Lead (Pb) continues to be a significant environmental toxin and remains an integral part of many industrial processes, hobbies, and tobacco smoke. Pb has been shown to be a potent toxin to the CNS and low levels of Pb (below the CDC established toxic blood level of 10 microg/dl) have been correlated with decreases in the IQ of children. Pb exposure is a risk factor for dyslexia, and significantly, dyslexics have deficits in auditory temporal processing, including backward masking and amplitude modulation detection. Importantly, Pb-exposed children have been found to be deficient in various aspects of auditory temporal processing, including backward masking. Auditory temporal information is vital for appropriate speech detection and it is not known where within the auditory axis temporal processing takes place, nor is it understood how Pb exposure modifies the cells of the auditory system. To address these questions, we have developed an animal model of auditory temporal processing using chickens and have established that Pb exposure during development results in deficits in backward masking in avians. The current study was undertaken to identify the cellular changes induced by Pb exposure in the auditory brainstem of chickens that are likely anatomical correlates of the observed deficits in backward masking. We found Pb exposure had no effect on neuron number or glial cells within the auditory brainstem. However, Pb exposure does result in significant decreases in the amount of the medium weight neurofilament protein (NFM) as well as decreased NFM phosphorylation within the axons connecting auditory nuclei in the avian brainstem. Because the amount of neurofilament can affect the conduction velocities of axons, these results may provide an anatomical link between Pb exposure, auditory temporal processing deficits, and dyslexia.