These preliminary results are consistent with a dysregulation of the g-aminobutyric acid A/benzodiazepine receptor complex during the premenstruum of women suffering from premenstrual dysphoric disorder.

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Nitric oxide (NO) plays a major role in cardiopulmonary regulation as illustrated by the alterations of the NO system described in cardiopulmonary illnesses. Recent studies have found an association between panic disorder and cardiovascular death and illness, as well as pulmonary diseases. Our objective was to investigate whether pulmonary or systemic NO production was altered during induced panic attacks (PAs). We used a double-blind placebo-controlled crossover design with randomization of the order of an injection of placebo and pentagastrin, a cholecystokinin-B receptor agonist that induces PAs in healthy volunteers (HVs). A total of 17 HVs experienced a PA after pentagastrin challenge. Exhaled NO and NO metabolites were measured by chemiluminescence. During pentagastrin-induced PAs, HVs displayed significant decreases in plateau concentrations of NO exhaled, which were associated with proportional increases in minute ventilation. There were no significant changes in pulmonary or systemic NO production. These results suggest that the decrease in exhaled NO concentration observed during pentagastrin-induced PAs is related to the associated hyperventilation, rather than to any change in lung NO production. This study is the first to evaluate changes in NO measurements during acute anxiety.

Cholecystokinin (CCK) is a peptide neurotransmitter that modulates hypothalamic-pituitary-adrenal (HPA) axis activity and may be involved in fear or anxiety states. Arginine vasopressin (AVP) also modulates HPA axis activity and may play a role in fear conditioning. Few human studies have examined interactions between CCK and AVP systems. To explore relationships between CCK-B receptor activation, the HPA axis response, and AVP release, a dose-response study using the CCK-B receptor agonist pentagastrin was conducted. Adrenocorticotropin (ACTH) and cortisol results have been previously reportedand AVP data is presented here. Thirty-five healthy subjects were randomly assigned to receive placebo, or 0.2, 0.4, 0.6, or 0.8 Cholecystokinin (CCK) is a peptide neurotransmitter that is widely distributed in brain areas involved with cognitive or emotional aspects of behavior, such as prefrontal cortex, cingulate, hippocampus, amygdala, and the locus coeruleus (Lindefors et al. 1993;Saito et al. 1980). Some evidence suggests it may modulate stress responsiveness, functioning as a neuromodulator of the hypothalamicpituitary-adrenal (HPA) axis (Abelson and Liberzon 1999). CCK-B agonists, such as pentagastrin, activate the HPA axis in humans, stimulating release of adrenocorticotropin (ACTH) and cortisol (Abelson and Liberzon 1999;de Montigny 1989;Degli Uberti et al. 1983;Späth-Schwalbe et al. 1988).Levels of CCK and corticotropin-releasing hormone (CRH) were found to be correlated in human cerebrospinal fluid, suggesting that central regulation of these two neuropeptides may be linked in humans; and this linkage may be tighter under conditions of stress (Geracioti et al. 1999). Animal work also demonstrates substantial interaction between CCK and the HPA axis. The axis is directly sensitive to CCK activation (Kamilaris et al. 1992;Matsumura et al. 1983;Mezey et al. 1986;Reisine and Jensen 1986); and CCK peptide is colocalized with other HPA axis secretagogues (Kiss et al. 1984;Larsson and Rehfeld 1981;Mezey et al. 1986; Mill- ington et al. 1992;Rehfeld 1978;Rehfeld and Larsson 1981;Rehfeld et al. 1987;Vanderhaeghen et al. 1985). Central CCK systems are stress and glucocorticoid sensitive (Mezey et al. 1986;Siegel et al. 1987); and peripheral CCK can regulate activity in central components of the HPA axis (Chen et al. 1993).Though CCK-HPA axis interactions are well established, the mechanisms by which they interact remain uncertain. Central regulation of the HPA axis is exerted primarily through corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), and negative glucocorticoid inhibition (Aguilera 1994). Animal work suggests that both CRH (Biró et al. 1993;Kamilaris et al. 1992) and AVP (Bondy et al. 1989;DeBold et al. 1984;Mezey et al. 1986;Verbalis et al. 1987) could mediate CCK effects on the HPA axis. However, due to substantial cross species variation in CCK function (Hinks et al. 1995;Woodruff et al. 1991), human studies will be needed to clarify these mechanisms in humans. CCK-induced release of ACTH...