summary: The presence of the MECP2 protein in parvalbumin (PV) neurons is essential for newborn mice to quickly learn and respond to their young’s distressed cries, showing how the brain is reorganized during a crucial stage of adult learning.
When MECP2 is absent, mother mice show inattentive behavior towards their pups, illustrating how defects in the protein can contribute to communication and interpretation deficits in neurodevelopmental disorders such as Rett syndrome in humans.
Furthermore, the study highlights the versatility of brain circuits, which, although they harden with age, retain the ability to reconnect during certain life events.
This important study opens new avenues, potentially pinpointing brain circuits involved in common neurological conditions, and provides a framework for exploring treatments.
Key facts:
Important for motherhood: In mice, the MECP2 protein, especially in PV neurons, is critical for allowing new mothers to learn and respond appropriately to their offspring’s needs.
Tautan’s Syndrome Rett: In humans, MECP2 dysfunction is responsible for Rett syndrome, and this research highlights a potential pathway for understanding and treating neurodevelopmental disorders and other similar conditions.
Brain circuit adaptability: Although brain circuits tend to stabilize with age, certain life experiences, such as motherhood, can reactivate mechanisms to change their function and wiring, which may have broader implications for understanding brain disorders that emerge later in life.
source: CSHL
The developing brain is shaped by the sights, sounds, and experiences of early life. Brain circuits become more stable with age. However, certain experiences later in life opened up opportunities to improve these circuits quickly.
New research conducted by Professor Stephen Shea of Cold Spring Harbor Laboratory helps explain how the brain adapts during the critical period of adulthood: the time when new mothers are learning to care for their children.
Shea’s research in mice shows how this learning process is disrupted when a small group of neurons lacks a protein called MECP2. In humans, MECP2 dysfunction causes a rare neurodevelopmental disorder, Rett syndrome.
Shea’s findings may point researchers toward brain circuits associated with Rett syndrome and potential treatment strategies. His research could also impact more common neurological conditions. Shea explained:
“We are aware that patients with Rett syndrome have difficulty interpreting and producing language. Communication difficulties are widespread in autism spectrum disorders. One of the reasons we study Rett syndrome is that it may be a valuable model for other forms of autism.
Shea’s laboratory studies of MECP2 began about 10 years ago when he first noticed female mice with the mutation in Mecp2 Genes are bad parents. When it comes to parenting, most rat mothers are fast learners. But without enough MECP2, “they ignore the baby and don’t listen to its cries,” Shea said.
Shea and his team tested how deletion of MECP2 from certain cells in the mouse brain affected maternal behavior. They found that to delay the pup’s retrieval, the protein only needed to be removed from a small portion of cells in the sound-processing part of the brain. These important cells are known as parvalbumin (PV) neurons. In order for mice to learn how to efficiently retrieve their young, they need MECP2 in certain brain cells when they first hear the young animals’ cries of distress.
Shea showed that PV neurons also play an important role in brain circuits early in life. These cells usually suppress signals from other neurons. But they release these constraints during development, creating conditions for change. Shea said:
“We found that some of the same mechanisms involved in development are actually at play in adults. These mechanisms can be reactivated and reused to reorganize the brain at new points in life.
In other words, it’s not just about development or maturity. This research may provide clues about brain disorders that develop later in life, such as dementia and Alzheimer’s disease.
About genetics and neuroscience research news
author: Samuel Diamond
source: CSHL
communication: Samuel Berlian – CSHL
picture: Image credited to Neuroscience News
Original search: Closed access.
“Selective deletion of Methyl CpG binding protein 2 from parvalbumin interneurons in the auditory cortex delays the onset of maternal retrieval in mice.“By Stephen Shea et al. Journal of Neuroscience
summary
Selective deletion of Methyl CpG binding protein 2 from parvalbumin interneurons in the auditory cortex delays the onset of maternal retrieval in mice.
Mutation in MECP2 Causes neurodevelopmental disorders and Rett syndrome. MECP2 Codes for methyl CpG binding protein 2 (MECP2), a transcriptional regulator that activates the genetic program for experience-dependent plasticity.
Many of the neurological and behavioral symptoms of Rett syndrome may be due to irregular plasticity timing and thresholds.
As a model of adult plasticity, we studied changes in the inhibitory circuitry of the auditory cortex in female mice when they were first exposed to pups; This plasticity facilitates the pup’s behavioral response of issuing a distress call.
Deletion at the brain level Mecp2 This alters the expression of markers associated with GABAergic interneurons parvalbumin (PVins) and disrupts the initiation of pup retrieval.
We assume that loss Mecp2 In PVins, it contributes disproportionately to the phenotype.
Here we find its elimination Mecp2 PVin delays the onset of maternal retrieval behavior and recapitulates key molecular and neurophysiological features of whole-brain deletion. Mecp2.
We observed that when selective PVin mutants were exposed to pups, expression of the auditory cortical marker PVin was increased compared with their wild-type counterparts.
PVin-specific mutants also failed to show the inhibitory auditory cortex plasticity seen in wild-type mice when exposed to pups and their sounds. Finally, using a versatile viral genetic strategy, we demonstrate such postdevelopmental losses Mecp2 PVins from the auditory cortex are sufficient to delay the onset of maternal intake.
Our results support a model in which PVin plays a central role in adult cortical plasticity and may be particularly vulnerable to its loss Mecp2.
2023-10-04 20:44:31
#protein #rewires #brain #adapt #motherhood
