Vasoactive intestinal polypeptide (VIP) expression and inhibitory circuitry

Abstract

The brain is composed of millions of neurons, which connect and influence each other. This neuronal cooperation leads to coordinated behaviors and cognition. These connections exist within circuits that are made up of both excitatory and inhibitory synaptic neurons. The excitatory neurons’ primary neurotransmitter is glutamate and interneurons are the inhibitory neurons whose neurotransmitter is γ-aminobutyric acid (GABA). The term interneuron refers to the fact that most of these neurons have very local axonal connections rather than the longer projecting axons that are common to principal cells. They make up approximately 20% of all neurons in the brain and exist across the brain but most research is focused on the cortex and hippocampus. Excitation and inhibition act in close partnership to direct and shape neural activity. Without inhibition, excitation can have a “run-away” or “ramp-up” effect. These states of over-excitation are thought to be symptomatic of epilepsy and schizophrenia. There are a few different models thought to represent the pattern of excitation and inhibition in the brain. They included: feedforward, feed-back and disinhibition. The disinhibitory model is somewhat recently and has been proven across cortical modalities. The vasoactive intestinal polypeptide (VIP) expressing interneurons act as disinhibitors of excitatory cells by inhibiting other interneurons. This allows for attenuating of the signal and more gain control. The report will elaborate on the VIP protein itself and then within the context of inhibitory circuitry.