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Oxytocin, a neuropeptide hormone, is indispensable for milk ejection during nursing and is important for uterine contractions during parturition. The exact functions of oxytocin in postpartum maternal behaviors and motivations require further investigation. To this end, we characterized the role of oxytocin in components of maternal motivations during the mid‐postpartum period, which has not been previously studied. To maintain suckling stimuli, postpartum oxytocin knockout (Oxt−/−) and heterozygous (Oxt+/−) littermates were co‐housed with a wild‐type lactating mother and its litter, and were examined for their ability to retrieve pups under standard or high‐risk conditions, nursing behavior, maternal aggression towards an unfamiliar intruder, and motivation to regain contact with separated pups. One‐third of Oxt−/− mothers exhibited prolonged parturition but were otherwise grossly healthy. Despite their inability to eject milk, Oxt−/− mothers displayed nursing behaviors for similar durations to Oxt+/− mothers during the second postpartum week. In addition, Oxt−/− mothers were essentially intact for pup retrieval under standard conditions and were motivated to stay close to pups, although they showed a mild decrease in maternal care under high‐risk conditions and increased anxiety‐like behaviors in pup‐related contexts. The present findings indicate that oxytocin is dispensable for nursing behavior and maternal motivations, yet suggest that oxytocin may be relevant for stress resilience in the postpartum period.
Within the past 20 years, particularly with the advent of exome sequencing technologies, autosomal dominant and de novo mutations in the gene encoding the neurone-specific α3 subunit of the Na+,K+-ATPase (NKA α3) pump, ATP1A3, have been identified as the cause of a phenotypic continuum of rare neurological disorders. These allelic disorders of ATP1A3 include (in approximate order of severity/disability and onset in childhood development): polymicrogyria; alternating hemiplegia of childhood; cerebellar ataxia, areflexia, pes cavus, optic atrophy and sensorineural hearing loss syndrome; relapsing encephalopathy with cerebellar ataxia; and rapid-onset dystonia-parkinsonism. Some patients present intermediate, atypical or combined phenotypes. As these disorders are currently difficult to treat, there is an unmet need for more effective therapies. The molecular mechanisms through which mutations in ATP1A3 result in a broad range of neurological symptoms are poorly understood. However, in vivo comparative studies using genetically altered model organisms can provide insight into the biological consequences of the disease-causing mutations in NKA α3. Herein, we review the existing mouse, zebrafish, Drosophila and Caenorhabditis elegans models used to study ATP1A3-related disorders, and discuss their potential contribution towards the understanding of disease mechanisms and development of novel therapeutics.
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