Conventional chemical synapses in the nervous system involve a presynaptic accumulation of neurotransmitter-containing vesicles, which fuse with the plasma membrane to release neurotransmitters that activate postsynaptic receptors. In taste buds, type II receptor cells do not have conventional synaptic features but nonetheless show regulated release of their afferent neurotransmitter, ATP, through a large-pore, voltage-gated channel, CALHM1. Immunohistochemistry revealed that CALHM1 was localized to points of contact between the receptor cells and sensory nerve fibers. Ultrastructural and super-resolution light microscopy showed that the CALHM1 channels were consistently associated with distinctive, large (1- to 2-μm) mitochondria spaced 20 to 40 nm from the presynaptic membrane. Pharmacological disruption of the mitochondrial respiratory chain limited the ability of taste cells to release ATP, suggesting that the immediate source of released ATP was the mitochondrion rather than a cytoplasmic pool of ATP. These large mitochondria may serve as both a reservoir of releasable ATP and the site of synthesis. The juxtaposition of the large mitochondria to areas of membrane displaying CALHM1 also defines a restricted compartment that limits the influx of Ca²⁺ upon opening of the nonselective CALHM1 channels. These findings reveal a distinctive organelle signature and functional organization for regulated, focal release of purinergic signals in the absence of synaptic vesicles.

神经系统中的常规化学突触涉及突触前含神经递质的囊泡的积聚，这些囊泡与质膜融合以释放激活突触后受体的神经递质。在味蕾中，II型受体细胞不具有常规的突触功能，但仍通过大孔，电压门控通道CALHM1调节其传入神经递质ATP的调节释放。免疫组织化学显示，CALHM1位于受体细胞和感觉神经纤维之间的接触点。超微结构和超分辨率光学显微镜显示，CALHM1通道始终与突触前膜之间相距20至40 nm的独特大线粒体（1至2μm）保持一致。线粒体呼吸链的药理破坏限制了味觉细胞释放ATP的能力，这表明释放的ATP的直接来源是线粒体而不是ATP的细胞质库。这些大的线粒体既可以作为可释放ATP的储存库，又可以作为合成位点。大线粒体与显示CALHM1的膜区域的并置还定义了一个有限的区室，该区室限制了Ca的流入打开非选择性CALHM1通道时为²⁺。这些发现揭示了在不存在突触小泡的情况下，嘌呤能信号的调节，局部释放的独特细胞器特征和功能组织。