Arylalkylamine N-acetyltransferase (AANAT) is expressed in astrocytes and melatonin treatment maintains AANAT in the gerbil hippocampus induced by transient cerebral ischemia

Ok Kyu Park, Ki Yeon Yoo, Choong Hyun Lee, Jung Hoon Choi, In Koo Hwang, Jun Hong Park, Young Guen Kwon, Young Myeong Kim, Moo Ho Won

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12 Citations (Scopus)


Melatonin is synthesized from serotonin by the action of arylalkylamine N-acetyltransferase (AANAT) and hydroxyindole-O-methyltransferase. In this study, we observed cellular changes of arylalkylamine N-acetyltransferase (EC; AANAT) in the hippocampal CA1 region at various time points after ischemia/reperfusion. In vehicle-treated sham group, AANAT immunoreaction was detected in pyramidal neurons of the CA1 region. AANAT immunoreactivity in the neurons was highest 2 days and disappeared from 4 days after ischemia/reperfusion. From 3 days after ischemia/reperfusion, AANAT immunoreaction was expressed in astrocytes in the strata oriens and radiatum of the CA1 region. AANAT protein and mRNA levels were significantly increased 2 days after ischemia/reperfusion, and markedly decreased from 5 days after ischemia/reperfusion. The repeated administration of melatonin (10 mg/kg, i.p.) 3 times (once a day) to gerbils before ischemia/reperfusion significantly reduced ischemia-induced hyperactivity as well as neuronal death compared to those in the vehicle-treated ischemia group. Melatonin treatment also maintained AANAT immunoreactivity and its protein levels in the CA1 region after ischemia/reperfusion. These results suggest that the reduction of AANAT in ischemic CA1 region is associated with delayed neuronal death following transient ischemia, and melatonin treatment shows neuroprotection with maintenance of AANAT levels in the ischemic CA1 region.

Original languageEnglish
Pages (from-to)7-17
Number of pages11
JournalJournal of the Neurological Sciences
Issue number1-2
Publication statusPublished - 2010 Jul 15

Bibliographical note

Funding Information:
We observed the neuroprotective effects of melatonin against ischemic damage. The administration of melatonin for 3 days significantly reduced the ischemia-related hyperactivity 1 day after ischemia/reperfusion. Spontaneous motor activity is a good method for evaluating the neuroprotection against ischemic damage in a gerbil ischemic model days after ischemia/reperfusion. This result was supported by previous studies that melatonin protects brain damage from the ischemic damage in rats [39,40] . The melatonin also reduced the ischemia-related neuronal death in the hippocampus 5 [30,31,41–44] and gerbils [29] .

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

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