resulting in nucleus accumbens neurons being in the down position. this is why people with schizophrenia display an inability for context-dependent memory and their inability to show proper affective valence. in addition, because accumbens neurons are in the down position they are not as receptive to pfc stimulation and therefore people with schizophrenia show problems with attentional deficits. the gating theory of schizophrenia posits a bistable nucleus accumbens neuron that when gated improperly leads to a wealth of behavioral and memory deficits. current and future research current research now has shed light on the fact that the bistability of a neuron may be part of a larger bistable neural network. evidence of a bistable network has been shown with the interneurons of the auditory cortex. the stable states of this auditory cortex network are either synchronous or antisynchronous, which illustrates its bistable nature. when auditory interneurons were coupled with electrical and chemical inhibitory synapses, a bimodal firing pattern was observed. this bimodal pattern illustrates the bistability of the network to fire at either a synchronous or antisynchronous state. these two states could be modes by which an individual perceives different frequencies in sound waves. future research is looking into whether this bistable network embodies many of the properties of a bistable neuron, and if there is a larger gatekeeper modulating the network as a whole. it has been shown that nucleus accumbens neurons are capable of being gated because they are bistable. recent evidence has shown that neurons in the cortex are also bistable, and thus also able to be gated. there appear to be three different types of gating circuits – one that is controlled by the cortex, one that is controlled by the association nuclei in the thalamus, and one that is controlled by circuits spanning the basal ganglia, cortex, and the thalamus. strong evidence has concluded that gating from thalamus impacts the prefrontal cortex response from the hippocampus. this is seen as either an enhancement or a suppression illustrating the bistability of the process. it has been proven that nucleus accumbens neurons act as a gate yet do the neurons in the cortex act in the same manner? future research will look at similarities between the two sets of bistable neurons. in addition, the mechanism of shifting the bistable neurons to their “down” state needs to be expanded upon. this state leads to inhibition and thus are their inhibitory interneurons that modulate this shift and if so are inhibitory neurotransmitters such as gaba involved? lastly, neurons capable of modulating gates such as hippocampal and thalamic neurons can contact many different areas of the brain. with increasing research saying that neurons in the cortex, nucleus accumbens, and cerebellum are all able to be gated, can the hippocampus modulate the signals for all of these and if so can it connect these different brain areas into a much larger neural network capable of being modulated all at once? these are the questions at the heart of synaptic gating in the future.