An Interview with Jonathan Bloom

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doi:10.5250/resilience.2.1.007

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“…In contrast to the CORT and cFos studies, all FSCV recordings occurred on the day immediately following the final stress exposure to examine an adaptive response. Our stimulation parameters examined light pulses (4ms duration) to various frequency (20 pulses at 1, 2, 5, 10, 15 Hz) and pulse number (1,2,5,10,20 pulses at 5 Hz or 10 Hz) protocols, and were chosen to encapsulate a range of physiologically relevant noradrenergic firing patterns [26][27][28] . Repeated restraint stress exposure significantly increased NE release across the range of stimulation frequencies with the largest differences observed at high phasic frequencies (Fig.…”

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confidence: 99%

“…Noradrenergic neurons project through two primary pathways in the brain: the dorsal noradrenergic bundle and ventral noradrenergic bundle. The pontine locus coeruleus (A6) gives rise to the dorsal noradrenergic bundle sending projections throughout the cortex, thalamus, hippocampus, cerebellum, and amygdala [5][6][7] . In contrast, the ventral noradrenergic bundle mainly arises from two nuclei, A1 of the rostral ventrolateral medulla and A2 of the nucleus of the solitary tract 6 , and projects mainly to hypothalamus, parabrachial nucleus, midbrain, and bed nucleus of the stria terminalis (BNST) 3,6,8 .…”

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Stress-Induced Alterations of Norepinephrine Release in the Bed Nucleus of the Stria Terminalis of Mice

Schmidt¹,

Makhijani²,

Boyt³

et al. 2018

ACS Chem. Neurosci.

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Stress can drive adaptive changes to maintain survival during threatening stimuli. Chronic stress exposure, however, may result in pathological adaptations. A key neurotransmitter involved in stress signaling is norepinephrine. Previous studies show that stress elevates norepinephrine levels in the bed nucleus of the stria terminalis (BNST), a critical node regulating anxiety and upstream of stress responses. Here, we use mice expressing channelrhodopsin in norepinephrine neurons to selectively activate terminals in the BNST, and measure norepinephrine release with fast-scan cyclic voltammetry. Mice exposed to a single restraint session show an identical norepinephrine release profile compared to that of unexposed mice. Mice experiencing five days of restraint stress, however, show elevated norepinephrine release across multiple stimulation parameters, and reduced sensitivity to the α 2 -adrenergic receptor antagonist idazoxan. These data are the first to examine norepinephrine release in the BNST to tonic and phasic stimulation frequencies, and confirm that repeated stress alters autoreceptor sensitivity.

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