ABSTRACT
Insomnia symptom is one of the most common types of sleep disturbances.Apart from being a risk factor for psychiatric disorders, insomnia symptom has been found to affect the course of psychiatric disorders and increase the relapse rate of psychiatric disorders.Therefore, insomnia treatment is beneficial to mitigate the psychiatric symptoms among chronic insomnia patients, which may help prevent mental health disorders.On the other hand, insomnia treatment for psychiatric patients is conductive to reduce the harm consequence in social function, which can help improving the prognosis of psychiatric disorders.Cognitive behavior therapy for insomnia (CBT-I) is a first-line treatment for chronic insomnia.This paper reviews the research progress on the efficiency of CBT-I on the psychiatric symptoms of chronic insomnia patients, as well as its application in comorbid psychiatric conditions.Findings from previous research suggested that CBT-I is effective to improve the psychiatric symptoms of insomnia patients through insomnia improvement, and it can also promote the remission of depression and anxiety symptoms, reduce the risk of substance disorder and suicide behaviors, and reduce the impairment of life quality and costs of treatment through insomnia improvement among psychiatric patients comorbid with insomnia, which indicated that CBT-I is a safe and effective treatment for insomnia symptoms in psychiatric patients.Moreover, this paper listed the contraindications and the decision-to-treat algorithm of CBT-I among psychiatric patients, as well as the CBT-I availability and adherence that limited the clinical application.More understanding of CBT-I is beneficial to provide support for a broad clinical application in mental health services.
ABSTRACT
Objective To investigate the expression of oxytocin ( OXT ) and oxytocin receptor (OXTR) in the prefrontal cortex of postpartum depression (PPD) rats induced by restraint stress during pregnancy and to observe the antidepressant effect of oxytocin and its analogue capitoxin and its mechanism. Methods Twenty-four adult female SD rats of SPF grade were randomly divided into control group,PPD +saline group,PPD + oxytocin group and PPD + captopril group with 6 rats in each group. Rats were subjec-ted to restraint stress for 2 hours every day on the 8th to 21st day of pregnancy to establish PPD model. While the rats in control group were not given any treatment. Rats in PPD + saline,PPD + oxytocin and PPD +captopril were injected bilaterally into prefrontal cortex (PFC) at 10 days postpartum (1 μl/side),oxytocin (30 ng/side) and captopril (45 ng/side) respectively once a day for 5 days. The depressive behaviors of rats were detected by sugar-water preference experiment. Rats were sacrificed 18 days after delivery. The ex-pression of OXT was detected by ELISA method,OXTR by Western blot,Iba-1 by immunofluorescence,and IL-1β,IL-6 and TNF-α by qRT-PCR. Results (1) The sucrose consumption of the PPD + saline group ((67. 1±10. 4)%) was significantly lower than that of the control group((92. 6± 3. 9)%,t=-5. 31,P<0. 01). (2) The expression of oxytocin in prefrontal cortex in PPD group was significantly lower than that in control group ((0. 03±0. 01) ng/mg) vs (0. 08 +0. 05) ng/mg,t=-2. 67,P<0. 05). However,there was no significant difference in the expression of oxytocin receptor between PPD group and control group ((0. 90 ±0. 06) vs (0. 90±0. 05),t=0. 709,P=0. 517). (3) The sucrose consumption of PPD+saline group de-creased than that of control group((65. 6±16. 9)% vs (91. 5±3. 5)%,t=3. 35,P<0. 001). Compared with PPD+saline group,the sucrose consumption of PPD+oxytocin group ((81. 8±8. 4)%) and PPD+carbetocin group ((78. 4±9. 4)%) increased(t=1. 98,1. 68,both P<0. 05). (4) The expression of Iba-1 in the pre-frontal lobe of PPD + saline group was higher than that of control group ((1. 15±0. 05) vs (1. 04 +0. 06), t=3. 50,P<0. 01). Compared with PPD + saline group,the expression of Iba-1 in PPD + oxytocin group (1. 03±0. 06) and in PPD + captopril group (1. 00±0. 02) were lower (t=-3. 50,-6. 55,both P<0. 01). (5) The expression of inflammatory factors IL-1β mRNA (1. 0±0. 1),IL-6 mRNA (1. 1±0. 1) and TNF-α mRNA (1. 7±0. 4) in the prefrontal cortex of rats in the PPD group were higher than that in the control group (IL-1β mRNA (0. 7± 0. 3),IL-6 mRNA (0. 9± 0. 1),TNF-α mRNA ( 1. 1± 0. 3),t=1. 92,3. 19, 2. 43 respectively,all P<0. 05). The expression of inflammatory factors IL-1β,IL-6 and TNF-α mRNA of the PPD+oxytocin group(IL-1β mRNA (0. 6±0. 1),IL-6 mRNA (0. 9±0. 1),TNF-α mRNA (1. 2±0. 4) )and the PPD+carbetocin group ( IL-1β mRNA ( 0. 7± 0. 1),IL-6 mRNA ( 0. 9 ± 0. 1),TNF-α mRNA ( 1. 0 ± 0. 2))in the prefrontal cortex were lower than that in the PPD group(t=-3. 17,-2. 78,-1. 84,t=-2. 76,-2. 40,-2. 94 respectively,all P<0. 05). Conclusion Oxytocin and capitoxin injected into prefrontal cortex can effectively improve depression-like behaviors in PPD model rats. Activation of microglia and decrease of inflammatory factors in prefrontal cortex may be the potential antidepressant mechanism.
ABSTRACT
Depression is the most common mental disorder in epilepsy, which means that they maybe have some common pathogene-sis. This paper discussed the biological relation mechanism, such as neurotransmitter, neuropeptide and its receptor, glial cell, immune-medi-ators, nerve signal transduction pathway, synaptic plasticity and nerve regeneration.