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Beta-endorphin
Adenylate
cyclase type 2
Voltage-
dependent
L-type calcium
channel subunit
beta-1
G protein-
activated
inward
rectifier
potassium
channel 3
Mu-type opioid
receptor
Gβ
Gγ
Neuronal
acetylcholine
receptor
subunit beta-2
Acetylcholine
Trimebutine
Na
+
Acetylcholine
Na
+
Ca
+
Ca
+
Na
+
Na
+
ATP
cAMP
PP
i
Trimebutine
GTP
Neuronal
acetylcholine
receptor
subunit alpha-4
nAchR Smooth
Muscle
Contraction
Guanine
nucleotide-
binding protein
G(i) subunit
alpha-1
Magnesium
Less nicotinic acetylcholine
receptors are actiavted.
Contraction of GI muscle is
reduced, motility and
secretion decreases.
Neuromuscular Junction
Smooth Muscle Myocyte
Decreased calcium levels
lead to decreased
neurotransmitter release.
Less acetylcholine is
available in the synapse to
bind to post synaptic
muscarinic receptors on the
muscle.
Trimebutine activates mu
opioid receptors inhibiting
the N-type calcium channels
on the neuron. This prevents
calcium to enter the neuron
and depolarize.
Mu opioid receptor is
coupled to Go and Gi
proteins. When diphenoxylate
activates the mu opioid
receptor, the Gi cascade
causes inhibition of
adenylate cyclase and the Go
signaling pathway causes
inhibition of Ca2+ channels
and activation of K+
channels.
Pre-Synaptic Neuron
Cytosol
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
Synaptic Vesicle
K+ channel is activated
allowing K+ to enter the
neuron and sodium to leave
the neuron. This results in
hyperpolarization, reducing
the ability of the neuron to
fire.
Trimebutine is taken orally
or intravenously
Unknown
ADCY2
CACNB1
KCNJ9
OPRM1
GNB1
GNG2
Unknown
Acetylcholine
Trimebutine
Sodium
Acetylcholine
Sodium
Calcium
Calcium
Sodium
Sodium
Adenosine
triphosphate
cAMP
Pyrophosphate
Trimebutine
Guanosine
triphosphate
Unknown
nAchR Smooth
Muscle
Contraction
GNAI1
ADCY2
CACNB1
KCNJ9
OPRM1
GNB1
GNG2
ACh
Trime
Na
+
ACh
Na
+
Ca
+
Ca
+
Na
+
Na
+
ATP
cAMP
PP
i
Trime
GTP