The paraventricular nucleus (PVN) of the hypothalamus is an important area in the maintenance of homeostasis and plays a vital role in cardiovascular regulation via autonomic control[1, 2]. The mechanisms underlying this control are not fully understood. Some of this control involves transient receptor potential (TRP) channels and we previously reported coupling between the known osmosensitive channel TRPV4 and small-conductance calcium-activated potassium channels (SK) in the parvocellular PVN[3]. Activation of TRPV4 by hypotonic challenge results in the opening of SK, leading to hyperpolarisation and a reduction in activity of neurones. As the PVN also has a thermoregulatory role [4] our results led us to investigate whether TRPV4 channels also have a thermosensitive role in the PVN. Immunofluorescence staining and single channel data from cell-attached patch clamp recording in CD1 mouse brain slices shows the clear presence of TRPV4 in the parvocellular PVN[3]. Here we recorded action current frequency (ACf) during temperature steps of 5oC from room temperature (22oC) to 37oC. All data was analysed with one-way ANOVA with Tukey post hoc test.Increasing temperature significantly decreased ACf of parvocellular neurones within the PVN (reductions of 49±11% at 27oC, 88±6% at 32oC and 97±2% at 37oC; n=6, p<0.001). This effect at physiological temperatures was not prevented by gadolinium (100 µM), a widely used, but non-selective inhibitor of many ion channels, including TRPV4. A significant decrease of ACf was still seen at 37oC (reduction of 94±2% n=4; p<0.005). This suggests that TRPV4 may not be involved, but a gadolinium sensitive TRP channel may be inhibited at these lower temperatures. Further investigation revealed TRPM2 as a potential candidate as this channel is activated at temperatures around 35oC, and is not inhibited by gadolinium. Pre-incubation with the TRPM2 inhibitor econazole (10 µM), prevented the decrease in ACf throughout increasing temperatures up to 37oC (n=5;p>0.05). We have shown the presence of the TRPV4 channel within the parvocellular region of the PVN, however, this study has ruled out TRPV4 as a simple temperature sensor within this same neuronal population at physiological temperatures of 37oC. Instead, our data suggests that TRPM2 may have a part to play in this complex process. It has been shown in other neurones within the brain that increases in temperature most typically leads to an increase in activity[5]. We therefore hypothesise that the decrease in activity we have seen is as an indirect effect of the TRPM2 channel present on the inhibitory GABAergic neurones innervating the parvocellular neurones patched.