Synaptic Transmission Flashcards
types of synapses
- electrical
- chemical
electrical synapse
gap junctions
- direct cell to cell contact
- cytoplasmic continuity
- conduct electrical signals very rapidly (no delay)
- 2-4 nm gap
- 2 way conductance
- diameter on the protein pores = 1.5 nm
- –> only ions/small molecules can pass
electrical synapse location
- immature neurons
- glacial cells to neurons
- cardiac muscle
- smooth muscle
chemical synapse
- synaptic cleft (10-20 nm gap) between 2 neurons
- AP in presynaptic neuron stimulates neurotransmitter release
- NT release across cleft (.2 msec delay) to bind to receptors on postsynaptic cleft
- one way flow
- amount of NT can be modified
- number of receptors for NT can be modified
level of excitability of a postsynaptic cellar any moment depends on:
- the number of synapses active at one time
- number the are excitatory
- number that are inhibitory
complexity altered by:
- number of neurons
2. number of synapses
plasticity
constantly making new synapses, basis for learning
excitatory postsynaptic potentials (EPSPs)
depolarizing graded potentials
- neuron more likely to generate action potential
NT’s that generate EPSPs
- Ach
- glutamate
- NE
EPSPs caused by:
Na+ flows in
inhibitory postsynaptic neuron (IPSPs)
hyper polarizing graded potenitals
- less likely to generate action potential
NT’s that generate IPSPs
- GABA
- glycine
IPSPs caused by:
- Cl- flow in
- K+ flow out
- most will K+ channels, Cl- doesn’t have much of an effect by itself
NT removal options
- diffuse away (glutamate)
- reuptake (serotonin)
- degradation by an enzyme (AchE –> degrade Ach)
summation
local potentials are small: need about 20 EPSPs to reach voltage (.5 mV)
temporal summation
multiple inputs in rapid success ion from one synapse
spatial summation
input from multiple different synapses arriving at the same time
convergence
many different presynaptic neurons can affect a single postsynaptic cell
divergence
a single presynaptic neuron that can affect many postsynaptic cells
presynaptic facilitation
increased number of Ca+ channels open on presynaptic neuron, increasing the quanta of NT released, increase the postsynaptic response
presynaptic inhabitation
decreased number of Ca+ channels open in presynaptic neuron, decreasing the quanta of NT released, decreasing the postsynaptic response (decreasing local potential)
desensitization
with persistent stimulus, receptor fails to respond (tolerance to drugs)
neuromodulation
modify the postsynaptic cells response to a specific NT (amplifying or dampening its effectiveness)
Ligand-gated ion channels
- ionotropic
- cellular response = local potential
- rapid response
ionotropic
receptor forms ion channel
G-protein coupled receptors
- metabotropic
- cellular response = activation of second messenger cascade
- slower response
- change in gene transcription, enzyme activity, etc.
metabotropic
change “metabolism”
metabotropic receptors
- usually small molecules, co-released with NT
- bind to receptors on pre- or postsynaptic membrane
- activate 2nd messenger signaling cascades –> have longer term effects
- ex: NTs, neuropeptides, nitric oxides, ATP
neuromodulators
- alter synthesis, release, uptake or metabolism of NT at the presynaptic cell
- increase or decrease the effectiveness of a NT at the postsynaptic cell
- are associated with longer term effects
Botulism Toxin mechanism of action
- prevents exocytosis of synaptic vesicles –> no NT released
- specific for excitatory neurons
Botulims Toxin consequence
- decrease in muscle contraction
- can paralyze respiratory muscles (fatale)
dystonia
too much muscle contraction
sarin (nerve gas) mechanism of action
- inhibits AchE
- increases Ach in synapse
sarin consequence
- uncontrolled muscle contraction
- desenitization –> paralysis
- respiratory arrest –> most common death
SSRI
selective serotonin reuptance inhibitor
Paxil (SSRI) mechanism of action
- prevents reuptake
- increases serotonin
Paxil consequence
- build up of serotonin in synaptic cleft
- stabilizes mood
xanax, valium, ethanol mechanism of action
- stimulate GABA-R
2. block Glut-R
xanax, valium, ethanol consequence
- decrease anxiety and increase sleep (GABA-R)
2. decrease mental processing (learning) and decrease sensory / motor (Glut-R)
