&alpha;MHC-GCaMP8 transgenic mice express the fluorescent calcium indicator GCaMP8 under control of the Myh6 (&alpha;MHC) minimal promoter/enhancer sequences. &alpha;MHC-GCaMP8 mice from founder line B4-10 exhibit robust expression levels of GCaMP8 in cardiomyocytes of the heart - consistent with endogenous Myh6. Additional details described further below. Calcium is a key molecular signal for cell functions including heart, smooth muscle, vessel, and airway contraction, lung secretion, autonomic neurotransmission and immunocyte function. GCaMP8 is a sensitive GCaMP variant with high dynamic range and fast response kinetics. In the absence of calcium binding, low/baseline EGFP fluorescence is observed. Following calcium binding (such as during heart contraction), bright EGFP fluorescence is observed at several-fold greater levels than baseline (see additional GCaMP8 information below). For &alpha;MHC-GCaMP8 transgenic mice, the donating investigator reports that expression patterns appear to mimic the endogenous Myh6 expression. Specifically, GCaMP8 expression in cardiomyocytes is demonstrated using anti-GFP antibody staining and RNA message levels by qPCR. As expected, low native fluorescence is observed in the absence of calcium binding, whereas increased bright fluorescence is observed during heart contraction (they report as much as ~38-fold increased fluorescence in vitro). The donating investigator has not tested expression in other tissues to date (March 2019). Mice hemizygous for the &alpha;MHC-GCaMP8 transgene are viable and fertile with normal breeding, and no reported gross phenotypic abnormalities. To date (March 2019), it has not been attempted to make this strain homozygous. The genetically encoded calcium indicator GCaMP8 is a sensitive GCaMP variant with high dynamic range and fast response kinetics (<a href="http://www.ncbi.nlm.nih.gov/pubmed/23240011">Ohkura et al. 2012 PLoS One 7:e51286</a>). Specifically, the high signal amplitude and low baseline fluorescence of GCaMP8 results in ability to detect single Ca2+ spikes / single neuronal action potentials. Compared to GCaMP3, the GCaMP8 has ~3-fold greater dynamic range, similar response kinetics, ~2-fold more rapid decay kinetics and lower baseline fluorescence. In the absence of calcium binding, dim EGFP fluorescence is expected as there is a pore from the outside of its barrel into the chromophore. Upon calcium binding, this pore becomes occupied and bright EGFP fluorescence is observed at several-fold greater levels than baseline (~16-fold greater or more). In the presence of Ca2+, GCaMP8 has absorbance and emission peaks (~488 nm and ~510 nm, respectively). This mouse model is available by way of a collaborative effort between Cornell/National Heart Lung Blood Resource for Optogenetic Mouse Signaling (<a href="http://chromus.vet.cornell.edu">CHROMus</a>) and The Jackson Laboratory.

&alpha;MHC-GCaMP8 transgenic mice express GCaMP8 (a sensitive GCaMP variant with high dynamic range and fast response kinetics) in cardiomyocytes. Upon GCaMP8 binding to calcium, increased EGFP fluorescence is observed. These &alpha;MHC-GCaMP8 mice may be useful to examine calcium signaling in cardiomyocytes both in vivo and in vitro.

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