Resilience and Psychosocial Function Among Mainland Chinese Parents of Children With Cancer: A Cross-sectional Survey.

BACKGROUND: Resilience is commonly used to refer to the capacity to resist negative psychological reactions when encountering aversive circumstances. However, clinicians generally define resilience as a lack of psychological distress or an adoption of positive attitude in response to a potentially traumatic event. Although resilience was initially considered to be a psychological variable, it has gradually become seen as a psychosocial indicator now used in clinical settings in the Western world but is still a relatively new topic in most Eastern countries. In this study, we aimed to extend our understandings of the psychological responses of a group of mainland Chinese parents upon being informed that their children were diagnosed with cancer, using resilience as a major indicator. OBJECTIVE: The aim of this study was to evaluate the level of resilience among mainland Chinese parents in response to knowing that their children were diagnosed with cancer and to examine the relationships between resilience and other psychosocial outcomes. METHODS: A descriptive and a cross-sectional survey design was used and involved a sample of 125 parents who visited a specialist cancer hospital in southeast China between September 2013 and February 2014. RESULTS: The participants reported lower level of resilience as compared with a control population in the Chinese community (P < .01). Resilience was negatively correlated with uncertainty in illness (P < .01) and depression (P < .01) and was positively correlated with social support (P < .01) and all other positive coping strategies subscales (P < .01). Parents from the high- resilience group reported better psychosocial functions than did those from the low-resilience group (P < .01). In addition, 6 influencing factors were identified and entered into the multiple linear regression equation of psychological resilience, which predicts 38.3% (adjusted R) of total variation in psychological resilience. CONCLUSION: A high level of resilience in parents of children diagnosed with cancer is associated with better psychosocial function in response to the traumatic event. IMPLICATIONS FOR CLINICAL PRACTICE: Additional attention should be given to those Mainland Chinese parents who demonstrated a low level of resilience in response to their child's diagnosis. This is particularly important because of the long and stressful process for cancer treatment. Clinicians should also provide targeted interventions to those parents to promote their psychological resilience.

Electric fields due to synaptic currents sharpen excitatory transmission.

The synaptic response waveform, which determines signal integration properties in the brain, depends on the spatiotemporal profile of neurotransmitter in the synaptic cleft. Here, we show that electrophoretic interactions between AMPA receptor-mediated excitatory currents and negatively charged glutamate molecules accelerate the clearance of glutamate from the synaptic cleft, speeding up synaptic responses. This phenomenon is reversed upon depolarization and diminished when intracleft electric fields are weakened through a decrease in the AMPA receptor density. In contrast, the kinetics of receptor-mediated currents evoked by direct application of glutamate are voltage-independent, as are synaptic currents mediated by the electrically neutral neurotransmitter GABA. Voltage-dependent temporal tuning of excitatory synaptic responses may thus contribute to signal integration in neural circuits.

Metabotropic glutamate receptors in the trafficking of ionotropic glutamate and GABA(A) receptors at central synapses.

The trafficking of ionotropic glutamate (AMPA, NMDA and kainate) and GABA(A) receptors in and out of, or laterally along, the postsynaptic membrane has recently emerged as an important mechanism in the regulation of synaptic function, both under physiological and pathological conditions, such as information processing, learning and memory formation, neuronal development, and neurodegenerative diseases. Non-ionotropic glutamate receptors, primarily group I metabotropic glutamate receptors (mGluRs), co-exist with the postsynaptic ionotropic glutamate and GABA(A) receptors. The ability of mGluRs to regulate postsynaptic phosphorylation and Ca(2+) concentration, as well as their interactions with postsynaptic scaffolding/signaling proteins, makes them well suited to influence the trafficking of ionotropic glutamate and GABA(A) receptors. Recent studies have provided insights into how mGluRs may impose such an influence at central synapses, and thus how they may affect synaptic signaling and the maintenance of long-term synaptic plasticity. In this review we will discuss some of the recent progress in this area: i) long-term synaptic plasticity and the involvement of mGluRs; ii) ionotropic glutamate receptor trafficking and long-term synaptic plasticity; iii) the involvement of postsynaptic group I mGluRs in regulating ionotropic glutamate receptor trafficking; iv) involvement of postsynaptic group I mGluRs in regulating GABA(A) receptor trafficking; v) and the trafficking of postsynaptic group I mGluRs themselves.

Antisecretory factor modulates GABAergic transmission in the rat hippocampus.

