Chronic lead exposure of the developing brain: electrophysiological abnormalities of cerebellar Purkinje neurons.
This manuscript reviews our recent research concerning electrophysiological effects of chronic low-level lead exposure on developing brain. We found that, although growth, survival and histological organization of in oculo cerebellar grafts appear normal after perinatal exposure to blood lead levels of 450 to 550 micrograms/liter, the physiological activity of Purkinje neurons in these lead-treated grafts is abnormally low after discontinuation of lead treatment. On the other hand, chronic low-level lead exposure postnatally via systemic injections or perinatally via the drinking water did not alter in situ cerebellar Purkinje cell activity. Moderate systemic doses (2 mg/kg) did cause a persistent slowing of Purkinje neuron firing rates; however, this effect was much smaller than in intraocular cerebellar grafts. The slowing may be mediated by lead actions on various transmitter systems. We have found that chronic lead induces catecholaminergic neurons to hyperinnervate target areas. Perhaps this hyperinnervation is initiated by the postsynaptic lead-induced blockade of the electrophysiological effects of norepinephrine which we have previously observed in the cerebellum in situ and in cerebellar grafts in oculo.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002526:Cerebellar Diseases / Q000139:chemically induced*; D002531:Cerebellum / Q000637:transplantation; D005333:Fetus; D007854:Lead / Q000633:toxicity*; D018377:Neurotransmitter Agents / Q000502:physiology; D009748:Nutrition Disorders / Q000150:complications; D011689:Purkinje Cells / Q000187:drug effects; D051381:Rats; D013569:Synapses / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects
D018377:Neurotransmitter Agents; D007854:Lead