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Conclusion Prazosin should be used in PTSD with caution because prazosin might exacerbate anxiety in non-traumatized subjects. However prazosin might as well alleviate stress responses very effectively. Stress induced changes included increased NA and GABA levels in the amygdaloid complex in our study, attributing noradrenaline a possible inhibitory role on fear acquisition. Acetylcholine also has a role in memory modulation in the brain. We also demonstrated increased choline esterase acitivity. Cholinergic modulation might be another target for indirect prazosin action which needs to be further studied.Objective Lithium is used as first line in treating bipolar patients to stabilize their mood. However, the exact mechanism of lithium is not yet established. One of the proposed mechanisms is that lithium depolarizes the hyperpolarized neuronal membrane of bipolar patients bringing it back to the normal potential. On the other hand, the only way that lithium causes significant therapeutic depolarization is to have a membrane conductance that must be at least an order of magnitude higher than that for sodium but this is not achieved since both; lithium and sodium have the same conductance because the membrane channels are selective for them approximately by the same degree. So, this study aimed to explain how lithium could achieve higher conductance than sodium. Methods The idea of quantum tunneling through closed channels was used in a way to calculate the tunneling probability and the quantum conductance for lithium ions. Results It was found that lithium could achieve higher conductance than sodium because it has a smaller mass than sodium making lithium to have higher probability of tunneling and consequently higher conductance through channels and membrane. Conclusion Lithium tunneling model provides a reasonable explanation for the therapeutic depolarization effect of lithium. This model is experimentally testable to prove the tunneling effect of ions through the closed channels and to show the variations of quantum conductance between ions according to their mass.Objective We conducted a meta-analysis of randomized controlled trials to explore whether vitamin D supplementation is beneficial for symptom improvement in children with autism spectrum disorder. Methods We systematically searched the PubMed database, EMBASE, Cochrane Library, Web of Science, Sino-Med, Wanfang Data, and China National Knowledge Infrastructure mainly up to September 2019. Using a fixed effects model, we calculated the standard mean difference with 95% confidence interval. Furthermore, we analyzed baseline serum 25-hydroxyvitamin D levels and outcome scores including the Social Responsiveness Scale and Child Autism Rating Scale scores after vitamin D supplementation. selleck chemical Results There was no significant difference in baseline serum 25-hydroxyvitamin D levels among 203 children included from three studies in the meta-analysis. After vitamin D supplementation, the outcome scores in the experimental group were dramatically elevated compared with those in the control group (p = 0.03). Conclusion Vitamin D supplementation improves the typical symptoms of autism spectrum disorder, as indicated by reduced Social Responsiveness Scale and Child Autism Rating Scale scores; thus, it is beneficial for children with autism spectrum disorder.Objective Antipsychotic and anticonvulsant medications are increasingly being used as pharmacotherapeutic treatments for maladaptive aggression in youth, yet no information is available regarding whether these drugs exhibit aggression- specific suppression in preclinical studies employing adolescent animal models of maladaptive aggression. This study examined whether the commonly used antipsychotics medications haloperidol and risperidone and the anticonvulsant medication valproate exert selective aggression-suppressing effects using a validated adolescent animal model of maladaptive aggression. Methods Twenty-seven-day old Syrian hamsters (Mesocricetus auratus) were administered testosterone for 30 consecutive days during the first 4 weeks of adolescent development. The following day (during late adolescence), experimental animals received a single dose of haloperidol (0.00, 0.025, 0.50, 1.0 mg/kg), risperidone (0.00, 0.01, 0.03, 1.0 mg/kg), or valproate (0.00, 1.0, 5.0, 10.0 mg/kg) and tested for offensive aggression using the Resident/Intruder Paradigm. As a baseline, non-aggressive behavioral control, a separate set of pubertal hamsters was treated with sesame oil vehicle during the first 4 weeks of adolescence and then tested for aggression during late adolescence in parallel with the haloperidol, risperidone or valproate-treated experimental animals. Results Risperidone and valproate selectively reduced the highly impulsive and intense maladaptive aggressive phenotype in a dose-dependent fashion. While haloperidol marginally reduced aggressive responding, its effects were non-specific as the decrease in aggression was concurrent with reductions in a several ancillary (non-aggressive) behaviors. Conclusion These studies provide pre-clinical evidence that the contemporary pharmacotherapeutics risperidone and valproate exert specific aggression-suppressing effects in an adolescent animal model of maladaptive aggression.The solute carrier (SLC) superfamily is one of the major sub-groups of membrane proteins in mammalian cells. The solute carrier proteins include more than 400 different membrane-spanning solute carriers organized with 65 families in the human. In solute carrier family neurons, neurotransmitter is considered to be a pharmacological target of neuropsychiatric drugs because of their important role in the recovery of neurotransmitters such as GABA, glutamate, serotonin, dopamine and noradrenaline and regulation of their concentration in synaptic regions. Therefore, solute carrier transporters play vital and different roles in neurodegenerative disorders. In this article, the role of solute carrier transporters in neurodegenerative disorders such as Alzheimer disease, amyotrophic lateral sclerosis, Huntington disease, Parkinson's diseases, depression, post-traumatic stress disorder, dementia, schizophrenia, and Epilepsy reviewed and discussed to see how defects or absences in SLC transporter cause neurodegenerative disorders.