State of the E-Mental Health Field in Australia: Where Are We Now?
State of the e-mental health field in Australia: Where are we now?
Filed under: Depression Treatment
Aust N Z J Psychiatry. 2013 Jan 7;
Christensen H, Petrie K
Objective:E-mental health technologies are increasing rapidly, both in number and in utilisation by consumers, health systems and researchers. This review aimed to: (i) examine the features and scientific evidence for e-mental health programs; (ii) describe the growth in these programs in the past decade, and track the extent and quality of scientific research over time; and (iii) examine Australian and international contribution to the field.Method:Two types of e-mental health programs; ‘web interventions’ and mobile applications’; targeting depression, bipolar disorder, generalised anxiety disorder, social anxiety, panic disorder and general stress were included. Data were collected from the Beacon website (www.beacon.anu.edu.au; last updated July 2011). Features of each program and their supporting scientific evidence were coded.Results:In total, 62 web interventions and 11 mobile applications were identified. Half of these were developed in Australia. The majority of programs were aimed towards adults and were based upon cognitive behavioural therapy. Approximately equal numbers of programs were developed for all targeted disorders except bipolar disorder, which was underrepresented. Only 35.5% of programs, all of which were web-based, had been evaluated by at least one RCT. The number of publications over the last decade is increasing. The majority were from Australian sources. Non-Australian research was lower in diversity and quantity.Conclusions:E-mental health research is increasing globally. Australia continues to be an international leader in this field. Depression, anxiety and panic disorder remain the disorders most targeted. Whilst the scientific evidence supporting e-mental health programs is growing, a substantial lack of high-quality empirical support was evident across the field, particularly for mobile applications and bipolar and social anxiety.
HubMed – depression
Gating of long-term depression by CaMKII through enhanced cGMP signaling in cerebellar Purkinje cells.
Filed under: Depression Treatment
J Physiol. 2013 Jan 7;
Kawaguchi SY, Hirano T
Long-term depression (LTD) at parallel fiber synapses on a cerebellar Purkinje cell has been regarded as a cellular basis for motor learning. Although Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has been implicated in the LTD induction as an important Ca(2+)-sensing molecule, the underlying signaling mechanism remains unclear. Here, we attempted to explore the potential signaling pathway underlying the CaMKII involvement in LTD using systems biological approach, combined with validation by electrophysiological and FRET imaging experiments on a rat cultured Purkinje cell. Model simulation predicted the following cascade as a candidate mechanism for the CaMKII contribution to LTD: CaMKII negatively regulates phosphodiesterase 1 (PDE1), subsequently facilitates the cGMP/protein kinase G (PKG) signaling pathway and down-regulates protein phosphatase 2A (PP-2A), thus supporting the LTD-inducing positive feedback loop consisting of mutual activation of protein kinase C (PKC) and mitogen activated protein kinase (MAPK). This model suggestion was corroborated by whole-cell patch clamp recording experiments. In addition, FRET measurement of intracellular cGMP concentration revealed that CaMKII activation causes sustained increase of cGMP, supporting the signaling mechanism of LTD induction by CaMKII. Furthermore, we found that activation of cGMP/PKG pathway by nitric oxide (NO) can support LTD induction without activation of CaMKII. Thus, this study clarified interaction between NO and Ca(2+)/CaMKII, two important factors required for LTD.
HubMed – depression
Hippocampal and cerebellar mossy fibre boutons – same name, different function.
Filed under: Depression Treatment
J Physiol. 2013 Jan 7;
Delvendahl I, Weyhersmüller A, Ritzau-Jost A, Hallermann S
Over a century ago, the Spanish anatomist Ramón y Cajal described “mossy fibres” in the hippocampus and the cerebellum, which contain several presynaptic boutons. Technical improvements in the last decades have allowed direct patch-clamp recordings from both hippocampal and cerebellar mossy fibre boutons (hMFBs and cMFBs, respectively), making them ideal models to study fundamental properties of synaptic transmission. HMFBs and cMFBs have similar size and shape, but each hMFBs contacts one postsynaptic hippocampal CA3 pyramidal neuron, while each cMFB contacts ~50 cerebellar granule cells. Furthermore, hMFBs and cMFBs differ in terms of their functional specialization. At hMFBs, a large number of release-ready vesicles and low release probability (<0.1) contribute to marked synaptic facilitation. At cMFBs, a small number of release-ready vesicles, high release probability (~0.5), and rapid vesicle reloading result in moderate frequency-dependent synaptic depression. These presynaptic mechanisms, in combination with faster postsynaptic currents of cerebellar granule cells compared with hippocampal CA3 pyramidal neurons, enable much higher transmission frequencies at cMFB compared with hMFB synapses. Analysing the underling mechanisms of synaptic transmission and information processing represents a fascinating challenge and may reveal insights into the structure-function relation of our brain. HubMed – depression
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