Synaptic gating
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).
Such mechanisms have been observed in the nucleus accumbens, with gatekeepers originating in the cortex, thalamus and basal ganglia.
When activated, the gatekeeper neuron alters the polarity of the presynaptic axon to either open or close the gate.
[1] Examples of this kind of gating have been found in visual cortical neurons[2] and areas of the prefrontal cortex (PFC) in primates that may be responsible for suppressing irrelevant stimuli.
[3] Studies suggest that this kind of inhibition can be attributed in part to GABA receptor-mediated synapses.
[2] In order for these inhibitory interneurons to act upon their targets, they must receive input from a gatekeeper signal that stimulates them.
Generally, this input occurs in the form of neuromodulatory substances, such as hormones, neuropeptides and other neurotransmitters that have been released from incoming neurons.
Studies have shown hippocampal neurons may gate the transmission of signals between the prefrontal cortex and the nucleus accumbens.
[11] Thus, the hippocampus serves as the gatekeeper for information flow from the prefrontal cortex to the nucleus accumbens, such that its action permissively gates these synapses.
It has been suggested that impaired synaptic gating processes in the nucleus accumbens are the underlying cause of this comorbidity.
[17] This defect causes a reduction in synaptic gating of dopamine input from the prefrontal cortex and hippocampus on the nucleus accumbens.
One theory supposes that this defect reduces the individual's ability to selectively inhibit fear responses from the amygdala, leading to anxiety.
[17] In studies with rodents, the prefrontal cortex, specifically the medial prefrontal cortex (mPFC) has been implicated in the processing of information lasting from milliseconds to several seconds, while the hippocampus has been implicated in the processing of information for longer time scales – such as minutes to hours.
Individuals that take medication such as methylphenidate (Ritalin) will increase their dopamine (DA) output along many of these synapses helping to compensate in the loss of synaptic activity generated from the pathophysiology of ADHD.
Taking methylphenidate can increase DA projections to the nucleus accumbens, which can not only act to increase synaptic activity between the prefrontal cortex and hippocampus (improving memory) but also act as a reward system as the nucleus accumbens is part of the mesolimbic pathway.
[20] Moreover, it is possibly why individuals on Ritalin have a “need” and “desire” to learn as it acts as a positive reinforcer in the brain.
In addition, this reward circuitry activation is most likely a reason why methylphenidate is highly addictive and carries great dependence.
People with schizophrenia have damage to the hippocampus and amygdala illustrating improper gating and resulting in nucleus accumbens neurons being in the down position.
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 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.
Strong evidence has concluded that gating from thalamus impacts the prefrontal cortex response from the hippocampus.
