Lecture 1 Synaptic transmission Flashcards Preview

202 Theme 1 > Lecture 1 Synaptic transmission > Flashcards

Flashcards in Lecture 1 Synaptic transmission Deck (45)
Loading flashcards...

what is a synapse

a specialised junction where part of a neuron contacts and communicates with another neuron or cell type (muscle or glandular)


what are the two main categories of synapses

chemical (majority) and electrical (minority)


how do electrical; synapses compare to chemical

simpler structure and function
passive signal transmission
minority (common in development)
allow synchronised electrical activity among populations of neurons


how do chemical synapses work simply

Arrives as electrical and converted to chemical and back to electrical in chemical synapses


what is a drug

a chemical substance, which when administered to a living organism, produces a biological effect
drugs affect how signals are communicated at a synapse
eg caffeine
affects learning and memory


what are the types of synapse



what is the presynaptic element

upstream neuron, source of current


what is the postsynaptic element

downstream neuron, into which current flows


how does synapse location link to function

where they are affected how strongly they affect the postsynaptic neuron


what is an axodendritic synapse

presynaptic axon to dendrite in postsynaptic neuron


what is an axosomatic synapse

presynaptic contact to postsynaptic soma (more synaptic weight)


what is an axoaxonic synapse

presynaptic axon contacts axon of another cell before attaching to postsynaptic soma, affects communication as can cancel each other out (signal integration to determine excitation/inhibition)


what is the chemical synapse

synaptic bouton - presynaptic element
cytoskeleton - aid function and passing signals
synaptic vesicles - cont nt
synaptic granules ^
active zone - membrane of presynaptic cell to optimise conditions of membrane for communication
synaptic cleft - gap btwn AZ and postsynaptic cell


what is the neuromuscular junction

similar to chemical synapse
one synapse innervates many muscle fibres
vesicles contain Ach, received by muscle fibres converted to electricity for contraction


what is the postsynaptic membrane at the neuromuscular junction called

motor end-plate
folds to inc SA for more powerful reception of signals


how does synaptic transmission occur

as an action potential reaches the synaptic terminal, nt molecules are released from presynaptic neuron and diffuse across cleft to post synaptic membrane


what do receptors on the postsynaptic membrane recognise

specific neurotransmitters to initiate a response


what are the types of responses

direct excitatory or inhibitory (on or off) neurotransmission

neuromodulation - lots of possible effects (dynamic so important in development and memory)


what is direct excitatory or inhibitory transmission

the membrane of the next cell becomes slightly depolarised (ex) or hyperpolarised (in)


what is neuromodulation

alters the presynaptic cell's ability to release more transmitter or the postsynaptic cell's ability to respond


how much transmitter is released

released in specific packages (quanta)


what criteria define a neurotransmitter

synthesised in the neuron
present in presynaptic terminal and released to exert a defined effect on postsynaptic neuron or effector organ
administered exogenously it mimics action of endogenously released transmitter
specific mechanism exists to remove it from cleft


what is the first step of typical chemical synapse transmission

transmitter synthesised then stored in vesicles


what is the 2nd step of typical chemical synapse transmission

action potential invades the presynaptic terminal


what is the 3rd step of typical chemical synapse transmission

presynaptic. terminal depolarises causes opening voltage gated ca2+ channels


what is the 4th and 5th step of typical chemical synapse transmission

influx of Ca2+ causing vesicles to fuse with presynaptic membrane


what is the 6th and 7th step of typical chemical synapse transmission

transmitter released int synaptic cleft by exocytosis
binds to receptor molecules in postsynaptic membrane


what is the 8th and 9th step of typical chemical synapse transmission

opening or closing of postsynaptic channels
postsynaptic current causes ex or in potential that changes the excitability of the postsynaptic cell


what is the 10th and 11th step of typical chemical synapse transmission

remove nt by glial uptake or enzymatic degradation
retrieve vesicular membrane from plasma membrane


where and how are vesicles anchored in the presynaptic cell

pool of vesicles anchored to cytoskeleton by synapsin


how does action potential flow through the cell

action potential to presynaptic terminal, voltage gated ca2+ channels open so ca2+ flows to cytoplasm activate calmodulin activated kinase II (CaMKII) which phos synapsin


How are synaptic vesicles released and recycled

activates calmodulin activated kinase II (CaMKII) which phos synapsin
P-synapsin can no longer bind to cytoskeleton, allows vesicles to dock to active zone to start fusion/exocytosis
vesicles reused


what is a SNARE complex

at active zone
enzyme (ATPase) docks vesicles to plasma membrane as a helical protein with v and t SNAREs


what are the mechanisms of exocytosis during neurotransmitter release

vesicle docks
entering Ca2+ allows binding to membrane
SNARE complex form to pull membranes together
entering Ca2+ binds to synaptotagmin
ca2+ bound synapto catalyses membrane fusion by binding SNAREs to plasma membrane


how are vesicles recycled

rapidly recovered by endocytosis (10-20 sec), new vesicles bud off and refilled with transmitter
whole cycle about 1min


how are SNARE proteins affected by clostridial toxins

sites of proteolysis blocking nt release
target amino acids in SNAREs
botox and tetanus prevent transmission release


how does botulinum toxin affect SNAREs

stops neuromuscular transmission of Ach - paralysis by relaxation (treatment for muscle paralysis)


how does tetanus toxin affect SNAREd

interneurons at spinal cord, GABA/gly to stop inhibitors - permanent contraction


where are botulinum and tetanus toxins from

from bacteria Clostridium botulinum and tetani respectively


what diseases affect the presynaptic terminal

cong myasthenia syndromes - impaired vesicle recycling
latrotoxin - trigger vesicle fusion
botox and tetanus
cog disorders impair transsynaptic signalling
LEMS attacks presynaptic Ca2+ channels


how are vesicular transporters powered

proton gradient
ATPase proton pump loads up vesicles with H+ to make acidic (pH 5.5 comp to cytoplasm 7.2)
eg 1 glut traded for 1 H+ (counter transport)


how are plasma membrane transporters powered

by electrochemical gradient
Na+ higher outside and K+ inside
eg glut co transported in with 2 Na+


what do glia do

part of tri-partite synapse - support and regulate
support synaptic transmission
express nt receptors (can respond to synaptic activity by changing intracellular Ca2+)
coordinate synapse formation and elimination with secreted and cell surface associated signals


what do glia control

synapse formation
crucial in development, learning, memory and disease


how do glia link to disease

reactive gliosis post injury (relevant to CNS regeneration)
aberrant synapse formation (link to epilepsy and neuropathic pain)
brain cancer
HIV induced dementia
neuroinflammatory response (depression)
neurodegernative diseases (Alzheimers, glaucoma, prion disease through aberrant synaptic stripping)