, 1993). Thus, reduced NMDA-receptor function may have a dual effect, an augmentation of local gamma activity and a liberation of local gamma oscillators from the www.selleckchem.com/products/PLX-4032.html coordinating action of long-range connections. The result would be increased autonomy of local processors and reduced coordination of globally ordered states. Thus, positive symptoms could be the result of impaired communication between cortical regions (Hoffman and McGlashan, 1993). Indeed, there is preliminary evidence

that suggests that local beta- and gamma-band oscillations are increased in patients with schizophrenia experiencing auditory hallucinations (Lee et al., 2006; Mulert et al., 2011). In interpreting the effects of NMDA-receptor blockade, it is important to consider the differential effects of acute versus chronic administration of NMDA-receptor antagonists (Jentsch and Roth,

1999) and further research has to compare the effects of acute versus chronic NMDA hypofunctioning on neural synchrony. This is because prolonged NMDA-receptor hypofunction is associated with reduced GABAergic neurotransmission, which has been confirmed in several studies (Behrens et al., 2007; Zhang et al., 2008), suggesting that the alterations of GABAergic interneurons Selleck Ipatasertib found in postmortem studies of schizophrenia patients (Lewis et al., 2012) could be a consequence of a NMDA-receptor hypofunctioning. However, it should be noted that altered neural synchrony can have many causes because several animal models of schizophrenia that involve quite different mechanisms are associated with aberrant synchrony and power of oscillatory activity (Table 1). Thus, it is unclear whether changes in the E/I balance reflect a primary pathophysiological

process or whether they are secondary consequences of altered network activity. In our previous review (Uhlhaas and Singer, 2006), we interpreted ASDs as a syndrome in which the pattern of cognitive impairments and known physiological abnormalities made the involvement of aberrant neural synchrony an important and testable (-)-p-Bromotetramisole Oxalate hypothesis (Uhlhaas and Singer, 2007). Yet at the time, very little direct evidence was available. By now, several EEG/MEG studies have examined neural synchrony during cognitive functions and resting state, supporting a role of altered neural synchrony in the pathophysiology of ASDs. In children with ASDs, there is consistent evidence for a reduction of high-frequency oscillations during sensory processing. Similar to patients with schizophrenia, children and adolescents with ASDs are characterized by reduced entrainability of auditory circuits to stimulation at 40 Hz. This reduction is particularly pronounced in the left hemisphere (Wilson et al., 2007).