Depression affects millions worldwide, thus underscoring the urgent need to optimize health care practices. To better understand the processes involved in psychotherapy gains, studies have emphasized the need to complement subjective reports with objective measures, in particular biological markers. Oxytocin (OT) has been proposed as a potential biomarker in the treatment of depression given its involvement in depression-related psychological and physiological functions and the formation of close relationships. Here, we assessed whether OT reactivity to therapeutic encounters (absolute and/or directional reactivity) is linked to improvements in depressive symptoms from session to session during psychotherapy. A total of 284 saliva samples were collected from 30 adult clients who underwent 16 sessions of manualized psychodynamic psychotherapy for depression in a university setting. Salivary OT was measured before and after five preselected sessions distributed evenly throughout the therapy. The Beck Depression Inventory-II (BDI-II) was administered at the beginning of each session. Multilevel growth models indicated that clients exhibiting greater absolute OT reactivity showed greater improvement in depressive symptoms throughout treatment. Directional reactivity was not associated with depressive symptom change. In addition, clients with higher baseline OT levels displayed less change in depressive symptoms. These findings highlight reactivity of the OT system, in either direction, as an important feature of the treatment response. Consistent with recent models of the neurobiology of resilience, OT reactivity appears to serve as an important biomarker of psychotherapy gain in the treatment of depression. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Animal studies demonstrate that maternal touch and contact regulate infant stress, and handling during periods of maternal deprivation attenuates the stress response. To measure the effects of touch on infant stress reactivity during simulated maternal deprivation, 53 dyads were tested in two paradigms: still-face (SF) and still-face with maternal touch (SF+T). Maternal and infant cortisol levels were sampled at baseline, reactivity, and recovery and mother's and infant's cardiac vagal tone were measured during the free play, still-face, and reunion episodes of the procedure. Cortisol reactivity was higher among infants in the SF condition and while cortisol decreased at recovery for infants in the SF+T, it further increased for those in the SF. Vagal tone showed a greater suppression when SF was not accompanied by maternal touch. Touch synchrony during free play was associated with higher infant vagal tone, whereas touch myssynchrony--maternal tactile stimulation while the infant gaze averts--correlated with higher maternal and infant cortisol. In humans, as in mammals, the provision of touch during moments of maternal unavailability reduces infants' physiological reactivity to stress.

The goal of this work was to elucidate the molecular events underlying stimulation of ciliary beat frequency (CBF) induced by acetylcholine (ACh) in frog esophagus epithelium. ACh induces a profound increase in CBF and in intracellular Ca(2+) concentration ([Ca(2+)](i)) through M(1) and M(3) muscarinic receptors. The [Ca(2+)](i) slowly decays to the basal level, while CBF stabilizes at an elevated level. These results suggest that ACh triggers Ca(2+)-correlated and -uncorrelated modes of ciliary stimulation. ACh response is abolished by the phospholipase C (PLC) inhibitor U-73122 and by depletion of intracellular Ca(2+) stores but is unaffected by reduction of extracellular Ca(2+) concentration and by blockers of Ca(2+) influx. Therefore, ACh activates PLC and mobilizes Ca(2+) solely from intracellular stores. The calmodulin inhibitors W-7 and calmidazolium attenuate the ACh-induced increase in [Ca(2+)](i) but completely abolish the elevation in CBF. Therefore, elevation of [Ca(2+)](i) is necessary for CBF enhancement but does not lead directly to it. The combined effect of Ca(2+) elevation and of additional factors, presumably mobilized by Ca(2+)-calmodulin, results in a robust CBF enhancement.

The intent of this work was to evaluate the role of cAMP in regulation of ciliary activity in frog mucociliary epithelium and to examine the possibility of cross talk between the cAMP- and Ca2+-dependent pathways in that regulation. Forskolin and dibutyryl cAMP induced strong transient intracellular Ca2+-concentration ([Ca2+](i)) elevation and strong ciliary beat frequency enhancement with prolonged stabilization at an elevated plateau. The response was not affected by reduction of extracellular Ca2+ concentration. The elevation in [Ca2+](i) was canceled by pretreatment with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM, thapsigargin, and a phospholipase C inhibitor, U-73122. Under those experimental conditions, forskolin raised the beat frequency to a moderately elevated plateau, whereas the initial strong rise in frequency was completely abolished. All effects were canceled by H-89, a selective protein kinase A (PKA) inhibitor. The results suggest a dual role for PKA in ciliary regulation. PKA releases Ca2+ from intracellular stores, strongly activating ciliary beating, and, concurrently, produces moderate prolonged enhancement of the beat frequency by a Ca2+-independent mechanism.