Expression of gLTP in Sympathetic Ganglia from Stress-hypertensive Rats: Molecular Evidence

Abstract

We previously reported behavioral and electrophysiological evidence indicating that superior cervical ganglia (SCG) from rats that developed hypertension as a result of chronic psychosocial stress expressed ganglionic long-term potentiation (gLTP) in vivo. In the present study, we present additional supportive evidence by measuring changes in protein levels of essential signaling molecules in ganglia from chronically stressed rats. We compared protein levels of essential, LTP-related signaling molecules in ganglia isolated from chronic stress-hypertensive rats, known to have expressed gLTP, with those of the same molecules in normal ganglia 1h after eliciting gLTP by high frequency stimulation (HFS) in vitro. Immunoblot analysis showed a significant increase in the levels of phosphorylated CaMKII, total CaMKII, nitric oxide synthase (NOS-1), and calmodulin in SCG from both chronically stressed rats and from normal rat ganglia in which gLTP was expressed by HFS in vitro. Additionally, there was a parallel reduction in calcineurin protein levels in ganglia from both groups. The present results confirm that ganglia from stressed rats have expressed gLTP in vivo and that synaptic plasticity in sympathetic ganglia may involve a molecular cascade largely similar to that of LTP in the hippocampal CA1 region.

Expression of gLTP in Sympathetic Ganglia of Obese Zucker Rats In Vivo: Molecular Evidence

“…To examine if these changes also occur in ganglia from OZR, we measured the protein levels of signaling molecules by immunoblot analysis to compare basal levels in ganglia from OZR and LZR. The levels of many of these essential signaling molecules were similar to those detected in normal ganglia in which gLTP was evoked with HFS in vitro (Alzoubi et al 2008).…”

“…Recently, we have shown that in vitro HFS-induced gLTP is associated with an increase in the protein levels of key signaling molecules, including P-CaMKII, neural nitric oxide synthase (NOS-1) and PKC, and a decrease in calcineurin levels (Alzoubi et al 2008). Similar changes were observed in these signaling molecules in unstimulated ganglia from psychosocially stressed rats where gLTP had been expressed in vivo (Alkadhi et al 2005b;Alzoubi et al 2008).…”

“…Similar changes were observed in these signaling molecules in unstimulated ganglia from psychosocially stressed rats where gLTP had been expressed in vivo (Alkadhi et al 2005b;Alzoubi et al 2008). To examine if these changes also occur in ganglia from OZR, we measured the protein levels of signaling molecules by immunoblot analysis to compare basal levels in ganglia from OZR and LZR.…”

“…Stimulation-evoked gLTP caused significant increases in the levels of CaMKII and P-CaMKII in SCG of normal rats (Alzoubi et al 2008). Therefore, if gLTP had been already expressed in ganglia, then there would be an increase in the protein levels of P-CaMKII.…”

“…This indicates that stressgenerated sustained increases in central sympathetic outflow to ganglia may have provided the repetitive activation of preganglionic nerve required to induce gLTP. This would result in a sustained increase in sympathetic tone to the vasculature, leading to hypertension (Alkadhi et al 2001b(Alkadhi et al , 2005bGerges et al 2002;Alzoubi et al 2008).…”