Neurotoxicity and Behavioral Effects of Environmental Chemicals - Organic Pollutants: An Ecotoxicological Perspective - page 301

Axon

Pre-Synaptic
Membrane

Post-Synaptic Membrane

Dendrites

Receptors

Pore Channels

Direction of
Transmission

Vesicles with
Neurotransmitter

Axon

Synaptic Cleft

Cholinergic (Nicotinic) Synapse

ACh Receptor

Vesicles with
Acetylcholine
(Ach)

ACh-ase

Na Channel

Direction of
Transmission

Synaptic Cleft

fIgure 16.2 Schematic diagram of synapse.

Section 8.2.4 and Section 8.2.5 in this topic). Neurotoxic effects in adult mammals
include ataxia, difficulty in locomotion, neurasthenia, tremor, impairment of vision
and, finally, loss of consciousness and death. Necrosis, lysis, and phagocytosis of neu-
rons are effects coinciding with these symptoms of toxicity. As described earlier, sub-
lethal neurotoxic effects on humans and wild vertebrates have occurred and still occur
as the result of environmental contamination by methylmercury. The mechanism of
neurotoxic action is complex and is not well understood. There is strong evidence
that methylmercury compounds can have adverse effects upon a number of proteins,
including enzymes and membrane-spanning proteins involved in ion transport (ETAC
101). It seems probable that the strong tendency of these compounds to bind with—and
thereby render ineffective—functional -SH groups of the proteins is the main reason
for this (see, for example, Jacobs et al. 1977, who studied the inhibition of protein syn-
thesis by methylmercury compounds). There is also evidence that exposure to sublethal
levels of methyl mercury can cause changes in the concentration of neurochemical
receptors in the brains of mammals and birds (Basu et al. 2006, Scheuhammer et al.
2008). Thus, an increase in concentration of brain muscarinic receptors for acetylcho-
line and a decrease in the concentration of brain receptors for glutamate was observed