The role of melatonin deficiency induced by pinealectomy on motor activity and anxiety responses in young adult, middle-aged and old rats

Author:

Tchekalarova Jana1,Krushovlieva Desislava1,Ivanova Petj1,Nenchovska Zlatina1,Toteva Gergana2,Atanasova Milena2

Affiliation:

1. Bulgarian Academy of Sciences (BAS)

2. Medical University – Pleven

Abstract

Abstract Background Aging affects anxiety levels in rats while the pineal gland, via its hormone melatonin, could modulate their inherited life “clock.” The present study aimed to explore the impact of plasma melatonin deficiency on anxiety responses and the possible involvement of the hypothalamic-pituitary-adrenocortical (HPA) axis and heat shock proteins (Hsp) 70 and 90 in the frontal cortex (FC) and the hippocampus in young adult, middle-aged and elderly rats with pinealectomy. Results Melatonin deficiency induced at different life stages did not affect the lifespan of rats. Pinealectomy abolished the circadian rhythm of motor activity, measured for 48 h in the actimeter, in young adult but not in middle-aged rats. Both 18-month-old sham- and rats with pinealectomy exhibited impaired circadian variations of motor activity. The same generations (3- and 18-month-old rats with pinealectomy) had lower anxiety levels than the matched sham groups, measured in three tests: elevated-plus maze, light-dark test, and novelty suppressing feeding test. While the activity of the HPA axis remained intact in young adult and middle-aged rats with melatonin deficiency, high baseline corticosterone level and blunted stress-induced mechanism of its release was detected in the oldest rats. Age-associated reduced Hsp 70 and 90 levels in the FC but not in the hippocampus were detected. Pinealectomy diminished the expression of Hsp 70 in the FC of middle-aged rats compared to the matched sham rats. Conclusions Our results suggest that while melatonin hormonal dysfunction impaired the circadian variations of motor activity and emotional behavior in young adult and elderly rats, the underlying pathogenic mechanism in these generations might be different and needs further verification.

Publisher

Research Square Platform LLC

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