Changes in Photoperiod Alter the Daily Rhythms of Pineal Melatonin Content and Hypothalamicβ-Endorphin Content and the Luteinizing Hormone Response to Naloxone in the Male Syrian Hamster*

This study examines the possible involvement of β-endorphin in the photoperiodic control of reproduction in the Syrian hamster. β-Endorphin and LHRH concentrations in the medial basal hypothalamus (MBH), anterior hypothalamus (AHA), and the preoptic area (POA) as well as pineal melatonin content were determined by RIA in male Syrian hamsters exposed to either a long day [(LD) 16-h light; 8-h dark; lights on 0700–2300] or short day [(SD) 8-h light, 16-h dark; lights on 0700–1500] for 8 weeks. Groups of eight animals from each photoperiod were killed by decapitation at 4-h intervals over 24 h. Twenty minutes before death half the animals from each photoperiod were given naloxone (5 mg/kg, sc), the other half saline. Exposure to a long photoperiod maintained testicular activity while a short photoperiod induced testicular regression. Pineal melatonin content in both photoperiods was maximal at 0500 h, i.e. 2 h before the onset of light (SD, 435.58 ± 82.7 pg/pineal; LD, 276.78 ± 56.8 pg/pineal). However, the duration of the nighttime rise in pineal melatonin content was increased in SD animals with elevated melatonin levels at 2100 h (157.10 ± 41.8 pg/pineal) and 0100 h (199.11 ± 58.9 pg/pineal). In contrast pineal melatonin content in LD animals was only higher than daytime values at 0500 h. A daily rhythm of β-endorphin content within both the AHA and MBH of animals exposed to a short photoperiod coincided with this prolonged nighttime rise in pineal melatonin content, although a causal relationship between the two was not established. Peak levels of β-endorphin occurred at 2100 h (AHA, 6.569 ± 1.2 pmol/mg protein; MBH, 4.877 ± 0.45 pmol/mg protein) and at 0100 h (AHA, 6.107 ± 0.66 pmol/mg protein; MBH, 4.49 ± 00.79 pmol/mg protein) which was 6 h and 10 h into the dark phase, respectively, with lowest levels in the middle of the light phase (AHA, 3.561 ± 0.56 pmol/mg protein; MBH, 2.688 ± 0.3 pmol/mg protein). This rhythm was absent in animals exposed to a long photoperiod. There was no effect of photoperiod or time of day on the content of β-endorphin in the POA. LHRH levels were not altered by changes in photoperiod in all three brain regions studied. In the AHA and MBH, concentrations of LHRH were similar at all times of day whereas, in the POA, LHRH levels varied with time in both photoperiods. Peak levels occurred in the middle of the dark phase at 0100 h (LD, 2.774 ± 0.24 pmol LHRH/mg protein; SD, 3.206 ± 0.48 pmol LHRH/mg protein) with lowest levels during the light phase (LD, 1.664 pmol LHRH/mg protein; SD, 1.775 pmol LHRH/mg protein). Animals kept in a long photoperiod and given naloxone showed a 3- to 4-fold rise in serum LH levels at all times of the day (2.239 ng/ml, mean of six time points) as compared to the saline-treated controls (0.740 ng/ml, mean of six time points). In contrast, animals in a short photoperiod failed to show a rise in LH in response to naloxone at any tihie of day (saline, 0.418 ng/ml; naloxone, 0.422 ng/ml; mean of six time points). Thus, exposure to a short photoperiod inhibited reproduction and prolonged the nighttime rise in pineal melatonin content. A marked diurnal rhythm in hypothalamic β-endorphin content was also present, a rhythm absent in animals exposed to a long photoperiod. SD exposure blocked the LH response to acute naloxone administration. These data demonstrate that exposure of adult Syrian hamsters to a photoperiod that inhibits reproductive activity produces striking changes in the activity of the opiate system as measured both by β-endorphin brain content and the LH response to naloxone. This Suggests a possible involvement of the β-endorphin system in the photoperiodinduced suppression of reproduction in a seasonally breeding mammal. (Endocrinology117: 141–148, 1985)