Synaptic gating is the ability of neural circuits to gate inputs by either suppressing or facilitating specific synaptic activity. Selective inhibition of certain synapses has been studied thoroughly (see Gate theory of pain), and recent studies have supported the existence of permissively gated synaptic transmission. In general, synaptic gating involves a mechanism of central control over neuronal output. It includes a sort of gatekeeper neuron, which has the ability to influence transmission of information to selected targets independently of the parts of the synapse upon which it exerts its action (see also neuromodulation).Bistable neurons have the ability to oscillate between a hyperpolarized (down state) and a depolarized (up state) resting membrane potential without firing an action potential. These neurons can thus be referred to as up/down neurons. According to one model, this ability is linked to the presence of NMDA and AMPA glutamate receptors. External stimulation of the NMDA receptors is responsible for moving the neuron from the down state to the up state, while the stimulation of AMPA receptors allows the neuron to reach and surpass the threshold potential. Neurons that have this bistable ability have the potential to be gated because outside gatekeeper neurons can modulate the membrane potential of the gated neuron by selectively shifting them from the up state to the down state. Such mechanisms have been observed in the nucleus accumbens, with gatekeepers originating in the cortex, thalamus and basal ganglia.