The interface of learning and cognition applied to the study of animal behavior represents a target for significant progress if conceptual barriers can be reduced. Is animal behavior exclusively a product of learning or cognition, or are both implicated? Are special (i.e., new) methods required to study cognition or will the enterprise be accomplished by using well-established methods from learning? What types of hypotheses need to be tested to dissociate cognition from learning, and may these hypotheses be profitably tested? This article addresses the above questions by focusing on conceptual, methodological, and hypothesis-testing perspectives for navigating the interface between learning and cognition. Examples from contemporary research are used to develop some suggestions for best practices. The development of a rodent model of episodic memory is used as a case study tofeature the validation of an animal model of cognition.

Roberts (2020, Learning & Behavior, 48[2], 191-192) discussed research claiming honeybees can do arithmetic. Some readers of this research might regard such claims as unlikely. The present authors used this example as a basis for a debate on the criterion that ought to be used for publication of results or conclusions that could be viewed as unlikely by a significant number of readers, editors, or reviewers.

Acute stress suppresses pain by activating brain pathways that engage opioid or non-opioid mechanisms. Here we show that an opioid-independent form of this phenomenon, termed stress-induced analgesia, is mediated by the release of endogenous marijuana-like (cannabinoid) compounds in the brain. Blockade of cannabinoid CB(1) receptors in the periaqueductal grey matter of the midbrain prevents non-opioid stress-induced analgesia. In this region, stress elicits the rapid formation of two endogenous cannabinoids, the lipids 2-arachidonoylglycerol (2-AG) and anandamide. A newly developed inhibitor of the 2-AG-deactivating enzyme, monoacylglycerol lipase, selectively increases 2-AG concentrations and, when injected into the periaqueductal grey matter, enhances stress-induced analgesia in a CB1-dependent manner. Inhibitors of the anandamide-deactivating enzyme fatty-acid amide hydrolase, which selectively elevate anandamide concentrations, exert similar effects. Our results indicate that the coordinated release of 2-AG and anandamide in the periaqueductal grey matter might mediate opioid-independent stress-induced analgesia. These studies also identify monoacylglycerol lipase as a previously unrecognized therapeutic target.