Low lead levels stunt neuronal growth in a reversible manner.
The developing brain is particularly susceptible to lead toxicity; however, the cellular effects of lead on neuronal development are not well understood. The effect of exposure to nanomolar concentrations of lead on several parameters of the developing retinotectal system of frog tadpoles was tested. Lead severely reduced the area and branchtip number of retinal ganglion cell axon arborizations within the optic tectum at submicromolar concentrations. These effects of lead on neuronal growth are more dramatic and occur at lower exposure levels than previously reported. Lead exposure did not interfere with the development of retinotectal topography. The deficient neuronal growth does not appear to be secondary to impaired synaptic transmission, because concentrations of lead that stunted neuronal growth were lower than those required to block synaptic transmission. Subsequent treatment of lead-exposed animals with the chelating agent 2,3-dimercaptosuccinic acid completely reversed the effect of lead on neuronal growth. These studies indicate that impaired neuronal growth may be responsible in part for lead-induced cognitive deficits and that chelator treatment counteracts this effect.
Cline
H T
HT
Cold Spring Harbor Laboratory, NY 11724, USA. cline@cshl.org
Witte
S
S
Jones
K W
KW
D000818:Animals; D015220:Calcium Channels / Q000378:metabolism; D004594:Electrophysiology; D007854:Lead / Q000633:toxicity*; D009474:Neurons / Q000187:drug effects*; D011145:Polyvinyls; D011894:Rana pipiens; D004113:Succimer / Q000494:pharmacology; D013477:Superior Colliculi / Q000187:drug effects / Q000254:growth & development; D009435:Synaptic Transmission / Q000187:drug effects
D015220:Calcium Channels; D011145:Polyvinyls; C016438:ethylenevinylacetate copolymer; D007854:Lead; D004113:Succimer