The action potential and its all-or-none nature is fundamental to neural communication, typically initiated once voltage-gated Na+ (NaV) channels are activated. In contrast, here we show that cerebrospinal fluid contacting neurons (CSFcNs) in spinal cord do not use Nav channels, but rather two different types of voltage-gated Ca2+ channel, enabling spikes of different amplitude. Spinal cord slices (300 μm) were obtained under terminal anaesthesia (100mg.kg-1 sodium pentobarbital (I.P) from C57/Bl6 mice (P30-P52) in which GCAMP6f was expressed under the vesicular GABA transporter promoter.  Imaging was performed on a custom built 2-Photon laser scanning microscope. Drugs were applied via microinjection. Analysis was performed in Igor Pro (Wavemetrics).  Spike amplitudes were measured as the difference between the peak ΔF/F signal occurring in a 333ms window around the spike time and the mean signal in the preceding 166ms. All data are expressed as mean ± SEM. Spontaneous activity occurred at a low frequency in CSFcNs (0.16 Hz; IQR = 0.12 – 0.23 Hz; 61 CSFcNs, N=7 mice). The distributions of inter-spike-intervals decayed exponentially and had coefficients of variation close to 1. Spikes in individual CSFcNs displayed distinct low and high amplitude events with multi-modal amplitude distributions. The frequency and amplitude of spontaneous activity of CSFcNs was unaffected by the voltage-gated sodium channel blocker tetrodotoxin (1μM; n=33 cells, 3 slices; Wilcoxon test, p=0.2011 and p=0.396 respectively). Bath application of the high voltage activated CaV channel blocker cadmium (Cd2+, 100μM) reduced the frequency and amplitude of spontaneous Ca2+ events in CSFcNs (to 56 and 54% of control respectively, n=31 cells, Wilcoxon test, p=>0.0001 and p=0.0012 respectively), although low amplitude events persisted in 30 out of 31 CSFcN. Cd2+ changed the event amplitude histograms from multi-modal to unimodal, selectively attenuating the larger amplitude event. Bath application of the selective T-type blocker ML218 (3μM) dramatically reduced the frequency of Ca2+ events in all CSFcNs (to 10% of control, n=27 cells, 4 slices, N=4 animals, Wilcoxon test, p=>0.0001) with complete inhibition observed in 20 of 27 spontaneously active CSFcNs. Bath application of Cd2+ (n=15 CSFcNs) or ML218 (n=27 CSFcNs) also significantly reduced the amplitude of K+-evoked Ca2+ events to 30% and 25% of control respectively Cd (Wilcoxon test, p0.0001). The amplitude of ACh-evoked Ca2+ responses were reduced by the nicotinic Ach receptor antagonist MCA (50μM, n=22 CSFcNs), but not ML218 (3 μM, n=68 CSFcNs; Kruskal-Wallis test, p=0.9999 respectively). The amplitudes of ATP-evoked Ca2+ responses were reduced by ML218 (n=43 CSFcNs, Wilcoxon test, p=<0.0001). In CSFcN therefore, T-type Ca2+ channels are required for spontaneous spiking and generate lower amplitude spikes, whereas large amplitude spikes require high voltage activated Cd2+ sensitive Ca2+ channels. These different amplitude spikes signal input from different transmitter systems; purinergic inputs evoke smaller T-type dependent spikes while cholinergic inputs evoke large T-type independent spikes. Different synaptic inputs to CSFcNs can therefore be signalled by the spike amplitude.