Cortical arealisation and thalamocortical connectivity
Key members involved in this project
- Dr Anna Hoerder-Suabedissen
- Dr Wei Zhi Wang
- Dr Chika Okusha
- Ms Elanor Grant
- Ms Jennifer Millar
- Mr Andre Marques Smith
Cortical areas do not appear to be fully pre-programmed and some of the differences arise by interactions with afferent neuronal projections. We are studying the signalling mechanisms that set the coordinates for the further establishment of cortical areas. Thalamic axons, which later will mediate most sensory information from the environment, reach the cortex at a very early stage, before the majority of cortical neurons have even been born.
Recent work points to the crucial role of the early-developing thalamocortical projections and their interactions with the developing cortical circuitry in establishing some aspects of the functional and structural organization of the cortex. Nevertheless some aspects of cortical specialisation do not require thalamic input. We are particularly interested in the cellular and molecular mechanisms involved in the cortico-cortical and thalamocortical connectivity.
To understand the function of early neuronal activity patterns we have been investigating mutants with disrupted synaptic vesicle release machinery due to lack of SNAP25, MUNC18 or MUNC13). These tools help us to dissect the various forms of early activity patterns based on regulated and spontaneous neurotransmitter release. Understanding the role of Snap25 (a presumed susceptibility genes in schizophrenia) could have general clinical implications. Combinations of genetic susceptibility and environmental perturbations are thought to be responsible for the diseases of: schizophrenia, autism, dyslexia, and attention deficit disorders. This field faces difficulties because no single gene or factor is responsible for driving a highly complex biological process.