Rapid eye movement (REM) sleep loss is associated with increased consumption of weight-promoting foods. The prefrontal cortex (PFC) is thought to mediate reward anticipation. However, the precise role of the PFC in mediating reward responses to highly palatable foods (HPF) after REM sleep deprivation is unclear. We selectively reduced REM sleep in mice over a 25-48 hr period and chemogenetically inhibited the medial PFC (mPFC) by using an altered glutamate-gated and ivermectin-gated chloride channel that facilitated neuronal inhibition through hyperpolarizing infected neurons. HPF consumption was measured while the mPFC was inactivated and REM sleep loss was induced. We found that REM sleep loss increased HPF consumption compared to control animals. However, mPFC inactivation reversed the effect of REM sleep loss on sucrose consumption without affecting fat consumption. Our findings provide, for the first time, a causal link between REM sleep, mPFC function and HPF consumption.

Corticosterone is released from the adrenal cortex in response to stress, and binds to glucocorticosteroid receptors (GRs) and mineralocorticosteroid receptors (MRs) in the brain. Areas such as the dorsal hippocampus (DH), ventral hippocampus (VH) and medial prefrontal cortex (mPFC) all contain MRs and have been previously implicated in fear and/or memory.
The purpose of the following experiments was to examine the role of these distinct populations of MRs in rats' unconditioned fear and fear memory.
The MR antagonist (RU28318) was microinfused into the DH, VH, or mPFC of rats. Ten minutes later, their unconditioned fear was tested in the elevated plus-maze and the shock-probe tests, two behavioral models of rat "anxiety." Twenty-four hours later, conditioned fear of a non-electrified probe was assessed in rats re-exposed the shock-probe apparatus.
Microinfusions of RU28318 into each of the three brain areas reduced unconditioned fear in the shock-probe burying test, but only microinfusions into the VH reduced unconditioned fear in the plus-maze test. RU28318 did not affect conditioned fear of the shock-probe 24 hr later.
MRs in all three areas of the brain mediated unconditioned fear to a punctate, painful stimulus (probe shock). However, only MRs in the ventral hippocampus seemed to mediate unconditioned fear of the more diffuse threat of open spaces (open arms of the plus maze). In spite of the known roles of the hippocampus in spatial memory and conditioned fear memory, MRs within these sites did not appear to mediate memory of the shock-probe. (C) 2011 Elsevier Inc. All rights reserved.

It was recently found that temporary inactivation of the dorsal hippocampus with lidocaine impaired fear memory, whereas temporary inactivation of the ventral hippocampus did not. These site-specific deficits, however, may have resulted from disruption of axonal signals arriving from structures outside of the hippocampus, or from disruption of axons that pass through the hippocampus entirely. This is problematic because the hippocampus receives extensive afferent input from both the amygdala and the septum, which also play very important roles in fear and fear memory. To mitigate this problem, rats were infused with the GABA(A) receptor agonist muscimol, into either the dorsal or the ventral hippocampus, just after an "acquisition" session in which the rats were shocked from an electrified probe. A "retention" test in the same apparatus was conducted 24 h later, when the hippocampus was no longer inactivated, and the probe was no longer electrified. Dorsal hippocampal inactivation just after acquisition impaired conditioned fear behavior (probe avoidance) during the retention test, whereas ventral hippocampal inactivation after acquisition did not. However, muscimol inactivation of the ventral hippocampus during an "acquisition" session selectively impaired unconditioned fear behavior, replicating earlier findings with lidocaine, a sodium channel blocker. Because muscimol hyperpolarizes neurons through a post-synaptic, GABAA receptor-mediated increase of chloride conductance whereas lidocaine produces indiscriminate disruption of all axonal signalling its effects are more likely to be restricted to intrinsic neurons within the area of infusion. These results provide strong evidence that afferent input from brain structures located outside of the hippocampus is not responsible for the differential effects of dorsal and ventral hippocampal inactivation on fear memory. (C) 2010 Elsevier B.V. All rights reserved.

The roles of the dorsal and ventral hippocampus in fear and memory are unclear. This study examined the effects of temporary inactivation of the dorsal or ventral hippocampus on unconditioned and conditioned fear, using the shock-probe test. In Experiment 1, rats received either dorsal or ventral hippocampal infusions of lidocaine or saline, before exposure to an electrified shock-probe (acquisition I). In Experiment 2, rats received lidocaine or saline infusions after exposure to the shock-probe (acquisition II). In both experiments, a retention test in the same apparatus was given 24 h later, at which time the hippocampus was no longer inactivated, and the probe was disconnected from the shock-source. Because ventral hippocampal inactivation impaired fear behaviour during acquisition, and dorsal hippocampal inactivation impaired fear behaviour (probe avoidance) during retention, we concluded that 1) the ventral hippocampus plays a role in the expression of untrained fear reactions whereas 2) the dorsal hippocampus plays a role in encoding memory of the fearful experience. (c) 2008 Elsevier B.V. All rights reserved.