Dendritic overgrowth and elevated ERK signaling during neonatal development in a mouse model of autism

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Cheng, N., Alshammari, F., Hughes, E., Khanbabaei, M., & Rho, J. M. (2017). Dendritic overgrowth and elevated ERK signaling during neonatal development in a mouse model of autism. PLOS ONE, 12(6), e0179409. https://doi.org/10.1371/journal.pone.0179409

Publication date: 13 Jun 2017 Added to AutiHub: 29 Aug 2026 Type: Article Article language: English
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Authors

Publication authors
5
Publication authors identified as autistic
1 / 5 (20.0%)
  1. Ning Cheng
  2. Fawaz Alshammari
  3. Elizabeth Hughes *
  4. Maryam Khanbabaei
  5. Jong M. Rho

Abstract

Autism spectrum disorder (hereafter referred to as "ASD") is a heterogeneous neurodevelopmental condition characterized by impaired social communication and interactions, and restricted, repetitive activities or interests. Alterations in network connectivity and memory function are frequently observed in autism patients, often involving the hippocampus. However, specific changes during early brain development leading to disrupted functioning remain largely unclear. Here, we investigated the development of dendritic arbor of hippocampal CA1 pyramidal neurons in the BTBR T+tf/J (BTBR) mouse model of autism. BTBR mice display the defining behavioural features of autism, and also exhibit impaired learning and memory. We found that compared to control C57BL/6J (B6) animals, the lengths of both apical and basal dendrites were significantly greater in neonatal BTBR animals. Further, basal dendrites in the BTBR mice had higher branching complexity. In contrast, cross-sectional area of the soma was unchanged. In addition, we observed a similar density of CA1 pyramidal neurons and thickness of the neuronal layer between the two strains. Thus, there was a specific, compartmentalized overgrowth of dendrites during early development in the BTBR animals. Biochemical analysis further showed that the extracellular signal-regulated kinases (ERK) pathway was up-regulated in the hippocampus of neonatal BTBR animals. Since dendritic structure is critical for information integration and relay, our data suggest that altered development of dendrites could potentially contribute to impaired hippocampal function and behavior observed in the BTBR model, and that this might be related to increased activation of the ERK pathway.

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Cited references
105
With a DOI
104
Without a DOI, from raw bibliography text
1
4 / 105 (3.8%) cited references include at least one author identified as autistic.
References with data to complete
2 / 105 (1.9%)
References with detected author names
103 / 105 (98.1%)
Without detected author names
2
Without a structured title
1
Without a stable identifier
1
References with raw author names still to review
1
References with external metadata lookup issues
0
These indicators apply to cited references displayed on this page, after technical duplicates have been merged. A reference without a DOI can still support author statistics when a title and author names are available.
Author names detected in the cited bibliography
692
From DOI or external metadata
692
From validated raw bibliography text
0
Raw names already validated
0
Raw names still to review
2
59 / 692 (8.5%) names are linked to an author already present in AutiHub. 633 / 692 (91.5%) names are not yet linked.
Names linked to a person identified as autistic
4 / 692 (0.6%)
Calculated across all author names detected in the cited bibliography. Among names linked to an author already present in AutiHub: 4 / 59 (6.8%). Distinct people identified as autistic: 2 / 618 (0.3%).
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