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Beta-endorphin
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
Nalbuphine
cAMP
Ca
+
Ca
+
Na
+
Na
+
γ-Aminobutyric acid
Nalbuphine
Nalbuphine
ATP
PP
i
GTP
Pain
Guanine
nucleotide-
binding protein
G(i) subunit
alpha-1
Magnesium
More GABA leads to
inhibition of dopamine cell
firing in the spinal cord
pain transmission neurons,
as well as the inhibition of
dopamine cell firing in the
reward system of the brain.
Increased calcium levels
lead to increased
neurotransmitter release.
GABA is released by synaptic
vesicles.
Nalbuphine prevents the
gamma subunit of the mu
opioid receptor from
inhibiting the N-type
calcium channels on the
neuron. This allows calcium
to enter the neuron and
depolarize.
The inhibition of Mu-type
opioid receptors prevents
the Gi subunit of the mu
opioid receptor from
activating the outward
rectifying sodium channel.
This prevents
hyperpolarization
Post-Synaptic Neuron
Pre-Synaptic Neuron
Synapse
Cytosol
Synaptic Vesicle
With the mu opioid receptor
unable to inhibit adenylate
cyclase, it is able to
synthesize cAMP which
increases the excitability
in spinal cord pain
transmission neurons.
Diffusion
Unknown
CACNB1
KCNJ9
ADCY2
GABRG2
GABBR1
OPRM1
GNB1
GNG2
γ-Aminobutyric
acid
Nalbuphine
cAMP
Calcium
Calcium
Sodium
Sodium
γ-Aminobutyric
acid
Nalbuphine
Nalbuphine
Adenosine
triphosphate
Pyrophosphate
Guanosine
triphosphate
Pain
GNAI1
CACNB1
KCNJ9
ADCY2
GABRG2
GABBR1
OPRM1
GNB1