Male and Female Prolactin Receptor mRNA Expression in the Brain of a Biparental and a Uniparental Hamster, Phodopus , Before and After the Birth of a Litter E. Ma,* J. Lau,* D. R. Grattan,† D. A. Lovejoy‡ and K. E. Wynne-Edwards* *Department of Biology, Queen’s University, Kingston, Canada. †Department of Anatomy and Structural Biology, University of Otago, Dunedin, New Zealand. ‡Department of Zoology, University of Toronto, Toronto, Canada. Key words: prolactin, prolactin receptor, choroid plexus, paternal behaviour, reverse transcription-PCR, Phodopus, males, PRL-R nucleotide sequence, hamster. Abstract Prolactin receptor (PRL-R) mRNA transcript level was quantified in the choroid plexus (ChP) of a naturally biparental hamster, Phodopus campbelli, and its otherwise similar, yet nonpaternal, sibling species, Phodopus sungorus. Pair-housed males and females on the day before the birth of their first litter (G17), the day after birth (L1), lactation day 5 (L5), and unpaired animals that were sexually naı ¨ve, were tested. PRL-R mRNA transcript level relative to total RNA, was evaluated by reverse transcriptase-polymerase chain reaction using primers common to the long- and short-form of the PRL-R in Phodopus. In the ChP, a region implicated in prolactin transport into the central nervous system, females had the expected increase in PRL-R mRNA transcript from dioestrus to L5, consistent with known actions of prolactin. As predicted, males and females of the biparental species were similar, although PRL-R mRNA in naı ¨ve males was higher than in dioestrus females. Males of the two species also differed as predicted. PRL-R mRNA transcript levels were higher in the biparental males. In addition, P. campbelli males had low PRL-R mRNA at G17 compared to L5. By contrast, non-paternal P. sungorus males had elevated PRL-R mRNA transcript levels on G17 relative to unpaired males. We conclude that PRL-R mRNA in the ChP is differentially regulated before and after birth in a paternal and a nonpaternal male. Although prolactin is well established as a regulator of lactation in females, it also exerts numerous neuroendocrine effects in the maternal brain, such as increasing feeding behaviour (1, 2), suppressing fertility (3), and decreasing stress responsiveness and anxiety in new mothers (4). How- ever, the most prominent actions of prolactin in the brain are seen in the display of maternal behaviour after parturition, which include actions such as pup retrieval, grouping and crouching, and licking of pups (5, 6). Evidence also supports a functional role for prolactin in male parental behaviour. Although widespread, including human fathers (7) and naturally paternal nonhuman primates (8, 9) and biparental rodents (10–12), much of the evidence remains correlational. Dwarf hamsters (genus Phodopus) provide an excellent model to study the neuroendocrinology of paternal behaviour in more detail. Two species in this genus, Phodopus campbelli and Phodopus sungorus, are closely related and were long considered subspecies (13, 14). They have the same body weight and the same reproductive timetable (15, 16). However, P. campbelli is naturally bipa- rental, whereas P. sungorus has uniparental maternal care, with only facultative, seasonal opportunities for biparental care (17–19). These differences are due to physiological adaptations that have arisen from contrasting ecological niches (15, 16). Peripheral prolactin profiles of males of both species have been described in detail (11), with concentrations being elevated in expectant P. campbelli fathers during the late afternoon of the day before birth, but not in P. sungorus fathers. To effect overt changes in behaviour, prolactin must first gain access to key hypothalamic regions in the brain. As a relatively large protein (197–199 amino acids), prolactin is thought to enter the brain via prolactin binding sites on the choroid plexus (ChP) (20). Located in the lateral, third and fourth ventricles of the brain, the ChP has fenestrated capillaries but maintains a blood-cerebrospinal fluid (CSF) Correspondence to: Dr Katherine E. Wynne-Edwards, Department of Biology, Queen’s University, Kingston, Ontario K7L 3N6, Canada (e-mail: wynneedw@biology.queensu.ca). Journal of Neuroendocrinology, 2005, Vol. 17, 81–90 doi:10.1111/j.1365-2826.2005.01278.x Ó 2005 Blackwell Publishing Ltd