There are significant neurogenic and inflammatory influences on blood pressure, yet the role played by each of these processes in the development of hypertension is unclear. Tumor necrosis factor alpha (TNFα) has emerged as a critical modulator of blood pressure and neural plasticity, however the mechanism by which TNFα signaling contributes to the development of hypertension is uncertain. We present evidence that the TNFα type 1 receptor (TNFR1) plays a key role in heightened glutamate signaling following slow-pressor angiotensin II (AngII) in the hypothalamic paraventricular nucleus (PVN), a key central coordinator of blood pressure control. Fourteen-day administration of a slow-pressor dose of angiotensin II (AngII) in male mice was associated with transcriptional and post-transcriptional (increased plasma membrane affiliation) regulation of TNFR1 in the PVN. Further, TNFR1 was shown to be critical for elevated NMDA-mediated excitatory currents in sympathoexcitatory PVN neurons following AngII infusion....