Classical conditioning of the rabbit eyeblink response was used to study the effects of cerebellar lesions on performance in animals trained with low-intensity unconditioned stimuli (US). Animals were trained with 1 of 2 low-intensity corneal-airpuff USs paired with a tone-conditioned stimulus. This study confirms earlier findings demonstrating the differential effects of lesions of deep cerebellar nuclei on the conditioned (CR) and unconditioned responses (UR). Lesions of the anterior interpositus nucleus of the cerebellum in animals that were successfully conditioned abolished CRs without affecting UR performance.

Previously, pA134 was identified as one of the mRNAs present in the squid giant axon. Comparative sequence analyses revealed that the pA134 gene product manifested significant similarity to the mammalian lipoprotein receptor adaptor protein also known as ARH (autosomal recessive hypercholesterolemia). ARH mRNA and protein displayed very similar pattern of expression throughout the mouse brain. Significant levels of expression were observed in cells with a predominantly neuronal profile in the cerebellum, brainstem, olfactory bulb, hippocampus, and cortex. A yeast two hybrid screen for ARH protein interactions in mouse brain identified the following binders: amyloid precursor-like protein 1, low density lipoprotein receptor-related protein (LRP) 1, LRP8, and GABA receptor-associated protein-like 1. The interactions of ARH with LRP1 and GABA receptor-associated protein-like 1 were subsequently verified by co-immunoprecipitation of the protein complexes from transfected human embryonic kidney cells. The presence of ARH mRNA in axon of primary sympathetic neurons was established by RT-PCR analyses and confirmed by in situ hybridization. Taken together, our data suggest that ARH is a multifunctional protein whose spectrum of function in the brain goes beyond the traditionally known metabolism of lipoproteins, and that ARH may be locally synthesized in the axon.

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The genotoxicity and airborne organic particles from forest fire smoke was compared to that from nonsmoky (ambient) urban air using the Salmonella reversion assay and the sister chromatid exchange (SCE) assay in cultured human lymphocytes. Salmonella strains TA98 and TA100 were used with and without the addition of Aroclor-induced rat liver homogenate (S9). Each sample induced dose-related increases in mutagenicity and SCE. However, on the basis of the volume of air sampled, the smoke-filled air induced 12 to 14 times more bacterial reversions in TA100 and 16-38 times more reversions in TA98 brain ambient air. Similarly, on a volume basis smoky air induced 43 times more SCE in human lymphocytes than did ambient air. The results indicate that the increased mutagenicity was due not only to the heavier particulate load of the air, but also to the increased specific mutagenicity of the particles.