When a nerve impulse arrives at a noradrenaline nerve terminal, noradrenaline is released from synaptic vesicles into the synaptic cleft. Noradrenaline molecules bind to their receptors on the post-synaptic membrane and the nerve impulse is propagated or inhibited, depending on the specific receptor. Noradrenaline molecules are then released from their receptors and taken back into the nerve terminal via the noradrenaline re-uptake transporter. Noradrenaline is degraded by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT).1,2
Related content
Fear, rejection, and “othering” of people living with epilepsy continues to be a major additional burden, a burden beyond seizures, for many people globally.
The complex interplay between metabolic dysfunction and brain insulin resistance in schizophrenia warrants further investigation as it represents a unique opportunity for both mechanistic inquiry and the development of novel therapeutic strategies that can improve metabolic and cognitive outcomes in this population.
Central and peripheral causes of brain insulin resistance in schizophrenia