M1 Lec 5 Flashcards
how do neurons connect at electrical synapses?
via gap junctions which allow ions to directly flow from presynaptic cell to post synaptic cell
what do gap junctions allow for
allows for faster transmission and synchronization of neuronal activity
what channel does ion current flow through? what is it?
* characteristics of the channel
connexon channels - structural components of the gap junction
* made of 6 connexin proteins
* one connexon: hemichannel
* two connexons: gap junction
gap junctions diseases
dysfunction of connexion causes:
* charcot-marie-tooth disease - non functional gap junctions
chemical synapses have no physical connection. how do they communicate? how can they amplify the signal
communicate with the release of chemical messengers called neurotransmitters (NT)
* NT bind to many receptors on postsynaptic neuron which amplifies signal
* they are slower than electrical synapses
chemical synaptic transmission
- Action potential arrives at the ___
- Depolarization opens __ channels in the ___ membrane.
- Ca2+ influx into the __
- Ca2+ triggers the fusion of ___ (with neurotransmitter) with the
presynaptic membrane. - NT released into the ___ (exocytosis).
- NT diffuses across the cleft and binds
to ___ on the ___ - Receptor binding causes a change in the
___ (e.g., opening of ___ channels). - NT is removed from cleft via ___,
___, or ___
- Action potential arrives at the axon terminal.
- Depolarization opens voltage-gated Ca2+ channels in the presynaptic membrane.
- Ca2+ influx into the terminal.
- Ca2+ triggers the fusion of synaptic
vesicles (with neurotransmitter) with the
presynaptic membrane. - NT released into the synaptic cleft (exocytosis).
- NT diffuses across the cleft and binds
to receptors on the postsynaptic membrane. - Receptor binding causes a change in the
postsynaptic cell (e.g., opening of ion channels). - NT is removed from cleft via diffusion,
degradation, or reuptake
what is the neuromuscular junction (NMJ)?
this is where the nerve meets muscle. its a synapse between motor neuron and mmuscle fiber.
* 1 to 1 contact: axon to muscle fiber
What are end plate potentials (EPPs):
* what causes the release
the changes in the postsynaptic potential at the neuromuscular junction (NMJ) caused by the release of acetylcholine (ACh).
This leads to depolarization of the muscle fiber, and if the depolarization reaches the threshold, it can trigger an action potential (AP) in the muscle, leading to contraction.
What are MEPPs:
* how do they occur
- small spontaneous depolarizations of postsynaptic membranes
- occur in absence of AP in presynaptic neuron
- can be summed to form EPP
whats a quantum
the amount of neurotransmitter released when one synaptic vesicle fuses with the presynaptic membrane
whats a subthreshold epp
* how does it occur
a depolarization at the neuromuscular junction that is not strong enough to reach the threshold required to generate a muscle fiber action potential, meaning it does not trigger muscle contraction.
- occurs if you remove Ca2+ from solution and continue to stimulate the motor neuron.
Types of neurotransmitters
- neuropeptides (larger, slower, synthesized in cell body)
- small molecules (small, rapid, synthesized in termal)
Neurotransmitters
* where are NT synthesized and stored
* where are they released
* what do they bind to
- within presynaptic neurons
- into the synaptic cleft
- specific postsynaptic receptors
NT requirements
- must be present in presynaptic neuron
- must be released during synaptic activity
- must bind to receptors on postsynaptic neuron
- neuron can sometimes synthesize and release more than one NT
Small Molecules: amino acids
* list two and what they are
Glutamate
* main excitatory NT
* is almost half of all CNS synapses
* acts on ionotropic receptors (AMPA, NMDA, and kainate receptors) and metabotropic receptors.
GABA
* main inhibitory NT
Small Molecules: biogenic amines
* list three and what they are
Dopamine (DA)
* movement, reward, motivation
Adrenaline
* stress response
Serotonin (5-HT)
* mood, sleep, appetite
what causes parkinsons disease
destruction of dopamine neurons in substantia nigra
What are ionotropic receptors
* how does the channel get opened
* ex
ligand-gated ion channels - the receptor itself is an ion channel
* NT binding causes channel to open and ions flow
* Ex: Nicotinic acetylcholine receptors
What is Nicotinic Acetylcholine receptor (nAChR)
* list the agonist and antagonists
nAChR is an ionotropic receptor found in NMJ - it is excitatory
- nicotine is a receptor agonist that mimics naturally occuring NT
- curare is a receptor antagonist and blocks the normal action of NT (can cause paralysis bc muscles dont contract)
What are metabotropic receptors
* how does the channel get opened
* ex:
G protein coupled receptors
* NT binding activates a G protein which signals a cascade to indirectly open/close channels
* ex: muscarinic acetylcholine receptors (mAChR)
* slower w longer lasting effects
what is muscarinic acetylcholine receptor (mAChR)
* list an agonist
it is a metabotropic receptor found in diff areas of the body - inhibitory
* agonist: muscarine
what determines if signal is inhibitory or excitatory
the receptor
