“NEURINT” and Neuroweapons - Neurotechnology in National Security and Defense - page 106

TABLE 7.4
Organic Neurotoxic Agents

Origin Agent Mechanism

Marine cone snails (genus
Conus , e.g., Conus
geographus )

Inhibits the inactivation of voltage-dependent
sodium channels; prolonged opening
Inhibits the inactivation of voltage-dependent
sodium channels; prolonged opening
Inhibits voltage-dependent sodium channels in
muscles
Inhibits N-type voltage-dependent calcium
channels

σ-Conotoxin

κ-Conotoxin

μ-Conotoxin

ω-Conotoxin

Symbiotic bacteria found
in rough-skinned newts,
pufferfish, and
procupinefish (e.g.,
Pseudoalteromonas
tetraodonis , certain
species of Pseudomonas
and Vibrio )

Tetrodotoxin Prevents action potential firing in neurons

Binds near the pore and blocks voltage-gated
fast sodium channels on presynaptic terminals

Symbiotic bacteria found
in blue-ringed octopus
( Hapalochlaena
maculosa )

Maculotoxin (a venomous
form of tetrodotoxin)

Presynaptic sodium channel pore blockade
Inhibition of action potential

Shellfish/mollusks
(e.g., Saxidomus
giganteus contaminated
by algal blooms [“red
tides”], e.g., Alexandrium
catenella )

Saxitoxins
(e.g., saxitoxin,
gonyautoxin,
neosaxitoxin)

Selective pore blocker of neuronal voltage-
gated sodium channels
Water soluble and dispersible by aerosols
Inhalation causes death within minutes

Cobra snake (Genus Naja ) Naja toxins

(e.g., α-cobratoxin)

Block nicotinic ACh receptors at NMJ
Also selective antagonist to α7-nicotinic ACh
receptors in the brain

Krait snakes ( Bungarus
multicinctus )

Bungarotoxins
(e.g., α-bungarotoxin)

Irreversible and competitive binding to NMJ
nicotinic ACh receptors
Also selective antagonist to α7-nicotinic ACh
receptors in the brain

Mamba snakes
( Dendroaspis )

Dendrotoxins
(e.g., α-dendrotoxin,
σ-dendrotoxin)

Block voltage-gated (A-type) potassium
channels at nodes of Ranvier in motor neurons
Prolong duration action potentials
Increase ACh release at NMJ

Australian taipan snakes
( Oxyuranus scutellatus )

Taipoxin Induced increasing blockade of presynaptic

ACh release from motor neurons

ACh, acetylcholine; NMJ, neuromuscular junction.