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McRae, B. R.

Publications and source records attributed to McRae, B. R..

2 recordsLinked to original sources

Maternal experience alters brain-wide representation of infant cries

One SentenceMaternal experience fundamentally reorganizes infant cue processing across the entire brain into a more efficient and specialized caregiving state. Pup calls signal the presence of a mouse infant in need of care (Bernd Haack et al., 1983; Ehret, 2005). Previous work demonstrated that experience-dependent plasticity within the left primary auditory cortex is oxytocin-facilitated and enhances neural and behavioral responses to these distress vocalizations (Marlin et al., 2015). However, whether maternal experience reshapes pup call processing beyond auditory regions remains unknown. Here, we show that both innate and learned maternal experience shape pup call-evoked behavior and brain-wide neural responses. Combining behavioral assays, whole-brain activity mapping, and oxytocinergic projection analyses, we find that pup calls recruit distinct large-scale neural networks in naive virgins, experienced virgins, and mothers. With more maternal experience we observe a distributed pup call response network that is sparser yet more strongly coactivated, consistent with a more efficient and specialized neural representation of infant cues. We identified an oxytocin-dense circuit that shows an experience-dependent pup call response pattern. Therefore, we propose that experience-dependent refinement of the brain-wide response to pup calls is facilitated by oxytocin. Taken together, our findings reveal that maternal experience refines brain-wide sensory processing to support adaptive caregiving behavior.

neuroscience↗

Sensory regulation of absence seizures in a mouse model of Gnb1 encephalopathy

Absence seizures, a type of non-convulsive epilepsy manifested by spike-wave discharges (SWD) in the electroencephalogram (EEG), display synchronous reciprocal excitation between the neocortex and thalamus. Recent studies have revealed that inhibitory neurons in the reticular thalamic (RT) nucleus and excitatory thalamocortical (TC) neurons are two key subcortical players in generating SWD. However, the signals that drive SWD-related thalamic activity remain elusive. Here, we show that SWD predominately occurs during wakefulness in several mouse models of absence epilepsy. In more focused studies of Gnb1 mutant mice, we found that sensory input regulates SWD. Using in vivo recording, we demonstrate that TC cells are activated prior to the onset of SWD and then inhibited during SWD. On the contrary, RT cells are slightly inhibited prior to SWD, but are strongly activated during SWD. Furthermore, chemogenetic activation of TC cells leads to the enhancement of SWD in Gnb1 mice. Together, our results indicate that sensory input in the periphery can regulate SWD by activating the thalamocortical pathway.

neuroscience↗