Chapter 3 - Synapses and Synaptic Transmission Flashcards
presynaptic terminal
located at the end of the axon
- projection specialized for the release of chemicals to the postsynaptic terminals
- contains neurotransmitters
Synaptic communication sequence
1) action potential arrives at the presynaptic terminal
2) membrane of the presynaptic terminal depolarizes, opening voltage-gated calcium channels
3) influx of Ca into neuron terminal combined with liberation of Ca from intracellular stores triggers the movement of the synaptic vesicles
4) synaptic vesicles fuse with the membrane, releasing neurotransmitters into the cleft
5) neurotransmitter diffuses across the cleft
6) neurotransmitter contacts and binds with receptor on the postsynaptic membrane
7) receptor changes shape by:
a) opens an ion channel
b) activates intracellular messengers
postsynaptic potentials
local changes in ion concentration across the postsynaptic membrane
Neurotransmitters
effect of the neurotransmitter is based on the receptor it binds(inhibitory or excitatory)
- determined by the nature of the post-synaptic receptor
Ligand-gated receptors
binding of neurotransmitter opens channels for action potential
- faster response, short duration
G-protein activated receptors
2nd messenger
- binds to membrane and then 2nd messenger begins cascade of response
- slower response, longer duration
Action at the Synapse
1) action potential arrives at the presynaptic terminal
2) membrane depolarizes
3) Ca in the nerve terminal
- Ca channels open -> into
- vesicles migrate to presynaptic terminal and releases neurotransmitter
4) neurotransmitter diffuses across
5) shape of membrane changes
EPSP
Excitatory postsynaptic potential
- local potential
- neurotransmitter binds to receptor and opens Na+ channels causing action potential(depolarization)
- if binds to neuromuscular junction = muscle contraction
IPSP
Inhibitory postsynaptic potential
- local potential
- hyperpolarization K+ channels open making it more negative making less possible for action potential
Facilitation
axoaxonic synapse
- if excitatory from presynaptic terminal = more neurotransmitter released
- therefore more effect on postsynaptic terminal
- more Ca into presynaptic terminal
Inhibition
axoaxonic synapse
- if inhibitory from presynaptic terminal = less neurotransmitter
- therefore less effect on postsynaptic terminal - less Ca into presynaptic terminal
Cholinergic Neurotransmitters
Acetylcholine(ACh)
- post ganglionic parasympathetic
- preganglionic parasympathetics and sympathetics
- in autonomic nervous system
- excitatory
Muscarinic receptors
activated by muscarine
- a poison from a mushroom
- cholinergic
Nicotinic receptors
activated by nicotine
- cholinergic
Amino acid transmitter substance
GABA = inhibits Glutamate = excitatory Glycine = primarily in spinal cord(inhibitory)
Amines
Dopamine(DA) Epinephrine(adrenaline) Histamine Norepinephrine(NE) Serotonin(5-HT)
Dopamine(DA)
excitatory or inhibiting
- low levels = Parkinson’s
- schizophrenia = give drugs to interfere with dopamine
- possibly have too much dopamine causing disease)
Epinephrine(adrenaline)
not a big effect on nervous system
Histamine
concentrated in hypothalamus
- inhibitory
Norepinephrine(NE)
sleep/wake cycle and alertness
- in locus cerelius
- neurons for postganglionic parasympathetic system
Serotonin(5-HT)
regulation of mood
- for raphe nuclei in brain stem
- descending pain control system
- decreased serotonin = depression
Neuroactive peptides
endorphins
enkephalins
substance P
Endorphins
powerful analgesic(feel better)
- everywhere
- opium releases endorphins
- runner’s high(exercise)
Enkephalins
located in dorsal gray horn(sensory)
- can suppress painful stimuli
- similar to endorphins
Substance P
excitatory
Agonist
can mimic the effects of a neurotransmitter
antagonist
blocks the release of a neurotransmitter or binds to a receptor to prevent neurotransmitter from binding
- Ex: blocks ACh binding
Skeletal muscle contraction
1) action potential arrives
2) nerve secretes acetylcholine into the synaptic cleft
3) ACh binds to receptors on muscle membrane that opens the ion channels
4) action potential depolarizes the muscle and travels along the T tubules
5) reaches the sarcoplasmic reticulum and causes the myofibrils to release calcium
6) calcium initiates attraction of actin and myosin causing them to slide together
7) get shortening of sarcomeres
8) muscle contraction would continue as long as calcium remains in the area
Myasthenia Gravis
autoimmune disorder
- body creates antibodies against ACh receptors
- ACh is released and binds wherever possible
- with repeated contractions of muscle, continuously gets weaker
- eyelids droopy, along with facial muscles
- proximal weakness sometims
