Synapses Flashcards
Synapses
Junction between two neurons
Primary means by which one neruon directly interacts with another neuron
Pre synaptic
Synapse
Post Synaptic
Converge and Divergence
Converge: many neurons into one
Divergence: one neuron into many
Synapse steps
- Action potential arrives at terminal end
- Voltage gated calcium channels open
- Calcium moves into knob (where synaptic vesicles are)
- Arrival of Calcium triggers the release of neurotransmitters
- NT migrate across synapse
- Binds to receptor sites
-opens ion gates
-triggers graded potiental
Neurotransmitter release
Calcium binds to synaptotagmin
-stimulates snare proteins which release NT
- Vesicles migrate down
Post synaptic membrane
Activates
-Ionotropic receptors- action ion charnels, first response
or
- Metabotropic receptors - 2nd messenger activation of channel
Synaptic delay
0.2msec for Ionotropic
0.5msec for metabotropic
- bigger delay then would think
Synapses in terms of IPSP or EPSP
Signal at synapse either excites or inhibits the postsynaptic neuron
Two types of synapses (binds to)
-Excitatory synapses (Na+ or ion gates)
-Inhibitory synapses (K+ gates or Cl- gates)
Direction of flow
Excitatory Synapse: out ward from synapse
Inhibitory Synapse: back towards the synapse
Refer to slide 65 if needing help
Size of post synaptic potential
Depends on:
Calcium levels (fatigue) (not enough neurotransmitter released)
NT levels
Desensitization / hypersensitization (desense= same message over and over, hypersense=small impulse high release)
Pre-synaptic inhibition or facilitation
Spatial vs temporal summation
Spatial:
Summation of many EPSP’s occur at
different locations on the dendrites at the same time
Temporal Summation:
Summation of many EPSP’s occurring at
the same location over a very short
period of time
Need both to reach threshold?
EPSP and IPSP interaction: some neurons have 200k terminals
Pre synaptic facilitation/inhibition
ex: Opiates, endorphins meaning they inhibit release of neuro transmitter
Neuron A releases neurotransmitter that can either increase or decrease release from neuron B
Neurotransmitters
Vary from synapse to synapse:
-Same neurotransmitter is always released at a particular synapse
-Quickly removed from the synaptic cleft
Some common neurotransmitters:
Acetylcholine
Dopamine / Serotonin
Norepinephrine / Epinephrine
Histamine
Glutamate
Gamma-aminobutyric acid (GABA)
Neuropeptides
Large molecules consisting of from 2 to 40 amino acids
Neuropeptides:
Substance P (pain)
Enkephalins /Endorphins
Dynorphins
Hypothalamic releasing
and inhibiting hormones
Angiotensin II (BP)
Cholecystokinin (gut)
Characteristics of Neurotransmitters and Neuropeptides
Neurotransmitters:
Small, one amino acid or smilier chemical. Rapid, brief response
Neuropeptides:
Large, 2 to 40 amino acids in length. Slow, prolonged response
Acetylcholine (Ach)
Cholinergic receptors
* Parasympathetic system / muscle
* Muscarinic vs nicotinic receptors
(agonists)
* Broken down by acetylcholinesterase
and recycled (send it out and then take it back)
⬧ Sarin – inhibits this enzyme
* Alzheimer’s Disease
Catecholamines
Epinephrine / norepinephrine
- Affect consciousness, mood,
attention
-BP, HR (fight or flight)
Adrenergic / noradrenergic
receptors
Broken down by MAO
(monoamine oxidase)
MAO inhibitors increase epi
levels in synapse
* Anti-depressant (affect mood and conciseness)
Serotonin
From tryptophan / modulates (slow onset)
Excitatory on muscle control
Inhibitory on sensory mediation
Mood, anxiety, wakefulness
-role with dopamine too
Block reuptake with
Paxil (anti-depressant)
Also LSD
Serotonin and dopamine work together
Examples:
Parkinson’s Disease
Decrease release of L- dopa (dopamine) from basal nucleii
Tremors / muscle rigidity
Synaptic drug interactions
Possible drug actions:
-Altering the synthesis, axonal transport, storage, or release of a neurotransmitter
-Modifying neurotransmitter interaction with the postsynaptic receptor
- Influencing neurotransmitter reuptake or destruction
- Replacing a deficient neurotransmitter with a substitute transmitter
Possible drug effects on synaptic effectiveness
A. release and degradation of the
neurotransmitter inside the axon
terminal
B. increased neurotransmitter release
into the synapse
C. prevention of neurotransmitter
release into the synapse.
D. inhibition of synthesis of the
neurotransmitter.
E. reduced reuptake of the
neurotransmitter from the synapse.
F. reduced degradation of the neurotransmitter in the synapse.
G. agonists (evoke same response as neurotransmitter) or antagonists
(block response to neurotransmitter) can occupy the receptors.
H. reduced biochemical response inside the dendrite
drug interactions
Agonists – mimic NT when they bind
Eg. Morphine (opiates), block pathway
Antagonists- bind but don’t activate
receptor – blocks site
Eg. Atropine (Ach), block binding site
drugs that alter synaptic transmission
Cocaine:
Blocks reuptake of neurotransmitter dopamine at presynaptic terminals, doesn’t take dopamine back
Strychnine
Competes with inhibitory
neurotransmitter glycine at
postsynaptic receptor site
* convulsions
Tetanus toxin
Prevents release of inhibitory
neurotransmitter GABA, affecting
skeletal muscles
* (destroys SNARE proteins)
Botulism
Interferes with SNARE proteins for
excitatory NT
-Muscle paralysis (can’t breath)
