GABAergic system abnormalities

There are few, if any, areas in the brain that are not affected by these two substances (Lam et al., 2006 Carlson, 2001). Several reports have demonstrated abnormalities involving the glutamatergic and GABAergic systems of subjects with autism (Blatt et al., 2001 Dhossche et al., 2002 Fatemi, 2008 Fatemi et al., 2009a, b). 

Figure 2 Anxiety pathways and their interactions. Two fundamentally different mechanisms involved in anxiety and anxiety-like behavior are proposed. The first mechanism is developmental, and its consequences are manifested later in life. Both genetic and environmental factors linked to anxiety can have a deveiopmental origin, as illustrated by the example of the s allele of the 5-HTT, the deficiency in the SHT receptor, and variability in maternal care. The second possible mechanism is not developmental but based on "acute" or current molecular abnormalities that result in anxiety or anxiety-like behavior. Examples include deficiencies in GABAergic neurotransmission and abnormalities in the central CRH system, which have the direct behavioral output of anxiety. It is also proposed that the developmental mechanisms lead to anxiety by converging on the "acute" mechanisms.

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