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Nicotinic ACh receptor
example of inotropic NT receptor
-receptor for ACh
-channel for cations but mainly Na+ (sometimes K+, Calcium, chloride)
Nicotinic ACh receptor leads to what and why
leads to initial depolarization & EPSP because it introduces cations into cell
what channels do metabotropic NT Receptors open
indirectly opens channels that are further along the post synaptic membrane
how do metabotropic NT Receptors open channels
by activating signal transduction pathways, which involves the use of G protien coupled receptors
-sequence of intracellular events
What does G protien consist of
3 subunits
-alpha, betta, gamma
G protien coupled receptors location
it is linked to the Metabotropic NT Receptors
example of Metabotropic NT Receptors
Adrenergic Norepinephrine Receptor
3 types of ionotropic glutamate receptors
NMDA, AMPA, kainate receptors
8 types of metabotropic glutamate receptors
mGluR1 to mGluR8
GABAA receptors =
ionotropic receptors
GABAB receptors
metabotropic receptors
some NTs can be excitatory or inhibitory depending on what
the receptor they bind to an the location of the receptor
when is ACh an excitatory NT
when it binds to nicotinic ACh
nicotinic ACh receptor location
skeletal muscle & ionotropic
when is ACh an inhibitory NT
when it binds to musscaranic ACh
musscaranic ACh receptor location and what kind of receptor
smooth muscle and metabatropic
when is GABA an inhibitory NT
in mature/adult brain
when is GABA an excitatory NT
in developing brain (child)
why is GABA an excitatory NT in child brain
Chloride gradient is reveres in chuld’s brain
CI- high inside cell → Cl- leaves → cell positive → depolarization
what is Nitric Oxide
a gas produced by some nuerons
how does Nitric Oxide diffuse
it diffuses ACROSS the presynaptic membrane → into a large area → then diffuses into target cell
NO receptor and its location
Guanylyl cyclase
-present inside target cell
Gaunylyl Cyclase dual function
receptor and enzyme
Gaunylyl Cyclase as a receptor
activates the production of cGMP as a second messenger
cGMP
activates protien Kinase G if PED-5 is inhibited (PKG)
activation of PKG leads to what
→ relax smooth muscle cells → vasodilation
cGMP if PDE-5 is active
leads to GMP production
NO release leads to what mainly
vasodilation
presence of PDE 5
breaks down cGMP into GMP which means no vasodilation
what happens to smooth muscles if cGMP breaks down
no smooth muscles relaxation, no vasodilation occurs
why would a phosphodiesterase 5 inhibitor cause vasodilation
no cGMP breakdown leads to PKG which relaxes smooth muscles
famous PDE 5 inhibitors
ED medicine
-erectile dysfunction medicine