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The lateral nucleus (LA) is the input station of the amygdala for information about conditioned stimuli (CSs), whereas the medial sector of the central nucleus (CeM) is the output region that contributes most amygdala projections to brainstem fear effectors. However, there are no direct links between LA and CeM. As the main target of LA and with its strong projection to CeM, the basomedial amygdala (BM) constitutes a good candidate to bridge this gap. Consistent with this notion, it was reported that combined posttraining lesions of the basal nuclei [BM plus basolateral nucleus (BL)] abolish conditioned fear responses, whereas selective BL inactivation does not. Thus, we examined the relative contribution of BM and BL to conditioned fear using unit recordings and inactivation with muscimol microinfusions in rats. Approximately 30% ofBMand BL neurons acquired robust responses to auditory CSs predicting footshocks. While most BL cells stopped firing at CS offset,BMresponses typically outlasted the CS byβ40 s, paralleling the persistence of conditioned fear after the CS. This observation suggests that BM neurons are not passive relays of rapidly adapting LA inputs about the CS. Surprisingly, independent inactivation of either BM or BL with muscimol did not cause a reduction of conditioned freezing even though an extinction recall deficit was seen the next day. In contrast, combinedBL-BMinactivation did. Overall, there results support the notion that the basal nuclei are involved in conditioned fear expression and extinction but that there is functional redundancy between them. [ABSTRACT FROM AUTHOR]

Abstract: The norepinephrine transporter (NET) plays a crucial role in noradrenergic neurotransmission and is a target of many antidepressants and psychostimulants. Intracellular Ca2+ is reportedly involved in regulating NET activity, but the detailed mechanism is not clear. We employed a norepinephrine uptake assay using SH-SY5Y cells and found that the IP3 receptor inhibitors, 2-aminoethoxydiphenyl borate and xestospongin C, reduced the NET V max. These reductions were accompanied by the decreased cell surface expression of NET. Our findings suggest that intracellular Ca2+ mobilized by IP3 receptor is required for the maintenance of NET activity. This adds another pathway involving Ca2+ for the regulation of NET to other known mechanisms providing intracellular Ca2+. [Copyright &y& Elsevier]

Laboratory work is an essential part of natural science education because it provides students with a valuable opportunity to experience practical scientific research firsthand. In laboratory work in pharmacology, students generally learn about biological mechanisms and drug action mechanisms by analyzing drug actions using laboratory animals. Actual experience with hands and eyes is an important factor in the laboratory work. Under the COVID-19 epidemic, however, we were forced to conduct the laboratory work online. For the laboratory work using isolated organs, we used simulation software, in which students can examine effects of a range of drugs on the smooth muscle within the guinea pig ileum. For the behavioral observation practice, we showed the video of the experiments conducted by the instructors beforehand to the students, and asked them to observe and analyze the behavior. In this review, we will share our challenges to online laboratory work.