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Lip stretching, a newly described behavior, was performed significantly more often in response to caffeine than to any other substance, suggesting an association with the response to bitter taste. The facial response to the artificial sweetener aspartame was generally similar to the response to water, corroborating the notion that Platyrrhines may be unable to detect its sweetness. Overall, the present study supports the idea of similarity of taste-induced facial responses in non-hominoid primates and humans, suggesting these displays to be evolutionarily conserved across the primate order.
In the current study, it was aimed to investigate the relationship between BDNF gene expression and childhood suicide attempt, childhood traumatic experiences, and problem-solving skills in children and adolescents.
The suicide group consisted of 100 children and adolescents aged 11-18 years who were referred to our outpatient department due to suicide attempt. For further comparisons, 100 children and adolescents who have no any psychiatric diagnosis were referred to our same outpatient department were selected. A sociodemographic data form, the Schedule for Affective Disorders and Schizophrenia for School-Age Children- Present and Lifetime version (K-SADS-PL), the Suicide Intent Scale (SIS), Problem Solving Inventory (PSI), and the Childhood Trauma Questionnaire (CTQ) were used for both groups. Total RNA was isolated from whole blood samples and BDNF gene expression levels were measured using quantitative real time-polymerase chain reaction (QRT-PCR).
The total and subscale scores of the PSI and CTQ were found to be significantly higher in the suicide group than in the control group. There was no significant difference between the groups in terms of BDNF gene expression levels. However, gene expression of BDNF was found significantly increased in patients who have any psychiatric disorder compared with the others.
Our results indicate that BDNF gene expression could be more associated with psychiatric disorders rather than suicide attempt in children and adolescents.
Our results indicate that BDNF gene expression could be more associated with psychiatric disorders rather than suicide attempt in children and adolescents.Reserpine (RES) is an irreversible inhibitor of VMAT2 used to study Parkinson's disease (PD) and screening for antiparkinsonian treatments in rodents. Recently, the repeated treatment with a low dose of reserpine was proposed as a model capable of emulating progressive neurochemical, motor and non-motor impairments in PD. Conversely, compared to Wistar rats, Spontaneously Hypertensive Rats (SHR) are resistant to motor changes induced by repeated treatment with a low dose of RES. Pim inhibitor However, such resistance has not yet been investigated for RES-induced non-motor impairments. We aimed to assess whether SHR would have differential susceptibility to the object recognition deficit induced by repeated low-dose reserpine treatment. We submitted male Wistar and SHR rats to repeated RES treatment (15 s.c. injections of 0.1 mg/kg, every other day) and assessed object memory acquisition and retrieval 48 h after the 6th RES injection (immediately before the appearance of motor impairments). Only RES Wistar rats displayed memory impairment after reserpine treatment. On the other hand, untreated SHR rats displayed object recognition memory deficit, but RES treatment restored such deficits. We also performed immunohistochemistry for tyrosine hydroxylase (TH) and α-synuclein (α-syn) 48 h after the last RES injection. In a different set of animals submitted to the same treatment, we quantified DA, 5-HT and products of lipid peroxidation in the prefrontal cortex (PFC) and hippocampus (HPC). SHR presented increased constitutive levels of DA in the PFC and reduced immunoreactivity to TH in the medial PFC and dorsal HPC. Corroborating the behavioral findings, RES treatment restored those constitutive alterations in SHR. These findings indicate that the neurochemical, molecular and genetic differences in the SHR strain are potentially relevant targets to the study of susceptibility to diseases related to dopaminergic alterations.Drug use among adolescents is a serious problem in our society, as some individuals develop dependence and addiction. MDMA/Esctasy is one of the most typically used substances by this age group. It is well known that environmental factors can alter the rewarding properties of drugs and the propensity to drug-related disorders. In this sense, exposure to social stress induces long-term effects in mice, enhancing the rewarding effects of MDMA in the conditioned place preference (CPP) paradigm. On the other hand, previous research has not provided conclusive results regarding the short-term effects of social defeat on MDMA reward in adolescent animals, probably due to the use of very low or very high doses. Thus, in the present study, we set out to evaluate whether exposure to social defeat immediately before each conditioning session with an intermediate dose of MDMA (2.25 mg/kg) modulates the rewarding effect of this drug in adolescent animals. Our results indicate that both control and socially defeated mice acquired CPP, but only stressed mice showed reinstatement. These findings indicate that social defeat induces an increase in the rewarding effect of MDMA, suggesting that this type of stress is a potential factor in the development of MDMA addiction.Mitochondrial dysfunction is now considered an important sign of neuronal death during cerebral ischemia/reperfusion (I/R) injury. Studies have shown that the transfer of mitochondria from astrocytes to injured neurons contributes to endogenous neuroprotection after stroke. Basic and clinical studies have shown that mild hypothermia exerts a clear protective effect on neurons after cerebral ischemic injury, but the role of mild hypothermia in this endogenous neuroprotective mechanism remains unclear. Here, we established a neuronal cell oxygen-glucose deprivation (OGD)/reoxygenation (OGD/R)-induced injury model and explored the effect of mild hypothermia on the transfer of mitochondria from astrocytes to injured neurons. Astrocytes in the hypothermia group (33 °C) released more functional mitochondria into the extracellular medium than those in the normal temperature group (37 °C). Compared with cells in the normal temperature group, OGD-injured neuronal cells in the mild hypothermia group exhibited an increased intracellular ATP content, mitochondrial membrane potential (MMP) and cellular viability and a decreased death rate after the addition of astrocyte-derived conditioned medium.
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