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Increasing evidence suggests the involvement of ghrelin (an orexigenic hormone) and its cognate receptor growth hormone secretagogue receptor (GHSR1a, also known as the ghrelin receptor) in extra‐hypothalamic functions such as hippocampal learning and memory. However, cellular and molecular mechanisms underlying the ghrelin‐ regulated hippocampal neuron activity are poorly understood. In this chapter, we show the fol‐ lowing: (1) ghrelin promoted phosphorylation of the N‐methyl‐d‐aspartate receptor (NMDAR) subunit 1 (GluN1) in a PKC/PKA‐dependent manner and amplified NMDAR‐ mediated excitatory postsynaptic currents, (2) ghrelin stimulated phosphorylation of CREB (cAMP response‐element‐binding protein), and (3) ghrelin increased phalloidin binding to F‐actin, suggesting possible reorganization of dendritic spines; all occurred through the activation of GHSR1a in the CA1 pyramidal cell of the hippocampus in cul‐ tured slice preparations. Interestingly, the ghrelin’s effects on GluN1 and CREB phos‐ phorylation were negatively modulated by exogenous application of endocannabinoids, 2‐arachidonoylglycerol (2‐AG), and anandamide (ANE), in type 1 cannabinoid receptor (CB1R)‐dependent and ‐independent manners, respectively. It is suggested that ghrelin and the ghrelin receptor regulate synaptic transmission and plasticity in the hippocam‐ pus, interacting with the endogenous cannabinoid system, which may be essential and necessary for successful acquisition of metabolic state–dependent learning and adaptive appetitive behavior.

The Ghrelin Receptor Regulates Dendritic Spines and the NMDA Receptor–Mediated Synaptic Transmission in the Hippocampus