The limited memory of value following value directed encoding.

Items associated with higher values during encoding are later recognized and recalled better than are lower valued items. During recall paradigms, these value directed encoding (VDE) effects heavily depend upon learned strategies acquired during repeated testing with earnings feedback. However, because VDE effects also occur in single test recognition designs, precluding such learning, it has been suggested that high value may automatically induce good encoding. We tested this by manipulating encoding instructions (Experiments 1a and 1b) and manipulating concurrent levels of processing (LOP) requirements during encoding (Experiment 2a and 2b). Two main findings emerged. First, subject initiated strategies played a dominant role in VDE effects with little evidence for automaticity. This was demonstrated in Experiment 1 by a more than three-fold increase in the VDE recognition effect when instructions specifically encouraged selective elaboration of high-value items. It was also shown by the complete elimination of VDE recognition effects in Experiment 2 when LOP tasks were concurrently performed during encoding. Critically, the blocking of VDE effects occurred even though a catch trial procedure verified that value was being processed during encoding and remained even when subjects had unlimited time to process the materials during encoding. Second, the data showed, for the first time, that when subjects attempted to specify the value of recognized items, they heavily depended upon a recognition heuristic in which increases in recognition strength, even when nondiagnostic, were inferred to reflect high encoding value. The tendency for subjects to conflate recognition strength and value may have important implications for behavioral economics.

MCH Neuron Activity Is Sufficient for Reward and Reinforces Feeding.

BACKGROUND: Melanin-concentrating hormone (MCH)-expressing neurons have been implicated in regulation of energy homeostasis and reward, yet the role of their electrical activity in short-term appetite and reward modulation has not been fully understood. OBJECTIVES: We investigated short-term behavioral and physiological effects of MCH neuron activity manipulations. METHODS: We used optogenetic and chemogenetic approaches in Pmch-cre transgenic mice to acutely stimulate/inhibit MCH neuronal activity while probing feeding, locomotor activity, anxiety-like behaviors, glucose homeostasis, and reward. RESULTS: MCH neuron activity is neither required nor sufficient for short-term appetite unless stimulation is temporally paired with consumption. MCH neuronal activation does not affect short-term locomotor activity, but inhibition improves glucose tolerance and is mildly anxiolytic. Finally, using two different operant tasks, we showed that activation of MCH neurons alone is sufficient to induce reward. CONCLUSIONS: Our results confirm diverse behavioral/physiological functions of MCH neurons and suggest a direct role in reward function.

NTS Catecholamine Neurons Mediate Hypoglycemic Hunger via Medial Hypothalamic Feeding Pathways.

Glucose is the essential energy source for the brain, whose deficit, triggered by energy deprivation or therapeutic agents, can be fatal. Increased appetite is the key behavioral defense against hypoglycemia; however, the central pathways involved are not well understood. Here, we describe a glucoprivic feeding pathway by tyrosine hydroxylase (TH)-expressing neurons from nucleus of solitary tract (NTS), which project densely to the hypothalamus and elicit feeding through bidirectional adrenergic modulation of agouti-related peptide (AgRP)- and proopiomelanocortin (POMC)-expressing neurons. Acute chemogenetic inhibition of arcuate nucleus (ARC)-projecting NTSTH neurons or their target, AgRP neurons, impaired glucoprivic feeding induced by 2-Deoxy-D-glucose (2DG) injection. Neuroanatomical tracing results suggested that ARC-projecting orexigenic NTSTH neurons are largely distinct from neighboring catecholamine neurons projecting to parabrachial nucleus (PBN) that promotes satiety. Collectively, we describe a circuit organization in which an ascending pathway from brainstem stimulates appetite through key hunger neurons in the hypothalamus in response to hypoglycemia.