Changes in acetylcholinesterase, Na+,K+-ATPase, and Mg2+-ATPase activities in the frontal cortex and the hippocampus of hyper- and hypothyroid adult rats.
The thyroid hormones (THs) are crucial determinants of normal development and metabolism, especially in the central nervous system. The metabolic rate is known to increase in hyperthyroidism and decrease in hypothyroidism. The aim of this work was to investigate how changes in metabolism induced by THs could affect the activities of acetylcholinesterase (AChE), (Na+,K+)- and Mg2+-adenosinetriphosphatase (ATPase) in the frontal cortex and the hippocampus of adult rats. Hyperthyroidism was induced by subcutaneous administration of thyroxine (25 microg/100 g body weight) once daily for 14 days, and hypothyroidism was induced by oral administration of propylthiouracil (0.05%) for 21 days. All enzyme activities were evaluated spectrophotometrically in the homogenated brain regions of 10 three-animal pools. A region-specific behavior was observed concerning the examined enzyme activities in hyper- and hypothyroidism. In hyperthyroidism, AChE activity was significantly increased only in the hippocampus (+22%), whereas Na+,K+-ATPase activity was significantly decreased in the hyperthyroid rat hippocampus (-47%) and remained unchanged in the frontal cortex. In hypothyroidism, AChE activity was significantly decreased in the frontal cortex (-23%) and increased in the hippocampus (+21%). Na+,K+-ATPase activity was significantly decreased in both the frontal cortex (-35%) and the hippocampus (-43%) of hypothyroid rats. Mg2+-ATPase remained unchanged in the regions of both hyper- and hypothyroid rat brains. Our data revealed that THs affect the examined adult rat brain parameters in a region- and state-specific way. The TH-reduced Na+,K+-ATPase activity may increase the synaptic acetylcholine release and, thus, modulate AChE activity. Moreover, the above TH-induced changes may affect the monoamine neurotransmitter systems in the examined brain regions.
Carageorgiou
Haris
H
Department of Experimental Pharmacology, Medical School, University of Athens, Goudi, GR-11527 Athens, Greece. xkarag@med.uoa.gr
Pantos
Constantinos
C
Zarros
Apostolos
A
Stolakis
Vasileios
V
Mourouzis
Iordanis
I
Cokkinos
Dennis
D
Tsakiris
Stylianos
S
D000110:Acetylcholinesterase / Q000378:metabolism*; D000818:Animals; D013956:Antithyroid Agents; D017301:Ca(2+) Mg(2+)-ATPase / Q000378:metabolism*; D006624:Hippocampus / Q000201:enzymology*; D006980:Hyperthyroidism / Q000139:chemically induced / Q000201:enzymology*; D007037:Hypothyroidism / Q000139:chemically induced / Q000201:enzymology*; D008297:Male; D017397:Prefrontal Cortex / Q000201:enzymology*; D011441:Propylthiouracil; D051381:Rats; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013974:Thyroxine
D013956:Antithyroid Agents; D011441:Propylthiouracil; D000110:Acetylcholinesterase; D017301:Ca(2+) Mg(2+)-ATPase; D000254:Sodium-Potassium-Exchanging ATPase; D013974:Thyroxine