs generated at the same synapse in rapid succesion
* this means at different times in the same space
* * multiple peaks, height gets larger w/ each input
contribution of denertic properties
dendritic cable properties
- considered dendrities w/o voltage-gated channels,a s they have a few compared to axons
contribution of dendrtic properties
Affecting ESPS summation
leaky membrane- deplorization drops off exponentially w/ increasing distance travelled
vx= vo/e^x
synaptic integration: excitable dendrities
there are voltage-gated na+, ca2+. k+ chnnels in dendrites
* but rarely have enough channels to turn PSPS deplorization into action potential
Synaptic integration: IPSP
takling the membranr potentila away from AP threshold
exers powerful control over neurons output
inhibitary Synapse
GABA, gly bidning to recpetors open cl- channels
* cl- entry drops memebrane poteinal below( -65 m/v) = hyperpolrization
Shuning inhibition
- inward movement of cl-
- inhibits deplorixation reacting( crossing soma to axon hillock
- drastically reduces membrane resistance * postive curernt flows out
- called “ shunt”when inhibitory synapse in closer to soma
hyperplexia
overactive startle response
* excessive startle to single events
Hyperplexia is caused by?
improper glycine receptor signaling
spasmodic and spastic
spasmodic
single aminoa cids change, channel doesn’t come
spastic
normal receptors; not enough of them
GPCR modualtion of synaptic response
modifies effectivesnness of EPSPs generated at other synapse
* transmitters bind metabotropic receptors to activate ion channels though 2nd messgener pathways
