The Experience of Partner Relationships for Male Survivors of Childhood Sexual Abuse: A Qualitative Synthesis.

Research has documented wide-ranging psychological impacts of childhood sexual abuse (CSA) for male survivors, but their experience of relationships is understudied. This qualitative review aimed to synthesize the qualitative literature concerning the experience of partner relationships for male CSA survivors. Electronic searches were conducted across PsycINFO, CINAHL, and PubMed, complemented by hand searches of references. Searches were limited to English-language peer-reviewed studies. Studies were included if they sampled adult male CSA survivors and reported qualitative data on their experience of partner relationships. Sixteen studies met the review criteria. Articles were quality-appraised using the Critical Appraisal Skills Programme qualitative checklist (2018), and narrative synthesis derived five themes: "sexual orientation confusion," "sexual intimacy difficulties," "the barrier of emotional intimacy," "navigating agency," and "healing and growth through love." Key findings were male CSA survivors can face considerable barriers to relational intimacy; however, romantic relationships also offer a space to heal and experience post-traumatic growth (PTG). Clinicians should be aware of the diffuse impacts CSA can have upon male survivors' intimate relationships. Helping survivors and their partners build a safe space in which to process CSA, reassert agency and relational boundaries, and express love and validation can support survivors toward PTG.

Expression of catechol-O-methyltransferase in the brain and periphery of normal and MPTP-treated common marmosets.

Catechol-O-methyltransferase (COMT) inhibition is widely used to potentiate the effects of levodopa in Parkinson's disease but the effects of nigral dopaminergic cell loss and levodopa treatment on COMT activity are not known. The present study investigated the expression of COMT in the brain and liver of normal common marmosets, and animals treated with MPTP and those treated with levodopa to induce dyskinesia. Reverse transcript PCR demonstrated the expression of COMT mRNA in the liver, cortex and striatum of normal marmosets. Using Western blotting, the presence of two subunits of COMT protein, membrane bound COMT (MB-COMT) and soluble COMT (S-COMT), was shown in the liver, cortex and striatum of normal marmosets. Quantitative analysis of the MB-COMT and S-COMT subunit bands showed that there was no significant difference in the density of bands in MPTP treated marmosets or those exposed to levodopa compared to normal animals. COMT immunoreactivity was expressed in many brain regions including the cortex and striatum. No difference in COMT staining intensity was observed between normal, MPTP exposed or MPTP plus levodopa treated animals. COMT immunostaining was present in most striatal neurones and it was occasionally seen in glial cells. The data from present study demonstrated the expression of COMT mRNA and protein in the brain of common marmoset contrary to a previous report that it is not expressed in this species. COMT activity appears unaffected by loss of the dopaminergic nigro-striatal pathway and levodopa treatment.

Ionic currents underlying the response of rat dorsal vagal neurones to hypoglycaemia and chemical anoxia.

A proportion of dorsal vagal neurones (DVN) are glucosensors. These cells respond to brief hypoglycaemia either with a K(ATP) channel-mediated hyperpolarization or with depolarization owing to an as yet unknown mechanism. K(ATP) currents are observed not only during hypoglycaemia, but also in response to mitochondrial inhibition. Here we show that similarly to the observations for K(ATP) currents, both hypoglycaemia and inhibition of mitochondrial function elicited a small inward current that persisted in TTX in DVN of rat brainstem slices. Removal of glucose from the bath solution induced this inward current within 50 +/- 4 s in one subpopulation of DVN and in 279 +/- 36 s in another subpopulation. No such subpopulations were observed for the response to mitochondrial inhibition. Biophysical analysis revealed that mitochondrial inhibition or hypoglycaemia inhibited an openly rectifying K+ conductance in 25% of DVN. In the remaining cells, either an increase in conductance, with a reversal potential between -58 and +10 mV, or a parallel inward shift of the holding current was observed. This current most probably resulted from inhibition of the Na+-K+-ATPase and/or the opening of an ion channel. Recordings with electrodes containing 145 mm instead of 5 mm Cl- failed to shift the reversal potential of the inward current, indicating that a Cl- channel was not involved. In summary, glucosensing and non-glucosensing DVN appear to use common electrical pathways to respond to mitochondrial inhibition and to hypoglycaemia. We suggest that differences in glucose metabolism rather than differences in the complement of ion channels distinguish these two cell types.

Neuronal responses to transient hypoglycaemia in the dorsal vagal complex of the rat brainstem.

Several regions of the mammalian brain contain glucosensing neurones. In vivo studies have suggested that those located in the hypothalamus and lower brainstem are involved in glucoprivic feeding and homeostatic control of blood glucose. We have identified and characterized hypoglycaemia-sensitive neurones in the dorsal vagal complex of the brainstem using in situ hybridization, single-cell RT-PCR and whole-cell patch-clamp recordings from rat brainstem slices. Approximately 80% of neurones did not respond to hypoglycaemia (changing artificial cerebrospinal fluid (ACSF) glucose from 10 mM to 0 mM) within 5 min (non-responsive: NR). Another 10% depolarized within 155+/-31 s (mean+/-s.e.m.) of glucose removal (glucose-inhibited: GI), and the remaining neurones hyperpolarized within 53+/-7 s (glucose-excited: GE). The hyperpolarization was reversed by the KATP channel blocker tolbutamide. Single-cell RT-PCR revealed that GI and GE, but not NR, cells expressed glucokinase (GLK). In contrast, SUR1, a KATP channel subunit, was expressed in GE and some NR cells. In situ hybridization with biotin-labelled riboprobes in the dorsal vagal complex revealed ubiquitous expression of SUR1, and widespread, but sparse, expression of GLK. Identification of astrocytes using a GFAP (glial fibrillary acidic protein) antibody showed that GLK and GFAP were not colocalized. In summary, we have demonstrated that GI and GE neurones exist in the brainstem and that GLK is essential for their function. It seems likely that GE neurones work in a way analogous to pancreatic beta-cells in that they require both GLK and KATP channels.