The synapse: mechanisms of communication between neurons Flashcards
Myasthenia Gravis: symptoms
dysfunction of synaptic transmission. Causes fluctuating muscle weakness, problems chewing (dysphagia) and talking (dysarthria) and respiratory weakness
Synapse
the place where neurons come into close proximity with other neurons
pre synaptic- before the synapse
post synaptic- after the synapse
Axodendritic synapse
the terminal buttons synapses with a dendrite of the post synaptic neuron
Axosomatic synapse
the terminal button synapses with the cell body (soma) of the post synaptic neuron
Axoaxonic
the terminal button synapses with the axon of the post synaptic neuron
presynaptic membrane
the membrane of the presynaptic terminal button
post synaptic membrane
the membrane of the postsynaptic neuron
dendritic spine
a ridge on the dendrite of the post synaptic neuron, with which a terminal button from a pre synaptic neuron forms a synapse
synaptic cleft
the tiny gap between the presynaptic and postsynaptic membrane (approximately 20 nanometers wide)
synaptic vesicles
tiny balloons filled with neurotransmitter molecules; found in the release zone of the terminal button
microtubules
long tubes that run down the axon and guide the transport of synaptic vesicles from the soma to the axon terminal
release zone
part of the interior of the presynaptic membrane to which synaptic vesicles fuse in order to release their neurotransmitter into the synaptic cleft
Release of a neurotransmitter 1
- vesicles contain neurotransmitter (NT) molecules
- an action potential in the pre synaptic cell triggers vesicles to move toward the cell membrane
- vesicles are guided towards the membrane by proteins
Release of a neurotransmitter 2
Guiding proteins act like ropes that help fuse the vesicle and pre synaptic membrane together
Release of a neurotransmitter 3
- an influx of calcium ions into the pre synaptic terminal button induces fusion of the two membranes
- neurotransmitter molecules are then released into the synaptic cleft
Excitatory post synaptic potential (EPSP)
Excitatory post synaptic potentials (EPSPs) depolarise the post synaptic cell membrane
EPSPs increase the likelihood that an action potential will be triggered in the post synaptic neuron
Inhibitory post synaptic potential (IPSP)
Inhibitory post synaptic potentials (IPSPs) hyperpolarise the postsynaptic cell membrane
IPSPs decrease the likelihood that an action potential will be triggered
neural integration
the interaction between the effects of EPSPs and IPSPs
IPSPs tend to cancel out the effects of EPSPs
Reuptake
the neurotransmitter is removed from the synaptic cleft via special transporter molecules in the terminal buttons. These molecules use energy to draw the neurotransmitter back into the cytoplasm of the pre synaptic neuron
Enzymatic deactivation
an enzyme in the synaptic cleft destroys the remaining neurotransmitter molecules. Such deactivation seems to occur only for one type of neurotransmitter, called acetylcholine (ACh). The enzyme that destroys ACh in the synapse is called acetylcholinesterase (AChE); it does the job of breaking ACh into its constituents, acetate and choline
Seven steps of neurotransmitter action at the synapse
- neurotransmitter (NT) molecules are synthesised from their precursors by enzymes
- NT molecules are stored in vesicles
- NT molecules that leak from vesicles are destroyed by enzymes
- action potentials cause vesicles to fuse with the presynaptic cell membrane, releasing their NT into the synaptic cleft
- released NT binds with autoreceptors in presynaptic membrane, limiting further release of the NT
- released NT binds with the receptors on postsynaptic membrane, causing ion channels to open
- free NT molecules in the synaptic cleft are taken back up by transporter molecules in the presynaptic membrane, or destroyed by enzymes- reuptake or enzymatic deactivation
Amino acids
Glutamate: the most common excitatory neurotransmitter in the CNS
GABA (gamma aminobutyric acid): the most common inhibitory neurotransmitter
Monamines
Dopamine and Norepinephrine (catecholamines)
Serotonin (Indolamine)
present in groups of neurons that are located mostly in the brainstem
Acetylcholine
Acetylcholine: the neurotransmitter that operates at synapses with muscles, as well as other parts of the CNS
Agonist
increases the activity of the synapse
Antagonist
decreases the activity of the synapse
Agonists do the following…
- increase the number of neurotransmitter (NT) molecules that are synthasised
- increase the number of NT molecules stored in the vesicles
- destroy the enzymes that attack NT molecules
- increase the number of vesicles that fuse with the pre synaptic cell membrane
- decrease the activity of autoreceptors
- binding directly with the post synaptic membrane, causing ion channels to open
- decreasing the amount of NT that is reuptaken or destroyed by enzymes
Anatgonists can do any of the following
- decrease the number of neurotransmitter (NT) molecules that are synthasised
- decrease the number of NT molecules stored in the vesicles
- cause NT to leak from vesicles where they are attacked by degrading enzymes
- decrease the number of vesicles that fuse with the pre synaptic cell membrane
- increase the activity of autoreceptors
- block the inotropic receptor, preventing the ion channels from opening
- increasing the amount of NT that is reuptaken or destroyed by enzymes in the synapse
Myasthenia Gravis
Autoimmune disorder where the person’s own immune system destroys ACh receptors which are located on synapses with the muscles
Treated with anticholinesterase (AChE) inhibitors- these increase and prolong the effects of ACh on the post synaptic membrane
Also treated with immunosuppressive drugs or by removal of the thymus gland
