Abstract
Stress leaves a lasting impression on an organism and reshapes future responses. However, the influence of past experience and stress hormones on the activity of neural stress circuits remains unclear. Hypothalamic corticotropin-releasing hormone (CRH) neurons orchestrate behavioral and endocrine responses to stress and are themselves highly sensitive to corticosteroid (CORT) stress hormones. Here, using in vivo optical recordings, we find that CRH neurons are rapidly activated in response to stress. CRH neuron activity robustly habituates to repeated presentations of the same, but not novel stressors. CORT feedback has little effect on CRH neuron responses to acute stress, or on habituation to repeated stressors. Rather, CORT preferentially inhibits tonic CRH neuron activity in the absence of stress stimuli. These findings reveal how stress experience and stress hormones modulate distinct components of CRH neuronal activity to mediate stress-induced adaptations.
Highlights
Stress leaves a lasting impression on an organism and reshapes future responses
One hypothalamic neural population, which are essential for controlling stress responses, are the corticotropin-releasing hormone (CRH) neurons located in the paraventricular nucleus (PVN)
While CORT feedback had no effect on the magnitude of threat-evoked activity, it did induce a slow suppression of tonic CRH neural activity
Summary
Stress leaves a lasting impression on an organism and reshapes future responses. the influence of past experience and stress hormones on the activity of neural stress circuits remains unclear. One hypothalamic neural population, which are essential for controlling stress responses, are the corticotropin-releasing hormone (CRH) neurons located in the paraventricular nucleus (PVN) In addition to their well-known role in controlling corticosteroid (CORT) secretion, this neural population has been shown to be important in mediating other stress-related functions, including shifts in behavior[7], pheromone release[8], and encoding of valence[9]. Repeated exposure to homotypic stress suppressed threat-evoked CRH neuron activity over a time course of minutes to days This adaptive response did not require stress hormone signaling. While CORT feedback had no effect on the magnitude of threat-evoked activity, it did induce a slow suppression of tonic CRH neural activity Together, these data reveal that neural and endocrine mechanisms regulate different components of hypothalamic CRH neuron activity dynamics
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