not possess the other CNS and autonomic nervous system effects of
cocaine. Such molecules include benzocaine, lidocaine (brand name
Xylocaine), and procaine (brand name Novocain).
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Cocaine
All these local anesthetic molecules exert their action by binding
to voltage-gated sodium channels and disrupting the ability to open
and close in a normal voltage-dependent fashion. Unlike TTX and
STX, they do not completely block Na* channels, but they do interfere
enough to significantly alter the generation of action potentials. This
results in a reduction in signals from neurons sending sensory infor-
mation to the brain—the local anesthetic effect.
Let’s now return to a discussion of the neurotransmitter acetylcholine
(ACh) and its ionotropic and metabotropic receptors. Many years
before the protein structures and properties of these receptors were
characterized as ionotropic Na* channels and G-protein-coupled re-
ceptors, it was appreciated that there were two different types of ACh
receptor (AChR) that could be characterized as having different phar-
macological properties, that is, different agonists and antagonists.
One type of AChR is activated by binding nicotine, a molecule iso-
lated and identified from the tobacco plant, Nicotiana tabacum.