Nervous - week 3 Flashcards
(18 cards)
what is a synapse
how neurons communicate
a site where neurons can exchange information
2 types: electrical and chemical synapse
electrical synapse
site of cell-to-cell communication where neurons directly exchange ions through channels that span the 2 communicating cells (like a bridge)
- exchange of ions can lead to an AP developing in the next cell
chemical synapse
cell-to cell communication where excitable cells release chemicals called neurotransmitters to communicate
3 main components:
- pre-synaptic neuron: transmits the info towards the synaptic cleft via its axon terminals, to the dendrites of the next neuron
- synaptic cleft: small space between the axon terminals of one neuron and dendrites of another
- post-synaptic neuron: transmits info away form the synaptic cleft, from its dendrites towards its own soma
neurotransmitters
chemicals that neurons release to communicate with one another
- chemicals bind to ion channels or receptors on the next cell, leading to ion influx into the cell
what is excitation-contraction coupling
graded potentials
changes in membrane potential that vary according to the size of the stimulus
EPSPs
sub threshold depolarizations
properties:
- don not produce AP
- localized - depolarization is confined to one area of the plasma membrane
- magnitude of depolarization = magnitude of stimulus (meaning they are graded
- can be summed to produce larger depolarizations
- therefore multiple EPSPs required to create an AP
- produced by neurotransmitters that open Na+ and K+ channels
IPSPs - inhibitory post-synaptic potentials
hyperpolarizing potentials
properties:
- localized - hyperpolarization is confined to one area of the plasma membrane
- magnitude of hyperpolarization = magnitude of stimulus meaning they are graded
- can be summed up like EPSPs
- bring neuron further away for AP
- produced by neurotransmitters that open K+ (moving it out of the cell) or Cl- channels (moving it into the cell)
axon hillock
the “trigger zone”
- both IPSPs and EPSPs decay as they move towards the axon hillock
- IPSPs and EPSPs sum up at the axon hillock
AP will only be elicited only if the depolarization at the axon hillock is large enough to reach threshold
2 ways to strengthen EPSPs
- temporal summation: additive effect produced by many EPSPs that have been generated at the same synapse by series of high frequency AP on the presynaptic neuron
one neuron fires repeatedly
- summation - additive effect
- produced by many EPSPs that have been generated at many different synapses on the same post-synaptic neuron at the same time
many neurons fire at the same time to produce EPSPs in post synaptic neuron
excitatory neurotransmitter
leads to depolarization of the membrane in form of EPSPs
- if depolarization strong enough, may fire and AP
inhibitory neurotransmitter
leads to hyperpolarization of the post synaptic membrane in the form of IPSPs
- makes it harder to generate AP
nicotinic receptors
type of ACh receptor
respond to acetylcholine at certain synapse
when ACh binds to them, they open ion channels –>Na+ flows in –> causes depolarization
found at NMJ
it is a ligand-gated ion channel
- ACh (ligand) binds → channel opens → ions flow (mainly Na⁺ in, K⁺ out)
easy way to remember: Nicotinic = fast + muscle and autonomic
they span the plasma membrane of the post synaptic cell
muscarinic receptors
not ion channels themselves but when they bind to ACh activate a series of biochem rxns on the cytoplasmic side cell
will further activate and open ion channels in the post synaptic cell membrane
known as slow transmission
Muscarinic = Slow + Smooth muscle & organs (parasympathetic)
(Think: “M for Muscles that Move slowly and Manage organ stuff”)\
found in organs
end plate current
generates end plate potentials could lead to AP causing contraction of muscles
myasthenia Gravis
chronic autoimmune neuromuscular disease that is characterized by weakness in the skeletal muscle
- weakness develops because body elicits antibodies against the nicotinic receptors and blocks the binding of ACh and degrading of nicotinic receptors
administering acetylcholinesterase blockers to delay symptoms and progression pf disease
what do acetylcholinesterase blockers for myasthenia Gravis
degradation of ACh is slowed down therefore ACh is present in the synaptic cleft for longer
this increases chances that it will bind to nicotinic receptors in muscle cells reducing weakness