Antisecretory Factor (AF) is a protein that has been implicated in the suppression of intestinal hypersecretion and inflammation. Intestinal secretion and inflammation are partly under local and central neural control raising the possibility that AF might exert its action by modulating neural signaling. In the present study we have investigated whether AF can modulate central synaptic transmission. Evoked glutamatergic and GABAergic synaptic transmissions were investigated using extracellular recordings in the CA1 region of hippocampal slices from adult rats. AF (0.5 microg/ml) suppressed GABA(A)-mediated synaptic transmission by about 40% while having no effect on glutamatergic transmission. Per oral administration of cholera toxin as well as feeding of rats with a diet containing hydrothermally processed cereals, known to upregulate endogenous AF plasma activity, mimicked the effect of exogenously administered AF on hippocampal GABAergic transmission. Our results identify AF as a neuromodulator and further raise the possibility that the hippocampus and AF are involved in a gut-brain loop controlling intestinal secretion and inflammation.

Expression of dominant negative cadherin in the adult mouse brain modifies rearing behavior.

The cadherin superfamily of cell-cell adhesion molecules (CAM) are crucial regulators of morphogenesis and axonal guidance during development of the nervous system and have been suggested to play important roles in neural plasticity of the brain. To study the latter, we created a mouse model that expressed a dominant negative classical cadherin in the brain of adult mice. The mice were tested for spontaneous motor activity and exploratory behavior in the open field, anxiety in the plus-maze, and spatial learning and memory in the water-T maze. Mice expressing the dominant negative cadherin displayed reduced rearing behavior, but no change in motor activity, in the open field, indicating deficits in exploratory behavior. In the water maze, animals expressing the mutant cadherin showed normal escape latencies and were indistinguishable from control littermates. Similarly, LTP in hippocampal slices of cadherin mutant and control mice were indistinguishable. These findings demonstrate intact spatial learning in mice expressing a dominant negative cadherin but altered rearing behavior, suggesting the involvement of classical cadherins in mechanisms mediating rearing behavior.

Creation of AMPA-silent synapses in the neonatal hippocampus.

In the developing brain, many glutamate synapses have been found to transmit only NMDA receptor-mediated signaling, that is, they are AMPA-silent. This result has been taken to suggest that glutamate synapses are initially AMPA-silent when they are formed, and that AMPA signaling is acquired through activity-dependent synaptic plasticity. The present study on CA3-CA1 synapses in the hippocampus of the neonatal rat suggests that AMPA-silent synapses are created through a form of activity-dependent silencing of AMPA signaling. We found that AMPA signaling, but not NMDA signaling, could be very rapidly silenced by presynaptic electrical stimulation at frequencies commonly used to probe synaptic function (0.05-1 Hz). Although this AMPA silencing required a rise in postsynaptic Ca(2+), it did not require activation of NMDA receptors, metabotropic glutamate receptors or voltage-gated calcium channels. The AMPA silencing, possibly explained by a removal of postsynaptic AMPA receptors, could subsequently be reversed by paired presynaptic and postsynaptic activity.

Active decay of composite excitatory postsynaptic potentials in hippocampal slices from young rats.

NMDA receptor dependent synaptic plasticity was examined in hippocampal slices using a novel pharmacological pairing procedure. Field excitatory postsynaptic potentials (EPSPs) were recorded from the CA1 area of slices maintained in a low Mg(2+) solution using a stimulus rate of 0.1-0.2 Hz. The NMDA receptor antagonist 2-amino-5-phosphonovalerate (AP5) was initially included in the perfusion solution to establish baseline recording of isolated AMPA EPSPs. Washing out AP5 led to the expression of composite EPSPs, containing both AMPA and NMDA receptor mediated components. Following an initial, transient potentiation of the AMPA component, the composite responses gradually decayed for several hours, involving AMPA and NMDA components to a similar extent. This decay was input specific and could be terminated at any stage by reapplication of AP5. Subsequent long-term potentiation (LTP) reversed the effect to an extent inversely related to the degree of depression. Experiments to test the interaction with long-term depression (LTD) revealed a significant but incomplete overlap between the two depression processes. In conclusion, pairing synaptic activation at test stimulus frequency with pharmacological unblocking of NMDA receptors allows for expression of composite EPSPs that decay substantially, due to an active mechanism. The underlying process appears to be at least partly distinct from those involved in homosynaptic LTP and LTD.