Researchers at NYU Grossman School of Medicine have shed new light on the biology behind a mother’s ability to release breast milk in response to her baby’s cries.
Published in the journal Nature, the study explores the complex neurological processes that occur in mothers upon hearing the sound of their newborns’ wails, triggering a surge of oxytocin — the hormone responsible for milk ejection. The research may pave the way for novel interventions for mothers who struggle with breastfeeding.
Historically, it has been observed in humans and other mammals that a baby’s cries alone can prompt its mother to release breast milk. However, this is the first study to delve into the underlying mechanisms at play.
According to the study’s findings, the cry of a mouse pup travels as sound information to a specific area in the mother’s brain known as the posterior intralaminar nucleus of the thalamus (PIL). This sensory hub then signals oxytocin-releasing neurons in the hypothalamus, a key control center for hormone activity.
This surge of hormones lasts for approximately five minutes, which is usually enough time for the infant to feed until they are full or resume crying.
The researchers also found that under normal conditions, the hypothalamus neurons are restricted by proteins that act as gatekeepers to prevent false alarms and wasted milk. However, after 30 seconds of consistent crying, signals from the PIL accumulate enough to overpower these proteins, initiating the release of oxytocin.
“Our findings uncover how a crying infant primes its mother’s brain to ready her body for nursing,” said study co-lead author Habon Issa, a graduate student at NYU Langone Health. “Without such preparation, there can be a delay of several minutes between suckling and milk flow, potentially leading to a frustrated baby and stressed parent.”
This study deployed a relatively new type of molecular sensor, iTango, to measure actual oxytocin release from brain cells in real time, marking a significant advance in the field. Previously, researchers relied on indirect measurements, as oxytocin degrades rapidly due to its small molecular size.
Another fascinating discovery was that the oxytocin boost only occurs in mother mice and not in females who have never given birth. Furthermore, the study found that the mother’s brain circuitry was only activated by the cries of her own pups and not by computer-generated tones mimicking natural wails.
The researchers extended their study to assess the impact of this brain circuitry on maternal behavior. They discovered that inhibiting the PIL’s communication with oxytocin neurons led to mothers tiring and ceasing to fetch their straying young. However, when this system was reactivated, the mothers persevered despite their fatigue.
“These results suggest that the crying-prompted brain circuit is not only important for nursing behavior, but also for maintaining a mother’s attention over time and encouraging effective care of her young even when she is exhausted,” said study senior author Dr. Robert C. Froemke, who also emphasized the potential human applications of these findings.
It’s important to note that the study focused on hormone release, rather than the act of lactation itself. Dr. Froemke expressed that understanding how this oxytocin system functions — or malfunctions — in humans may offer new insights into aiding mothers who face difficulties with breastfeeding.
This seminal study provides invaluable insights into the sensory experiences and neural pathways that enable mothers to nurse their young. As we learn more about these processes, we move a step closer to helping human mothers who struggle with the natural, yet sometimes challenging, act of breastfeeding.
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