Activation of CRH Receptor Type 1 Expressed on Glutamatergic Neurons Increases Excitability of CA1 Pyramidal Neurons by the Modulation of Voltage-Gated Ion Channels.

Activation of CRH receptor type 1 expressed on glutamatergic neurons increases excitability of CA1 pyramidal neurons by the modulation of voltage-gated ion channels.

Front Cell Neurosci. 2013; 7: 91
Kratzer S, Mattusch C, Metzger MW, Dedic N, Noll-Hussong M, Kafitz KW, Eder M, Deussing JM, Holsboer F, Kochs E, Rammes G

Corticotropin-releasing hormone (CRH) plays an important role in a substantial number of patients with stress-related mental disorders, such as anxiety disorders and depression. CRH has been shown to increase neuronal excitability in the hippocampus, but the underlying mechanisms are poorly understood. The effects of CRH on neuronal excitability were investigated in acute hippocampal brain slices. Population spikes (PS) and field excitatory postsynaptic potentials (fEPSP) were evoked by stimulating Schaffer-collaterals and recorded simultaneously from the somatic and dendritic region of CA1 pyramidal neurons. CRH was found to increase PS amplitudes (mean ± Standard error of the mean; 231.8 ± 31.2% of control; n = 10) while neither affecting fEPSPs (104.3 ± 4.2%; n = 10) nor long-term potentiation (LTP). However, when Schaffer-collaterals were excited via action potentials (APs) generated by stimulation of CA3 pyramidal neurons, CRH increased fEPSP amplitudes (119.8 ± 3.6%; n = 8) and the magnitude of LTP in the CA1 region. Experiments in slices from transgenic mice revealed that the effect on PS amplitude is mediated exclusively by CRH receptor 1 (CRHR1) expressed on glutamatergic neurons. The effects of CRH on PS were dependent on phosphatase-2B, L- and T-type calcium channels and voltage-gated potassium channels but independent on intracellular Ca(2+)-elevation. In patch-clamp experiments, CRH increased the frequency and decay times of APs and decreased currents through A-type and delayed-rectifier potassium channels. These results suggest that CRH does not affect synaptic transmission per se, but modulates voltage-gated ion currents important for the generation of APs and hence elevates by this route overall neuronal activity. HubMed – depression

Prevalence of metabolic syndrome and its association with depression in patients with schizophrenia.

Neuropsychiatr Dis Treat. 2013; 9: 941-6
Suttajit S, Pilakanta S

To identify the point prevalence of metabolic syndrome in patients with schizophrenia and to evaluate the association between depressive symptoms and metabolic syndrome in patients with schizophrenia.Metabolic syndrome was assessed based on an updated definition derived from the modified National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) and the International Diabetes Federation criteria. The 17-item Hamilton Depression Rating Scale (HDRS-17) was used to measure depressive symptoms in 80 patients with schizophrenia. Odds ratios and 95% confidence intervals were calculated using logistic regression for the association between each depressive symptom and metabolic syndrome.The point prevalence rates of metabolic syndrome according to the modified NCEP-ATP III and International Diabetes Federation criteria were 37% and 35%, respectively. The risk of having metabolic syndrome significantly increased in those who were widowed or separated, or had longer duration of illness. Central obesity was the metabolic feature with the highest odds ratios for metabolic syndrome at 19.3. Three out of 17 items of HDRS subscales were found to be significantly associated with metabolic syndrome, including depressed mood, middle insomnia, and retardation with the odds ratios of 3.0, 3.4, and 3.6, respectively.This study showed that the prevalence of metabolic syndrome in patients with schizophrenia was higher than the overall rate but was slightly lower than in the general population in the USA. Central obesity, measured by waist circumference, was found to be highly correlated with metabolic syndrome. Depressed mood, middle insomnia, and retardation were significantly associated with metabolic syndrome in patients with schizophrenia. Waist circumference and screening for depression should be done at the clinics during patient follow-up. HubMed – depression

Effectiveness of controlled breathing techniques on anxiety and depression in hospitalized COPD: a randomized clinical trial.

Respir Care. 2013 Jul 23;
Valenza MC, Valenza-Peña G, Torres-Sánchez I, González-Jiménez E, Conde-Valero A, Valenza-Demet G

Anxiety and depression are highly prevalent comorbid complications in COPD. Breathing techniques can improve anxiety and depression in subjects hospitalized due to COPD exacerbation. We conducted a randomized clinical study using two groups. The sample comprised 46 male patients aged 67-86 years hospitalized with acute COPD exacerbation. Patients were randomly and equally divided into the control and controlled breathing intervention groups.The sample comprised 46 male patients aged 67-86 years hospitalized with acute COPD exacerbation. Patients were randomly and equally divided into the control and controlled breathing intervention groups.Baseline and post-intervention recordings of Dyspnea, Anxiety and depression, Quality of life (SGRQ and EURQoL), Respiratory pressures (PImax-PEmax), Hand-grip test and Sleep quality were taken in all subjects. Subjects hospitalized due to acute COPD exacerbation showed high levels of dyspnea and low values in overall quality of life as measured with the St. George’s Respiratory Questionnaire (SGRQ).Controlled breathing techniques had a significant effect on dyspnea, anxiety and mobility (p<0.05). All the measured areas were improved in the intervention group. The control group had poorer values in all the areas after the hospitalization period.Controlled breathing exercises benefit patients hospitalized due to COPD exacerbation in anxiety and depression values. HubMed – depression

Response to Comment on: Kan et al. A Systematic Review and Meta-analysis of the Association Between Depression and Insulin Resistance. Diabetes Care 2013;36:480-489.

Diabetes Care. 2013 Aug; 36(8): e124
Kan C, Silva N, Golden SH, Rajala U, Timonen M, Stahl D, Ismail K

HubMed – depression