Oxytocin reactivity to the therapeutic encounter as a biomarker of change in the treatment of depression.

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).

Touch attenuates infants' physiological reactivity to stress.

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 mechanism of ciliary stimulation by acetylcholine: roles of calcium, PKA, and PKG.

Stimulation of ciliary cells through muscarinic receptors leads to a strong biphasic enhancement of ciliary beat frequency (CBF). The main goal of this work is to delineate the chain of molecular events that lead to the enhancement of CBF induced by acetylcholine (ACh). Here we show that the Ca(2+), cGMP, and cAMP signaling pathways are intimately interconnected in the process of cholinergic ciliary stimulation. ACh induces profound time-dependent increase in cGMP and cAMP concentrations mediated by the calcium-calmodulin complex. The initial strong CBF enhancement in response to ACh is mainly governed by PKG and elevated calcium. The second phase of CBF enhancement induced by ACh, a stable moderately elevated CBF, is mainly regulated by PKA in a Ca(2+)-independent manner. Inhibition of either guanylate cyclase or of PKG partially attenuates the response to ACh of [Ca(2+)](i), but completely abolishes the response of CBF. Inhibition of PKA moderately attenuates and significantly shortens the responses to ACh of both [Ca(2+)](i) and CBF. In addition, PKA facilitates the elevation in [Ca(2+)](i) and cGMP levels induced by ACh, whereas an unimpeded PKG activity is essential for CBF enhancement mediated by either Ca(2+) or PKA.