Gastrin/cholecystokinin-like immunoreactivity (G/CCK-LI) was localized by immunocytochemistry in neurons in the central nervous system of Aplysia californica. Neuronal cell bodies were specifically immunostained in the buccal, cerebral, pedal, and abdominal ganglia but not in the pleural ganglia. Neural G/CCK-LI processes were observed in the neuropil of all ganglia and connectives and in some but not all of the peripheral nerves examined. Somata containing G/CCK-LI ranged from 15 to 200 micron in diameter. Ganglionic G/CCK-LI was most efficiently extracted in neutral or basic solutions and consisted mainly of a substance eluting in a volume corresponding to a peptide of between 8 and 17 amino acid residues on gel filtration. This G/CCK-LI diluted in parallel to mammalian gastrin in radioimmunoassays using two antisera differing in their specificities for the bioactive COOH-terminal region of mammalian G/CCK. We conclude that G/CCK-LI is distributed widely in the central and peripheral nervous systems of Aplysia californica and that this immunoreactivity probably represents a small peptide which is similar but not identical to mammalian gastrins and cholecystokinins at the functionally critical COOH terminus.

There is increasing concern regarding the potential health effects associated with exposure to plastic nanoparticles and the chemicals released when plastic is heated or dissolved in water. Although exposure to plastic particles and their composite chemicals can be generated by a number of different processes, 3D printers used in manufacturing, schools and homes, are sources of fumes and particulate that humans are exposed to. This study examined whether inhalation of particulate and fumes generated during 3D printing with polycarbonate (PC) affects the OB and neuroendocrine system, and if there is a dose‐response relationship between exposure levels and measures of cell function. Methods Male rats (n= 6/group, 200 – 250 g at arrival) were exposed to filtered air, or black PC particulate and fumes generated by 3 desktop 3D‐printers (exposure was 4 h/day). The 4h average particulate concentration delivered to the animals breathing space was 500 µg/m3. Animals were exposed 4 days/week until the specified number of days of exposure (1, 4, 8, 15 or 30) had been reached. The morning after the last exposure, animals were euthanized, blood was collected and circulating hormone levels were measured in serum samples using ELISAs. The OB and brain were also collected, frozen, sectioned and stored at ‐80°C until processed for immunohistochemistry. Results In the OB, exposure to 3D‐emissions resulted in reductions in tyrosine hydroxylase (TH; rate limiting enzyme in dopamine synthesis) and glial derived neurotrophic factor immunolabeling. There were also reductions in myelin basic protein and cAMP nucleotide phosphatase staining, suggesting that there was myelin damage and dysfunction in the OB. In the hypothalamus, the major effects of exposure to 3D‐emissions were reductions in immunostaining for TH and glial fibrillary acidic protein, a marker of astrocyte activation. Changes in immunostaining in the OB suggest there is cellular dysfunction and potentially an alteration in the transmission of olfactory information to the brain. Changes in activity and morphology of astrocytes in the hypothalamus have been shown to affect the release of hormones, including those regulating reproductive and metabolic processes; In the current study, exposure to 3D‐emissions also resulted in changes in circulating concentrations of follicle stimulating hormone, and thyroid stimulating hormone. Conclusions Inhalation of PC particulate and/or fumes may act through olfactory pathways and affect neuroendocrine function. Although is not clear if these changes are the result of particulate matter interfering with various cellular and physiological processes, or due to endocrine disrupting bisphenols that are present in polycarbonate plastics, the results of this study are consistent with other experiments showing that exposure to PC particulate and the composite chemicals interfere with neuroendocrine processes that regulate reproduction and metabolism.