An fMRI study examining the role of the extended amygdala and amygdala in emotion and inhibitory control in native versus second language processing.

The role of the extended amygdala and amygdala in mediating emotion and inhibitory control in native language versus second language processing is currently not well understood. The current study examined activity in the extended amygdala and amygdala when twelve healthy young adults were exposed to emotional-linguistic stimuli in either their native language (i.e.

Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption.

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.

Adenosine A receptors in the olfactory bulb suppress rapid eye movement sleep in rodents.

Rapid eye movement (REM) sleep behavior disorder in humans is often accompanied by a reduced ability to smell and detect odors, and olfactory bulbectomized rats exhibit increased REM sleep, suggesting that the olfactory bulb (OB) is involved in REM-sleep regulation. However, the molecular mechanism of REM-sleep regulation by the OB is unknown. Adenosine promotes sleep and its A receptors (AR) are expressed in the OB.

Mineralocorticoid receptors in the medial prefrontal cortex and hippocampus mediate rats' unconditioned fear behaviour.

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.

Inactivation of the dorsal or ventral hippocampus with muscimol differentially affects fear and memory.

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.

The role of the dorsal and ventral hippocampus in fear and memory of a shock-probe experience.

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).