BIPN 100 Lecture Notes - Lecture 6: Acetyl Group, Botulinum Toxin, Acetylcholinesterase Inhibitor
26 Jun 2018
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BIPN100 Lecture 6 Notes 4/13/18
- Chemical synapses: synaptic transmission
oSignal travels down axon to synaptic terminal, releasing
neurotransmitters across the synapse, which bind to
receptors on the postsynaptic cell. These neurotransmitters
send signals to either excite or inhibit the response
oCan modulate how much neurotransmitters are released
depending on the number of action potentials, telling the
postsynaptic cell how strong the stimulus is
oNeuromuscular junction (NMJ): most widely studied synaptic
transmission
‘A’ alpha motor neuron sends signals to skeletal muscle fibers
nature of receptor in postsynaptic cell and effect on
postsynaptic cell varies depending on different synapses
- Function of NMJ in somatic nervous system
o‘A’ alpha motor neuron acts as presynaptic cell which affects skeletal muscle fibers that
act as postsynaptic cell
obetween the 2 cells, there’s a synaptic cleft, about 30 nm wide
oAction potential travels down axon to presynaptic terminal
oActivates voltage-gated calcium channels (p/q Calcium channels) at presynaptic
terminal. Calcium moves into presynaptic terminal due to concentration driving force
oThere are presynaptic vesicles present in the presynaptic terminal. They contain
neurotransmitters acetylcholine (ACh)
oCalcium binds to component of protein in cell membrane and signals presynaptic
vesicles to dislodge and fuse to the cell membrane. Fusion causes exocytosis of ACh to
diffuse into the synaptic cleft
Quanta: release of neurotransmitters from vesicles
Each quanta generates miniature end plate potential. Sum of miniature EPP
generates EPP (graded potential)
oSpecialized site that is folded to increase SA called motor end plate on postsynaptic cell
contains nicotinic muscle ACh receptors (AChR). 2 ACh bind to each receptor. Receptor
activates to allow ion movement. Nonspecific/ionotropic. Na+ moves into the cell and
K+ moves out of the cell. More Na+ goes in because there’s a larger driving force for Na+
due to the greater difference in equilibrium potential compared to the resting
membrane potential
oInflux of Na+ generates end plate potential (graded potential; happens at motor end
plate). Local propagation of Na+ activates voltage-gated Na+ channels on muscle fibers.
If the end plate potential (EPP) is above the voltage threshold (VT), this can activate a
muscle action potential (MAP)
- Mechanisms of neurotransmitter termination
oStop exocytosis of neurotransmitter
find more resources at oneclass.com
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Document Summary
Chemical synapses: synaptic transmission: signal travels down axon to synaptic terminal, releasing neurotransmitters across the synapse, which bind to receptors on the postsynaptic cell. A" alpha motor neuron sends signals to skeletal muscle fibers. Nature of receptor in postsynaptic cell and effect on postsynaptic cell varies depending on different synapses. Calcium moves into presynaptic terminal due to concentration driving force: there are presynaptic vesicles present in the presynaptic terminal. They contain neurotransmitters acetylcholine (ach: calcium binds to component of protein in cell membrane and signals presynaptic vesicles to dislodge and fuse to the cell membrane. Fusion causes exocytosis of ach to diffuse into the synaptic cleft. Sum of miniature epp generates epp (graded potential: specialized site that is folded to increase sa called motor end plate on postsynaptic cell contains nicotinic muscle ach receptors (achr). Local propagation of na+ activates voltage-gated na+ channels on muscle fibers.
