Our results are in line with the proposal that a deficiency in serotonergic modulation of the dPAG is involved in triggering the panic attack and the 5-HT1A receptors might be essential for the panicolytic-like response.
Experimental results obtained in rat models of panic indicate that serotonin interacts synergistically with endogenous opioids in the dorsal periaqueductal gray through 5-HT1A and μ-opioid receptors to inhibit proximal defense and, supposedly, panic attacks.
The 5-HT1A receptor-1019C/G polymorphism was strongly associated with response to treatment, in which 20 subjects with the GG genotype showed minimal changes in panic attack frequency with a relative risk of no response of 4.73.