Metal neurotoxicity is a global health concern. This paper summarizes the evidence for metal interactions with synaptic transmission and synaptic plasticity. Presynaptically metal ions modulate neurotransmitter release through their interaction with synaptic vesicles, ion channels, and the metabolism of neurotransmitters (NT). Many metals (e.g., Pb 2+, Cd 2+, and Hg +) also interact with intracellular signaling pathways. Postsynaptically, processes associated with the binding of NT to their receptors, activation of channels, and degradation of NT are altered by metals. Zn 2+, Pb 2+, Cu 2+, Cd 2+, Ni 2+, Co 2+, Li 3+, Hg +, and methylmercury modulate NMDA, AMPA/kainate, and/or GABA receptors activity. Al 3+, Pb 2+, Cd 2+, and As 2 O 3 also impair synaptic plasticity by targeting molecules such as CaM, PKC, and NOS as well as the transcription machinery involved in the maintenance of synaptic plasticity. The multiple effects of metals might occur simultaneously and are based on the specific metal species, metal concentrations, and the types of neurons involved.

Metal neurotoxicity is a global health concern. This paper summarizes the evidence for metal interactions with synaptic transmission and synaptic plasticity. Presynaptically metal ions modulate neurotransmitter release through their interaction with synaptic vesicles, ion channels, and the metabolism of neurotransmitters (NT). Many metals (e.g., Pb 2+ , Cd 2+ , and Hg + ) also interact with intracellular signaling pathways. Postsynaptically, processes associated with the binding of NT to their receptors, activation of channels, and degradation of NT are altered by metals. Zn 2+ , Pb 2+ , Cu 2+ , Cd 2+ , Ni 2+ , Co 2+ , Li 3+ , Hg + , and methylmercury modulate NMDA, AMPA/kainate, and/or GABA receptors activity. Al 3+ , Pb 2+ , Cd 2+ , and As 2 O 3 also impair synaptic plasticity by targeting molecules such as CaM, PKC, and NOS as well as the transcription machinery involved in the maintenance of synaptic plasticity. The multiple effects of metals might occur simultaneously and are based on the specific metal species, metal concentrations, and the types of neurons involved.

In cats, larvae of the dipteran fly, Cuterebra, sometimes cause severe disease by their migration through the tissues of the larynx, pharynx, nasal sinuses, brain, and spinal cord; such infected cats may die without the maggots ever reaching the subcutaneous tissues where they would typically mature. The current study examines the ability of an indirect enzyme-linked immunosorbent assay (ELISA) using crude Cuterebra antigen from maggots to detect parasite-specific immunoglobulin (Ig)G in cats with known ( n = 42), suspected ( n = 25), or no known exposure to the infection ( n = 68). The probability of a given optical density (OD) predicting the infection status of a given animal was determined using logistic regression, and both 1:20 and 1:80 serum dilutions were highly predictive of the potential of a cat being infected with a larval Cuterebra. In 5 cases where 2 samples were collected 1–2 weeks apart, there was a mean OD increase in the second sample for both the 1:20 and 1:80 dilutions, but it was significant ( P = 0.044) only at the 1:20 dilution. Sex of the sampled cat was not a significant contributor to the ability of the OD to predict the presence of a larva, but the age of the cat added significantly to the predictive value of the generated curves, with the only exception being with the 1:20 serum dilution with the curve being generated only using the cats known to be positive for larval presence. This ELISA should aid in ruling cuterebriasis in or out in suspect systemic and, specifically, neurologic cases and provide information on kinetics of antibody presence postexposure.

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