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Smiley, K. O.

Publications and source records attributed to Smiley, K. O..

2 recordsLinked to original sources

Parental state dynamically reshapes auditory processing of offspring vocalizations in zebra finches

Parental care is critical for offspring survival. For many species, including humans, auditory cues unique to dependent offspring, such as baby cries, elicit the necessary behavior from parents to care for young. Despite this, we know little about how the brain encodes auditory cues specific to offspring. Zebra finches are an excellent model to study this. Zebra finches are biparental, meaning both male and female parents raise the young and rely on auditory cues (begging calls) to elicit chick feeding responses (parental behavior). Begging calls also become individually identifiable by the parents, necessitating higher-order learning/ association neural processes. It is well established that the caudomedial nidopallium (NCM), a higher-order region of secondary pallial cortex (analogous to the mammalian secondary auditory cortex), is involved in the perception of complex auditory signals in birds. It is unknown, however, if/how NCM responds to offspring begging calls. To begin testing this, we used high density silicon probes to record single-unit in vivo electrophysiology activity in the NCM of adult parenting and non-parenting zebra finches exposed to playbacks of their own chicks begging calls (parents only), novel age-matched begging calls (parents and non-parents), as well as novel adult male song and pure tone controls. Our results show that NCM neurons in parents respond more strongly (i.e., higher evoked firing rates) to both their own and novel chick begging calls and have higher baseline (spontaneous) firing rates in narrow spiking units relative to non-parents. Furthermore, NCM neurons in parenting females tend to show more selective responses towards their own chick begging calls, whereas those in males do not show similar levels of selectivity. These studies lay essential groundwork for future studies on how auditory responses can elicit parental behavior and how these responses may change over the chick-rearing period.

neuroscience↗

Prolactin action is necessary for parental behavior in male mice

Parental care is critical for successful reproduction in mammals. In comparison to maternal care, the neuroendocrine mechanisms supporting paternal care are less well-studied. Laboratory mice show a mating-induced suppression of infanticide (normally observed in virgins) and onset of paternal behavior. Using this model, we sought to investigate whether the hormone prolactin plays a role in paternal behavior, as it does for maternal behavior. First, using c-fos immunoreactivity in Prlr-IRES-Cre-tdtomato reporter mouse sires, we show that the circuitry activated during paternal interactions contains prolactin-responsive neurons, including the medial preoptic area, bed nucleus of the stria terminalis, and medial amygdala. To evaluate whether prolactin action is required for the establishment and display of paternal behavior, we conditionally deleted the prolactin receptor (Prlr) from 3 distinct cell types: glutamatergic, GABAergic, and CaMKII-expressing forebrain neurons. Prlr-deletion from CaMKII-expressing forebrain neurons, but not from glutamatergic or GABAergic cells, resulted in a profound effect on paternal behavior, as none of these males completed the pup retrieval task. Finally, although sires do not show an acute increase in circulating prolactin levels in response to pups, pharmacological blockade of prolactin-release at the time of pup exposure resulted in failure to retrieve pups, similar to when the Prlr was deleted from CaMKII neurons, with prolactin administration rescuing this behavior. Taken together, our data show that paternal behavior in sires is dependent on basal levels of circulating prolactin acting at the Prlr on CaMKII-expressing neurons. These new data in male mice demonstrate that prolactin has a similar action in both sexes to promote parental care.

neuroscience↗