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Gq protein
signaling
cascade
Choline O-
acetyltransferase
Acetylcholinesterase
N-type calcium
channel
Vesicular
acetylcholine
transporter
High affinity
choline
transporter 1
Ca
+
Acetylcholine
Rivastigmine
Rivastigmine
Ca
+
Choline
Choline
Rivastigmine
Rivastigmine
Acetyl-CoA
Choline
CoA
H
2
O
Acetic acid
Acetylcholine
Muscarinic
acetylcholine
receptor M1
Acetylcholine
Magnesium
Presynaptic Neuron
Post-Synaptic Neuron
2. An action potential
arrives at the nerve
terminal and stimulates the
opening of the calcium
channel, causing an influx
of calcium ions
1. Acetylcholine is
synthesized and stored in
synaptic vesicles at the
nerve terminal
3. Calcium ions stimulates
the release of
neurotransmitter
acetylcholine into the
synaptic cleft via
exocytosis
4. Acetylcholine in the
synaptic cleft activates
muscarinic receptors on the
post-synaptic membrane
6. Acetylcholine is broken
down by acetylcholinesterase
into choline and acetyl-coa
7. Choline is taken back up
into the nerve terminal and
recycled to create more
acetylcholine
Rivastigmine inhibits
acetylcholinesterase,
preventing acetylcholine
breakdown
5. M1 receptor activation
stimulates the Gq signaling
cascade. The downstream
effects are responsible for
improving learning and
memory
↓ Amyloid-Beta Production
↓ Tau Phosphorylation
↑ Neuronal Survival
↑ Cerebral Blood Flow
Vesicle
Rivastigmine is administered
orally and diffuses into the
bloodstream and travels to
its target within the brain
Rivastigmine inhibits
choline-o-acetyltransferase,
leading to accumulation of
acetylcholine in the
synaptic cleft.
GNAQ
CHAT
ACHE
CACNB1
SLC18A3
SLC5A7
Calcium
Acetylcholine
Rivastigmine
Rivastigmine
Calcium
Choline
Choline
Rivastigmine
Rivastigmine
Acetyl-CoA
Choline
Coenzyme A
Water
Acetic acid
Acetylcholine
CHRM1
Acetylcholine
GNAQ
CHAT
ACHE
CACNB1
SLC18A3
SLC5A7
Ca
+
ACh
Rivasti
Rivasti
Ca
+
Choline
Choline
Rivasti
Rivasti
Ac-CoA
Choline
CoA
H
2
O
Acoh
ACh
CHRM1
ACh
Mg2+
Presynaptic Neuron
Post-Synaptic Neuron
2. An action potential
arrives at the nerve
terminal and stimulates the
opening of the calcium
channel, causing an influx
of calcium ions
1. Acetylcholine is
synthesized and stored in
synaptic vesicles at the
nerve terminal
3. Calcium ions stimulates
the release of
neurotransmitter
acetylcholine into the
synaptic cleft via
exocytosis
4. Acetylcholine in the
synaptic cleft activates
muscarinic receptors on the
post-synaptic membrane
6. Acetylcholine is broken
down by acetylcholinesterase
into choline and acetyl-coa
7. Choline is taken back up
into the nerve terminal and
recycled to create more
acetylcholine
Rivastigmine inhibits
acetylcholinesterase,
preventing acetylcholine
breakdown
5. M1 receptor activation
stimulates the Gq signaling
cascade. The downstream
effects are responsible for
improving learning and
memory
↓ Amyloid-Beta Production
↓ Tau Phosphorylation
↑ Neuronal Survival
↑ Cerebral Blood Flow
Vesicle
Rivastigmine is administered
orally and diffuses into the
bloodstream and travels to
its target within the brain
Rivastigmine inhibits
choline-o-acetyltransferase,
leading to accumulation of
acetylcholine in the
synaptic cleft.
GNAQ
CHAT
ACHE
CACNB1
SLC18A3
SLC5A7
Ca2+
ACh
Rivasti
Rivasti
Ca2+
Choline
Choline
Rivasti
Rivasti
Ac-CoA
Choline
CoA
H2O
Acoh
ACh
CHRM1
ACh