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POSTSYNAPTIC ADRENERGIC‐CYCLIC AMP CONTROL OF THE SEROTONIN CONTENT OF CULTURED RAT PINEAL GLANDS
Author(s) -
Klein D. C.,
Yuwiler A.,
Weller Joan L.,
Plotkin Selma
Publication year - 1973
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1973.tb07580.x
Subject(s) - medicine , endocrinology , cycloheximide , serotonin , norepinephrine , postsynaptic potential , pineal gland , adenosine , propranolol , adrenergic , dopamine , receptor , chemistry , adrenergic receptor , phenoxybenzamine , 5 ht receptor , biology , biochemistry , protein biosynthesis , melatonin
— This investigation was designed to determine whether the amount of serotonin (5‐HT) in cultured pineal glands can be altered by norepinephrine (NE). Treatment with l ‐NE (10 −5 ‐10 −7 m ) for 4‐6 h caused a gradual decrease in the concentration of 5‐HT to a value that was less than 30% of that in the untreated control gland. This effect was observed using chronically denervated pineal glands. d ‐Norepinephrine (10 −6 ‐10 −7 m ) and dopamine (10 −4 m ) were ineffective in lowering 5‐HT. The effect of l ‐NE was completely blocked by a β‐adrenergic receptor blocker, propranolol and was only slightly decreased by α‐adrenergic receptor blockers. These observations indicate that l ‐NE acts post‐synaptically via a highly specific β‐adrenergic mechanism. The effect of l ‐norepinephrine was mimicked by theophylline and N 6 , 2′0‐dibutyryl adenosine 3′,5′‐monophosphate, an indication that adenosine 3′,5′‐monophosphate is involved in the effect of l ‐NE on 5‐HT. Treatment with cycloheximide, which by itself caused a decrease in pineal 5‐HT, also blocked any further decrease caused by treatment with l ‐NE, an indication that protein synthesis is necessary for maintenance of baseline levels of serotonin and for the effect of l ‐NE to be observed. The total amount of l ‐[ 3 H]NE and degradation products of L‐[ 3 H]NE in the gland after 6 h of treatment with l ‐[ 3 H]NE was less than 3 pmol. This amount of l ‐NE and degradation products of l ‐NE could not account for the decrease of 100‐200 pmol of 5‐HT on the basis of a mole for mole replacement of 5‐HT by l ‐NE. These findings are consistent with the hypothesis that non‐neuronal pineal 5‐HT is physiologically regulated by the release of l ‐NE from the sympathetic nerve network.