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      The Nature and Magnitude of in vivo 5-Hydroxyindoleacetic Acid Output from 5-Hydroxytryptamine Terminals Is Related to Specific Regions of the Suprachiasmatic Nucleus

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          Eight cycling female rats were implanted with push-pull cannulae over the region of the suprachiasmatic nuclei (SCN) and allowed 7–10 days for recovery. Perfusion of the SCN continued in these freely behaving rats for 5–6 h of the light period and the subjective scotophase. The release of 5-hydroxyindoleacetic acid (5-HIAA) ranged from 10 to 350 pg 5-HIAA/min. Significantly, the amplitude and characteristics of the output of 5-HIAA were highly location dependent in that rostral cannulae placements revealed high amplitude changes with initial mean values of 40 pg 5-HIAA/min, which increased toward the dark phase to mean peak values of 195 pg 5-HIAA/min. Caudal cannulae placements revealed a low amplitude, high frequency, basal type of 5-HIAA release which did not increase toward the dark period (approximately 5 pg/min). 5-Hydroxytryptophan infusion resulted in a significant marked increase in the basal release of 5-HIAA confirming the biochemical viability of the area undergoing perfusion. These results suggest that the in vivo measurement of 5-HIAA from 5-hydroxytryptamine (5-HT) terminals in the region of the SCN could reflect discrete functional activity of serotonergic terminals within specific regions of the SCN in a freely behaving rat. Furthermore, the biochemical viability of these 5-HT terminals and the ability of the rat’s SCN to exhibit marked differential changes in 5-HT activity emphasizes the physiological relevance of this model system to study neuroendocrine events in freely behaving animals.

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          Author and article information

          S. Karger AG
          02 April 2008
          : 46
          : 5
          : 430-438
          aDepartment of Physiology and Biophysics, University of Illinois at Urbana-Champaign, Urbana, Ill.; bDepartment of Physiology, Eastern Virginia Medical School, Norfolk, Va., USA
          124857 Neuroendocrinology 1987;46:430–438
          © 1987 S. Karger AG, Basel

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          Pages: 9
          Original Paper


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