Literature on the neurological effects of lead in animals is extensive and comparable to the effects observed in human studies. Animals appear to be affected generally at the same PbB levels. Effects include impaired motor function and reflexes in rats , decreased NCV in rats  and impaired behavior/learning in rats and monkeys (see ATSDR  for a more complete review).
Several histopathological studies have shown a variety of adverse effects, including reductions or delays in the development of the hippocampus or other hippocampal changes , reductions or delays in the development of the cerebral cortex , reductions in the number and size of axons in the optic nerve of mice , and demyelination of peripheral nerves . Cytoarchi-tectural changes have also been noted in limited studies of the eyes of monkeys chronically exposed to lead beginning at or shortly after birth .
Neurochemical changes have been observed in the brains of rats exposed both pre- and postnatally to lead . These include decreased brain norepinephrine and 7-aminobutyric acid (GABA) levels, decreased glutamic acid decarboxylase (GAD) activity, increased brain glutamate, glutamine + asparagine, tyrosine levels, and monoamino oxygenase (MAO) activity. Kala and Jadhav  reported increases and decreases in the levels of several neurotransmitters in the rat brain. Other studies have found that lead disrupts the dopaminergic systems in rats [139-141].
Monkeys (Macaca fascicularis) treated for a lifetime with 0.5 mg lead/kg/day exhibited a slight decrease in vibration sensitivity (increased threshold to stimuli) when tested at the age of 18 years  and increased thresholds for pure tones  consistent with results reported in humans . Lilienthal and Winneke  reported increased latencies of waves of brain stem auditory-evoked potentials until about 10 years of age in monkeys exposed in utero, with no improvement observed 18 months after exposure ceased.
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