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N-type calcium
channel
potassium
voltage-gated
channel
subfamily J
Adenylate
cyclase type 2
GABAA receptor
Gamma-
aminobutyric
acid type B
receptor
Mu-type opioid
receptor
Gβ
Gγ
γ-Aminobutyric acid
Remifentanil
cAMP
Ca
+
Ca
+
Na
+
Na
+
γ-Aminobutyric acid
Remifentanil
Remifentanil
ATP
PP
i
GTP
Pain
Guanine
nucleotide-
binding protein
G(i) subunit
alpha-1
Magnesium
Remifentanil inhibits neuron
in the brain leading to
analgesic and anesthetic
effects
Less GABA leads to
disinhibition of dopamine
cell firing in the spinal
chord pain transmission
neurons. This leads to
inhibition of brain
signalling
Decreased calcium levels
lead to decreased
neurotransmitter release.
Less GABA is released for
synaptic vesicles.
Remifentanil binds to pre
synaptic mu opioid type
receptors.
The Gi subunit of the mu
opioid receptor activates
the inwardly rectifying
potassium channel increasing
K+ conductance. This causes
membrane hyperpolarization
decreasing the chances of
neuronal firing/action
potential.
Post-Synaptic Neuron
Pre-Synaptic Neuron
Synapse
Cytosol
Synaptic Vesicle
The mu opioid receptor
through the gamma subunit
inhibits voltage gated
N-type calcium channels
stopping the influx of
calcium into the neuron.
Blood-Brain Barrier
Diffusion
Remifentanil is taken
intravenously
With the inhibition of
adenylate cyclase, it is
unable to synthesize cAMP
which further prevents
calcium from entering the
neuron and depolarization of
the neuron
CACNB1
KCNJ9
ADCY2
GABRG2
GABBR1
OPRM1
GNB1
GNG2
γ-Aminobutyric
acid
Remifentanil
cAMP
Calcium
Calcium
Sodium
Sodium
γ-Aminobutyric
acid
Remifentanil
Remifentanil
Adenosine
triphosphate
Pyrophosphate
Guanosine
triphosphate
Pain
GNAI1
CACNB1
KCNJ9
ADCY2
GABRG2
GABBR1
OPRM1
GNB1
GNG2
GABA
Remfnl