title: Arylalkylamine N-acetyltransferase (AANAT) is expressed in astrocytes and melatonin treatment maintains AANAT in the gerbil hippocampus induced by transient cerebral ischemia.
abstract: 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 2.3.1.87; 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.
authors.affiliation: Department of Anatomy and Neurobiology, and Institute of Neurodegeneration and Neuroregeneration, College of Medicine, Hallym University, Chuncheon 200-702, Republic of Korea.
authors.forename: Ok Kyu
authors.initials: OK
authors.lastname: Park
authors.forename: Ki-Yeon
authors.initials: KY
authors.lastname: Yoo
authors.forename: Choong Hyun
authors.initials: CH
authors.lastname: Lee
authors.forename: Jung Hoon
authors.initials: JH
authors.lastname: Choi
authors.forename: In Koo
authors.initials: IK
authors.lastname: Hwang
authors.forename: Jun Hong
authors.initials: JH
authors.lastname: Park
authors.forename: Young-Guen
authors.initials: YG
authors.lastname: Kwon
authors.forename: Young-Myeong
authors.initials: YM
authors.lastname: Kim
authors.forename: Moo-Ho
authors.initials: MH
authors.lastname: Won
mesh_terms: D000818:Animals; D047068:Arylalkylamine N-Acetyltransferase / Q000378:metabolism*; D001253:Astrocytes / Q000187:drug effects / Q000201:enzymology* / Q000378:metabolism; D056547:CA1 Region, Hippocampal / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D005849:Gerbillinae; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000201:enzymology* / Q000378:metabolism; D008550:Melatonin / Q000008:administration & dosage / Q000627:therapeutic use*; D009043:Motor Activity / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D017966:Pyramidal Cells / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D015427:Reperfusion Injury / Q000188:drug therapy / Q000201:enzymology / Q000378:metabolism; D013997:Time Factors
chemical_list: D005904:Glial Fibrillary Acidic Protein; D018696:Neuroprotective Agents; D012333:RNA, Messenger; D047068:Arylalkylamine N-Acetyltransferase; D008550:Melatonin