Neurochemical changes in rat nucleus tractus solitarii after ablation of neurons with neurokinin‐1 receptors

Abstract

Ablation of nucleus tractus solitarii (NTS) neurons that express neurokinin‐1 (NK1) receptors attenuates baroreflexes, increases blood pressure lability and causes cardiac damage. Mechanisms for these effects are not clear. NK1 receptors colocalize with N‐methyl‐D‐aspartate (NMDA) receptors and alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionat (AMPA) receptors in NTS. Decreased glutamate transmission in NTS through loss of NK1 cells could be responsible for the effects. We tested this hypothesis by fluorescent immunohistochemistry after injecting stabilized substance P‐saporin (SSP‐SAP) unilaterally into the NTS. We assessed changes in NMDAR1 (NMDA receptor subunit 1), GluR2 (AMPA receptor subunit 2), gamma‐aminobutyric acid (GABA) receptor type a and b, neuronal nitirc oxide synthase (nNOS), tyrosine hydroxylase (TH), vesicular glutamate transporter (VGluT), choline acetyl transferase (ChAT), glial fibrillary acidic protein (GFAP), and protein gene product 9.5 (PGP 9.5). Immunoreactivity (IR) for NMDAR1, GluR2, GABAb, VGluT3, ChAT, GFAP, and PGP9.5 decreased in the injected NTS. In contrast, IR for VGluT2, nNOS and TH increased. We conclude that physiologic and pathologic effects following ablation of neurons with NK1 receptors in NTS may result from interruption of neurotransmission produced by neurochemicals other than SP. Support: NIH HL59593, NIH HL088090 and VA Merit Review.