Loewi's experiment demonstrating chemical neurotransmission. (A) Diagram of experimental setup. (B) Where the vagus nerve of an isolated frog's heart was stimulated, the heart rate decreased (upper panel). If the perfusion fluid from the stimulated heart was transferred to a second heart, its rate decreased as well (lower panel).
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Loewi's experiment demonstrating chemical neurotransmission. (A) Diagram of experimental setup. (B) Where the vagus nerve of an isolated frog's heart was.
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Loewi's experiment demonstrating chemical neurotransmission. (A) Diagram of experimental setup. (B) Where the vagus nerve of an isolated frog's heart was stimulated, the heart rate decreased (upper panel). If the perfusion fluid from the stimulated heart was transferred to a second heart, its rate decreased as well (lower panel).
Demonstrating the identity of a neurotransmitter at a synapse requires showing (1) its presence, (2) its release, and (3) the postsynaptic presence of specific receptors.
Demonstrating the identity of a neurotransmitter at a synapse requires showing (1) its presence, (2) its release, and (3) the postsynaptic presence of specific receptors.
Demonstrating the identity of a neurotransmitter at a synapse requires showing (1) its presence, (2) its release, and (3) the postsynaptic presence of specific receptors.
Oxydenitrique
Les amines biogènes
Acides aminés Peptides Others
Acetylcholine Monoamines
Sérotonine Catécholamine
NoradrénalineDopamine Adrénaline
Substance P
ATPGlutamate GABA
Neurotransmetteurs à petites molécules
B) Small-molecule neurotransmitters are synthesized at nerve terminals. The enzymes necessary for neurotransmitter synthesis are made in the cell body of the presynaptic cell (1) and are transported down the axon by slow axonal transport (2). Precursors are taken up into the terminals by specific transporters, and neurotransmitter synthesis and packaging take place within the nerve endings (3). After vesicle fusion and release (4), the neurotransmitter may be enzymatically degraded. The reuptake of the neurotransmitter (or its metabolites) starts another cycle of synthesis, packaging, release, and removal (5).
(C) Peptide neurotransmitters, as well as the enzymes that modify their precursors, are synthesized in the cell body (1). Enzymes and propeptides are packaged into vesicles in the Golgi apparatus. During fast axonal transport of these vesicles to the nerve terminals (2), the enzymes modify the propeptides to produce one or more neurotransmitter peptides (3). After vesicle fusion and exocytosis, the peptides diffuse away and are degraded by proteolytic enzymes (4).
M1 M2 M3 M4 M5
DistributionCortex,
hippocampusHeart
Exocrine glands, GI tract
NeostriatumSubstantia
nigra
G protein Gq/11 Gi/o Gq/11 Gi/o Gq/11
Intracellular response
Phospholipase C
Action stimulanteAdenylyl cyclase
inhibitionPhospholipase C
Action stimulanteAdenylyl cyclase
inhibitionPhospholipa
se C
Acetylcholine metabolism in cholinergic nerve terminals. The synthesis of acetylcholine from choline and acetyl CoA requires choline acetyltransferase. Acetyl CoA is derived from pyruvate generated by glycolysis, while choline is transported into the terminals via a Na+-dependent transporter. After release, acetylcholine is rapidly metabolized by acetylcholinesterase and choline is transported back into the terminal.
Series of endplate potentials/action potentials in frog muscle under the increasing effect of a concentration of tubocurarine added at b. As endplate potential falls below threshold, action potential fails and there is no mechanical response. Series summarized in h.
Clostridium botulinum
Acétyl choline
GABA
Traitement de la myasténie grave
Receptor Tissue Response
Muscarinic (M1) Smooth muscles and glands of the gut
Smooth muscle contraction and glandular secretion (relatively slow response)
Muscarinic (M2) Smooth and cardiac muscle of cardiovascular system
Smooth muscle contraction; some inotropic effect on cardiac muscle
Muscarinic (M3) Smooth muscles and glands of all targets