Stress-evoked increases in serotonin in the auditory midbrain do not directly result from elevations in serum corticosterone.

نویسندگان

  • Ian C Hall
  • Gabrielle L Sell
  • Emily M Chester
  • Laura M Hurley
چکیده

Neurochemicals such as serotonin convey information about behavioral context to sensory processing. In the auditory system, serotonin modulates the responses of neurons in the inferior colliculus (IC) to acoustic stimuli, including communication vocalizations. Levels of extracellular serotonin in the IC can change rapidly in response to stressful situations such as social challenge and limited movement. Since activation of the hypothalamo-pituitary-adrenal (HPA) axis can influence serotonin in other brain regions, we examined the relationship between serum corticosterone and serotonin release in the IC. We used voltammetry to measure extracellular serotonin in the IC of male CBA/J mice during restriction of movement, a low-intensity restraint stress. Enzyme immunoassay (EIA) was used to measure the concentration of corticosterone circulating in the blood serum as an indicator of the activation of the HPA axis. Changes in serotonin and corticosterone were also compared with behavioral performance. Restriction stress caused increases in serotonin in the IC and circulating corticosterone, and changes in behavior. Changes in serotonin and corticosterone were not correlated with each other across individuals. Individual behavioral performance was correlated with elevations in corticosterone, but not in serotonin. We further explored the relationship between physiological pathways by directly manipulating serum corticosterone. Injections of corticosterone elevated circulating levels beyond normal physiological ranges, but had no effect on serotonin in the IC. These findings suggest that, within the auditory system, serotonin is released during stressful events, but this is a correlate of behavioral arousal, rather than a direct response to elevations in serum corticosterone.

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عنوان ژورنال:
  • Behavioural brain research

دوره 226 1  شماره 

صفحات  -

تاریخ انتشار 2012