. Author manuscript; available in PMC: 2013 Jan 1.

Published in final edited form as: Trends Neurosci. 2011 Jul 26;35(1):24–35. doi: 10.1016/j.tins.2011.06.007

Table 1.

Other ligand-receptor systems involved in the regulation of Pavlovian fear conditioning¹

System	Function	Supporting Evidence
Norepinephrine (NE)	Consolidation	Enhanced with alpha1-adrenergic receptor antagonists ¹³⁸ Impaired by siRNA for beta(1) adrenergic receptors ¹³⁹
	Extinction	Impaired by antagonizing NE receptors in the infralimbic cortex^{140, 141}

NOS-cGMP	Consolidation	Enhanced by PKG activation in the LA ¹³³ Impaired contextual conditioning in nNOS KO mice ¹³⁴ Impaired in cGMP mutant mice ¹³⁵ Impaired by NOS and PKG inhibition in the LA¹³⁶

Endocannabinoid	Consolidation	CB1 mRNA increases 48 hrs after fear conditioning ¹³² Enhanced by inverse agonist of CB1 in the CeA or BLA ¹³² Impaired by CB1 receptor agonist or AEA transport inhibition into the vmPFC¹³²
	Extinction	Impaired by pharmacological blockade or genetic deletion of CB1 receptors ^{137, 148}

Dopamine (DA)	Consolidation	Enhanced by D2 receptor agonists in the VTA^{142, 143} D2 receptor antagonists in the BLA impair fear potentiated startle ¹⁴² Impaired by D1 receptor loss (genetic KO or siRNA in hippocampus)¹⁴⁴
	Extinction	Impaired by systemic or intra-IL PFC infusion of D2 antagonist ¹⁴⁵

Acetylcholine (Ach)	Consolidation	Enhanced by nicotinic Ach (nACh) agonists in the hippocampus ^149–151 Impaired by alpha7 nAch receptor antagonists¹⁵².
	Extinction	Impaired by nAch agonists ¹⁵³

Abbreviations: CB1 (Cannabinoid Receptor type 1), PKG (cGMP-dependent protein kinase), NOS (Nitric Oxide Synthase), KO (Knock out), siRNA (Small Interfering RNA), IL (Infralimbic)