Abstract
Impaired social cognition is a common component of many neurodevelopmental conditions. These impairments impair quality of life. However, the factors shaping social development and accompanying neural circuitry are not well understood.The brain regions that contribute to social cognition are called the “social brain”. The orbitofrontal cortex is one of the brain regions that constitute the “social brain”. Damage to the orbitofrontal cortex causes profound deficits in social cognition, including disinhibition and aggression. Dysfunctional circuitry in the orbitofrontal cortex may contribute to impaired social cognition in neurodevelopmental disorders. However, the role played by neuronal circuitry in the orbitofrontal cortex to social cognition is unclear.
I sought to examine the role of excitatory circuitry within the orbitofrontal cortex in social cognition. I first explored the contribution of excitatory circuitry in the orbitofrontal cortex to impaired social behaviour in Nrxn1α KO mice. These mice carry a genetic microdeletion that is a risk factor for multiple neurodevelopmental disorders, including autism and schizophrenia. Previous experiments have demonstrated that these mice display impaired social behaviour. I found that impaired social behaviour in Nrxn1α KO mice was accompanied by a reduction in short-term facilitation of pyramidal synapses.
The second aim of my thesis was to investigate the role of sensory experience in shaping the development of social cognition and accompanying “social brain” circuitry. This was achieved by depriving rodents of whisker input during a sensitive period of social development. I found that a short period of whisker deprivation led to long-lasting changes in rodent play behaviour. However, this was not accompanied by changes in excitatory circuitry in the orbitofrontal cortex.
| Date of Award | 2018 |
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| Original language | English |
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| Supervisor | Gerald Finnerty (Supervisor) & Cathy Fernandes (Supervisor) |