Early Life Damage to the Anterior Cingulate Cortex Impairs the Postnatal Development of Social Vocalizations in Marmoset Monkeys

Concetti Chiave

Early life damage to the anterior cingulate cortex (ACC) compromises the normal maturation of social contact calls and their associated acoustic characteristics in marmoset monkeys.

Sintesi

This study investigated the role of the anterior cingulate cortex (ACC) in the postnatal development of vocal behavior in marmoset monkeys. The researchers created ACC lesions in neonatal marmosets and compared their pattern of vocalization to age-matched controls throughout the first 6 weeks of life.
Key findings:

While the ACC lesion did not affect the production of basic call types, it led to significant changes in the development of social contact calls.
At 6 weeks of age, ACC-lesioned animals showed a substantial reduction in the proportion of social contact calls (e.g., phee, trill, twitter) compared to controls.
The acoustic structure of the phee call, a long-distance contact call, was also altered in the lesioned animals, with the calls being shorter in duration, louder in amplitude, and less acoustically complex.
The researchers found permanent changes in the inhibitory neurotransmitter GABA in the amygdala and periaqueductal gray, two brain regions interconnected with the ACC and involved in vocal behavior.
These results indicate that the normal development of social vocal behavior depends on the ACC and its interactions with other areas in the vocal network during early life. The ACC appears to play a critical role in shaping the emotional and social content of vocalizations, which has important implications for understanding the neural basis of social communication.

Statistiche

The ACC lesion caused a reduction in the average number of phee syllables at postnatal week 3.
The duration of phee syllables was shorter in ACC-lesioned animals, particularly in the later syllables of a multi-syllabic phee call.
The amplitude of phee syllables was higher in ACC-lesioned animals, with the difference increasing until postnatal week 5.
ACC-lesioned animals exhibited lower entropy in phee syllables relative to controls, indicating more stereotyped and less complex phee calls.

Citazioni

"Together, our data suggest that the ACC mediates developmental changes within the first 6 weeks of life that lead to the dominant production of isolation-induced contact calls and the gradual reduction of cries and other calls."
"The long-term behavioral implications of such imperfect vocalizations is currently unknown but could, ostensibly, affect their ability to use long distance social vocalizations to maintain intragroup functions such as warn of predators, strengthen family bonds, and maintain group cohesion more generally."

Approfondimenti chiave tratti da

Cingulate cortex shapes early postnatal development of social vocalizations

by Nagarajan,G.... alle www.biorxiv.org 02-21-2024

https://www.biorxiv.org/content/10.1101/2024.02.17.580738v1

Domande più approfondite

How might the altered social vocalizations in ACC-lesioned marmosets impact their social development and interactions later in life?

The altered social vocalizations in ACC-lesioned marmosets could have significant implications for their social development and interactions later in life. Social vocalizations play a crucial role in communication and social bonding among primates, including marmosets. By disrupting the normal development of social contact calls, the ACC lesions may hinder the marmosets' ability to effectively convey social messages to their group members. This could lead to difficulties in initiating and maintaining social interactions, coordinating group activities, and establishing social hierarchies within the group.
Furthermore, social vocalizations are essential for maintaining group cohesion, signaling danger, and facilitating social bonding. Marmosets rely on vocalizations to coordinate activities such as foraging, grooming, and territorial defense. The altered vocalizations in ACC-lesioned marmosets may result in misunderstandings, miscommunications, or reduced responsiveness from other group members, potentially leading to social isolation or exclusion.
Overall, the impaired social vocalizations in ACC-lesioned marmosets could impact their social development by limiting their ability to engage in normal social behaviors, establish social relationships, and navigate complex social dynamics within the group.

How might the altered social vocalizations in ACC-lesioned marmosets impact their social development and interactions later in life?

In the absence of normal ACC function, other brain regions and neural mechanisms may compensate to maintain basic vocal production in the lesioned animals. One possible compensatory mechanism could involve the recruitment of alternative neural pathways or circuits that are involved in vocalization. For example, the premotor cortex, supplementary motor area, or primary motor cortex may play a more prominent role in initiating and coordinating vocalizations in the absence of ACC input. These regions are known to be involved in motor planning and execution, and they may take on a greater role in controlling vocal output in ACC-lesioned marmosets.
Additionally, the amygdala, which is interconnected with the ACC and plays a key role in emotional processing, may also contribute to modulating vocalizations in response to social cues or emotional states. The amygdala's involvement in vocal behavior and its connections with other vocalization-related brain regions suggest that it could play a compensatory role in regulating vocalizations in ACC-lesioned animals.
Moreover, plasticity in the neural circuits involved in vocal production may allow for reorganization and adaptation in response to the ACC lesion. Neural plasticity mechanisms, such as synaptic strengthening or reorganization, may enable the remaining brain regions to compensate for the loss of ACC function and maintain basic vocal production in the lesioned animals.

Could similar disruptions to the development of social vocalizations be observed in human infants with early life damage to the anterior cingulate cortex, and how might this relate to social communication deficits seen in neurodevelopmental disorders?

Similar disruptions to the development of social vocalizations could potentially be observed in human infants with early life damage to the anterior cingulate cortex (ACC). The ACC is known to play a crucial role in socioemotional regulation and vocal behaviors in primates, including humans. Damage to the ACC in early infancy could impact the normal development of social vocalizations, leading to deficits in the expression of social contact calls, emotional vocalizations, and communicative behaviors.
In human infants, the ACC is involved in processing emotional cues, regulating social behaviors, and coordinating vocal responses in social contexts. Damage to the ACC could result in altered emotional expression, impaired social communication, and difficulties in interpreting and responding to social cues. This could manifest as deficits in social engagement, emotional reciprocity, and the ability to establish and maintain social relationships.
The disruptions in social vocalizations and social communication deficits observed in individuals with neurodevelopmental disorders, such as autism spectrum disorder (ASD), may be related to dysfunction in the ACC and its connections with other brain regions involved in social processing. Individuals with ASD often exhibit challenges in social communication, including atypical vocalizations, difficulties in interpreting emotional cues, and impaired social interactions. These deficits may reflect underlying abnormalities in the ACC and its impact on the development of social vocalizations and socioemotional behaviors.
Overall, damage to the ACC in human infants could lead to similar disruptions in social vocalizations and social communication deficits, highlighting the critical role of the ACC in the development of social behaviors and the potential implications for neurodevelopmental disorders characterized by social communication impairments.