ABSTRACT
Neural plasticity in the form of long-term potentiation (LTP) of synaptic transmission is known to occur in a variety of synapses including those of autonomic ganglia (Scott and Bennett 1993; Alkadhi et al. 1996). LTP of sympathetic ganglia (gLTP) is expressed in vitro following a brief period of high-frequency preganglionic nerve stimulation. Ganglionic LTP can also be produced in vivo by chronic psychosocial stress, which provides the repeated high-frequency presynaptic activity required for gLTP induction resulting in sustained elevation of sympathetic tone to cardiovascular system (Alkadhi and Alzoubi 2007). Ganglionic LTP in the rat sympathetic superior cervical ganglion is triggered by a serotonin receptor-dependent mechanism (Alkadhi et al. 2005a). The functional consequence of the chronic stress-induced expression of gLTP in sympathetic ganglia has been reported as marked elevation of blood pressure in various rat models including stressinduced hypertensive, spontaneously hypertensive (SHR), aged, and Zucker obese rats (Alkadhi et al. 2001; Alzoubi et al. 2008a,b; Alzoubi and Alkadhi 2009; Alzoubi et al. 2010). Expression of gLTP in sympathetic ganglia results in a significantly higher tonic sympathetic outflow to peripheral effector organs including the heart and blood vessels.
