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Environmental Neurotoxicology (1992)
Commission on Life Sciences (CLS)

Page
118
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Environmental Neurotoxicology

TABLE 6-1 Some Neurotoxicants That Act on Receptors

Receptor or Channel

Blocker (Antagonist)

Modulator (Agonist)

Acetycholine receptor

Lacticotoxin

 

 

Erabutoxin

 

 

α-Conotoxins

 

 

Anatoxin-a

 

 

Nereistoxin

 

 

Atropine

 

 

Scopolamine

 

Acetycholine-activated channel

Histrionicotoxin

 

 

Amantidine

 

 

N-Alkylguanidines

 

Excitatory amino acid

AP-5 (2-amino-5-phosponopentanoate)

Oxotremorine

 

AP-7 (2-amino-5-phosponopentanoate)

 

 

Nephila orb web spider toxins

 

 

Argiope orb web spider toxins

 

 

γ-Philanthotoxin

 

 

MK 801

 

 

Ketamine

 

GABAA receptor or channel

Bicuculline

N-Methyl-D-aspartate

 

Lindane

1-Glutamate

 

Dieldrin

Kainate

 

Picrotoxinin

Quisqualate

GABAB receptor or channel

Phaclofen

Muscimol

 

 

Avermectin Bla

 

 

Barbituates

 

 

Benzodiazepines

 

 

Ethanol

Glycine receptor or channel

Strychnine

Baclofen

Presynaptic tunnel

β-Bungarotoxin

α-Latrotoxin

 

Botulinum toxin

 

 

Tetanus toxin

 

 

Taipoxin

 

linear no-threshold model might be appropriate to estimate he effects of cytotoxic agents encountered during critical periods of development. Radiation is the classic example of such an exposure. The results of animal studies are consistent with the hypothesis of a lack of threshold for prenatal irradiation during the critical period of organogenesis of the cortex (Schull et al., 1990). The available human data are also consistent with the hypothesis (Otake and Schull, 1984; NRC, 1990). As shown in Figure 6-3, there is no clear evidence of a threshold for the effects of prenatal irradiation encountered during the critical period of fetal development, with respect to

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118