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Types of receptors
ionotropic
metabotropic
receptors
proteins embedded in the postsynaptic membrane which recognize a specific NT (lets bind to it)
Ionotropic receptors
aka ligand gated, when NT bind to this receptor it causes an ion channel to open
Metabotropic receptors
aka G-protein coupled receptors:
when NT binds to this receptor a chain of reactions are set off, sometimes involving a 2nd messenger
Ionotropic receptor structure (+open, +closed) and function
4 or 5 subunits forming a “pore”
this pore is closed when no NT is bonded
when NT binds it slightly twists the pore opening it
opening it allows ions to come through, which helps cause Post synaptic potential
Nicotinic Acetylcholine Receptor (ACh)
structure, how it functions
an ionotropic receptor
nicotinic ACh receptor has 5 subunits with two ligand binding sites that like to take in Acetylcholine but will take in agonists from outside body too (exogenous) like nicotine
two acetylcholine molecules must bind to the receptor to open and allow Na+ inside the cell
Properties of Ionotropic Receptors
these ligand gated channels usually get help from amino acid NTs like (G.G.G.)
and a couple non-amino acid NT (nicotine ACH)\
need to take into account
Pharmacology
Kinetics
Selectivity
Pharmacology (property of ionotropic receptor)
which neurotransmitters and drugs bind to receptor
(interact with receptor)
Kinetics (property of ionotropic receptor)
(how long channels open after NT molecule binds to receptor)
how it affects the duration of opening
Selectivity of ion channels
what type of ions are able to pass through ion channels. it determines whether there is an excitatory or inhibitory effect
Transmitter gated channels vs Voltage gated channels selectivity
Voltage gated channels are more selective about which ion molecules can go through
compared to Transmitter gated channels (ex. Na+, K+ both can go through Nicotinic ACh channels)
Excitatory PSP by Na+
a recorded excitatory membrane potential
when Na+ positive comes through the open channels into cell, it membranes depolarizes
causing an excitatory membrane potential (mV increased)
How Metabotropic receptors work
the NT binds to the g coupled receptors
this activates a g protein which splits into a alpha and beta subunits
these subunits go to their own effector proteins. subunits open an ion channel or activate second messengers (enzymes)
Shortcut pathway of Metabotropic receptors
receptor → G protein → ion channel
no 2nd messenger, it is fast and localized
(ex. musacarnic ACh receptors in heart: NT binds to receptor, acitiving G protein, Beta subunit opens ion channel, K+ flows thru, causing hyperpolzarization that slows the heart)
Second messenger cascades (metabotropic recpetor long route)
NT binds to receptor
receptor activates G protein
G protein spitls into subunits
activating effector enzyme
effector enzyme creates 2nd messengers
the 2nd messengers activate other enzymes
signal stops eventually
Second messenger function
they are the intermediary between first effector enzyme and last enzymes that cause a cellular response (ex. opening ion channel, gene expression, etc)
when you have the same NT causing different effects in two neurons, what is happening
one receptors could be excitatory like when NT binds it opens to Na+ and receptor is inhibitory since when NT binds it opens to Ka+ causing hyperpolarization
Different receptor subtypes can cause very different responses in the target cells
same NT affecting cells in very different ways
different areas of the brains different receptor subtypes importance
the distribution of receptors subtypes also varies across the NS, so the same NT when binding to diff receptor can have completely different effect
Divergence
when one single NT can affect multiple receptor subtypes, causing different postsynaptic responses
can happen not just to different neurons but different parts of the same neuron
divergance can happen at any step of metabotropic cascading reaction
Convergence
when multiple diff NTs bind to their specifc receptor type and they affect the same effector system (ex. both NT A and B cause hyperpolzation)