Abstract

Embryonic diapause is a widespread phenomenon in mammals and may be controlled either by lactation or by seasonal environmental factors1. A few species, such as the tammar wallaby, Macropus eugenii, use both mechanisms, depending on the time of year. On Kangaroo Island, South Australia (latitude 36° S), female tammars give birth to a single young in late January or early February2. Mating occurs on the day after birth and the resulting conceptus grows to a 100-cell blastocyst before entering a state of embryonic diapause. This arrest of embryonic growth is due to a suppression of the corpus luteum by prolactin induced by the young in the pouch sucking the teat (lactational diapause)3,4. If the young is removed from the teat between February and early June, the corpus luteum hypertrophies, the blastocyst resumes growth and birth occurs 27 days later5. In the second half of the year (June to December), diapause is not solely dependent on the sucking stimulus as it is maintained after weaning, which usually occurs in October, or following experimental removal of the pouch young. This is referred to as seasonal diapause5. Reactivation occurs on or about the summer solstice (22 December) and there is evidence that it is photoperiodically induced6 (Fig. 1). We report here that bilateral removal of the superior cervical ganglion in female tammars eliminates seasonal embryonic diapause, but has no effect on lactational diapause. This is the first evidence that the pineal gland may be involved in regulation of embryonic diapause in mammals.

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