Kisspeptins are G protein-coupled receptor ligands originally identified as 
human metastasis suppressor gene products that have the ability to suppress 
melanoma and breast cancer metastasis and recently found to play an important 
role in initiating the secretion of gonadotropin-releasing hormone at puberty. 
Kisspeptin-13 is an endogenous isoform that consists of 13 amino acids. The 
action of kisspeptin in the regulation of gonadal function has been widely 
studied, but little is known as concerns its function in limbic brain 
structures. In the brain, the gene is transcribed within the hippocampal dentate 
gyrus. This paper reports on a study the effects of kisspeptin-13 on passive 
avoidance learning and the involvement of the adrenergic, serotonergic, 
cholinergic, dopaminergic and GABA-A-ergic, opiate receptors and nitric oxide in 
its action in mice. Mice were pretreated with a nonselective α-adrenergic 
receptor antagonist, phenoxybenzamine, an α2-adrenergic receptor antagonist, 
yohimbine, a β-adrenergic receptor antagonist, propranolol, a mixed 5-HT1/5-HT2 
serotonergic receptor antagonist, methysergide, a nonselective 5-HT2 
serotonergic receptor antagonist, cyproheptadine, a nonselective muscarinic 
acetylcholine receptor antagonist, atropine, D2, D3, D4 dopamine receptor 
antagonist, haloperidol, a γ-aminobutyric acid subunit A (GABAA) receptor 
antagonist, bicuculline, naloxone, a nonselective opioid receptor antagonist and 
nitro-l-arginine, a nitric oxide synthase inhibitor. Kisspeptin-13 facilitated 
learning and memory consolidation in a passive avoidance paradigm. 
Phenoxybenzamine, yohimbine, propranolol, methysergide, cyproheptadine, 
atropine, bicuculline and nitro-l-arginine prevented the action of kisspeptin-13 
on passive avoidance learning, but haloperidol and naloxone did not block the 
effects of kisspeptin-13. The results demonstrated that the action of 
kisspeptin-13 on the facilitation of passive avoidance learning and memory 
consolidation is mediated, at least in part, through interactions of the 
α2-adrenergic, beta-adrenergic, 5-HT2 serotonergic, muscarinic cholinergic and 
GABA-A-ergic receptor systems and nitric oxide.