Long-term potentiation in autonomic ganglia: Potential role in cardiovascular disorders

Table 1 Summery of studies reporting ganglionic long-term potentiation of the nicotinic pathway in various animal species

Animal species	Specific ganglia	Ref.
Rat	Superior cervical ganglion	Brown and McAfee[4]
		Briggs and McAfee[6]
		Alkadhi et al[15]
		Alzoubi et al[25]
		Alkadhi et al[28]
		Alkadhi et al[29]
		Alkadhi and Alzoubi[36] Alzoubi et al[30]
Cat	Superior cervical, lumbar and stellate ganglia	Alonso-deFlorida et al[7]
		Bachoo and Polosa[8]
Guinea pig	Superior cervical ganglion	Weinreich et al[9]
Chick	Parasympathetic ciliary ganglion	Scott and Bennett[14]
Bullfrog	Sympathetic ganglia	Koyano et al[11]
		Kumamoto and Kuba[13]
		Minota et al[10]

Adapted from Alkadhi K, Alzoubi K. In: Sudden Death in Epilepsy: Forensic and Clinical Issues (Chapter 26). CRC Press, 2011: 395-426.

Table 2 Effects of various 5-HT₃ receptor agonists and antagonists on compound action potential during ganglionic long-term potentiation induced in vitro by high frequency repetitive stimulation

Serotonergic drugs	Mode of action	Compound AP
Serotonin (10-20 μmol/L)	Agonist	Increased
Fluoxetine (10 μmol/L)	SSRI	Increased
m-CPBG (1 μmol/L)	Receptor agonist	Increased
Tropisetron (5 μmol/L)	Receptor antagonist	Reduced
Ondansetron (5 μmol/L)	Receptor antagonist	Reduced
MDL 72222 (0.5 μmol/L)	Receptor antagonist	Reduced
Reserpine pretreatment (3 mg/kg)	5-HT3 depletion	No gLTP
m-CPBG (1 μmol/L) + reserpine	Receptor agonist	Increased

The same drugs produced no significant effect on basal synaptic transmission in control ganglia (adapted from ref. [15,25,29,30,32,33,36]). SSRI: Selective serotonin reuptake inhibitor; AP: Action potential.