Basic and Clinical Neuroscience最新文献

Introduction: Vitamin D deficiency has been linked to the evolution of ischemic stroke, but the data regarding the association between stroke severity and vitamin D level is scarce.

Methods: Patients with first-ever ischemic stroke in the middle cerebral artery territory, within seven days after the stroke, were recruited. The control group included age- and gender-matched individuals. We compared 25-OH vitamin D (vitamin D), high sensitive C-reactive protein (hsCRP), serum amyloid A (SAA), and osteopontin levels between stroke patients and the control group. The association between stroke severity according to the National Institutes of Health Stroke Scale (NIHSS) and the Alberta stroke program early CT score (ASPECTS) and levels of vitamin D and inflammatory biomarkers were also studied.

Results: There was an association between hypertension (P=0.035), diabetes mellitus (P=0.043), smoking (P=0.016), history of ischemic heart disease (P=0.002), higher SAA (P<0.001), higher hsCRP (P<0.001), and lower vitamin D levels (P=0.002) and stroke evolution in a case-control study. Meanwhile, in stroke patients, its severity was associated with higher SAA (P=0.04) and hsCRP (P=0.001), and lower vitamin D levels (P=0.043) according to clinical scale (higher admission NIHSS). According to the ASPECT score, higher SAA (P=0.017) and hsCRP (P=0.007), but not lower vitamin D levels, were associated with more infarct areas (P=0.149).

Conclusion: Vitamin D may play a role in both the evolution and severity of stroke.

Introduction: Autism is a heterogeneous neurodevelopmental disorder associated with social, cognitive and behavioral impairments. These impairments are often reported along with alteration of the brain structure such as abnormal changes in the grey matter (GM) density. However, it is not yet clear whether these changes could be used to differentiate various subtypes of autism spectrum disorder (ASD).

Method: We compared the regional changes of GM density in ASD, Asperger's Syndrome (AS) individuals and a group of healthy controls (HC). In addition to regional changes itself, the amount of GM density changes in one region as compared to other brain regions was also calculated. We hypothesized that this structural covariance network could differentiate the AS individuals from the ASD and HC groups. Therefore, statistical analysis was performed on the MRI data of 70 male subjects including 26 ASD (age=14-50, IQ=92-132), 16 AS (age=7-58, IQ=93-133) and 28 HC (age=9-39, IQ=95-144).

Result: The one-way ANOVA on the GM density of 116 anatomically separated regions showed significant differences among the groups. The pattern of structural covariance network indicated that covariation of GM density between the brain regions is altered in ASD.

Conclusion: This changed structural covariance could be considered as a reason for less efficient segregation and integration of information in the brain that could lead to cognitive dysfunctions in autism. We hope these findings could improve our understanding about the pathobiology of autism and may pave the way towards a more effective intervention paradigm.

Introduction: This study aimed to assess the effect of controlled mouth breathing during the resting state using functional magnetic resonance imaging (fMRI).

Methods: Eleven subjects participated in this experiment in which the controlled "Nose" and "Mouth" breathings of 6 s respiratory cycle were performed with a visual cue at 3T MRI. Voxel-wise seed-to-voxel maps and whole-brain region of interest (ROI)-to-ROI connectome maps were analyzed in both "Nose>Mouth" and "Mouth>Nose" contrasts.

Results: As a result, there were more connection pairs in the "Mouth" breathing condition, i.e., 14 seeds and 14 connecting pairs in the "Mouth>Nose" contrast, compared to 7 seeds and 4 connecting pairs in the "Nose>Mouth" contrast (false discovery rate [FDR] of P<0.05).

Conclusion: The present study demonstrated that mouth breathing with controlled respiratory cycles could significantly induce alterations in functional connectivity in the resting-state network, suggesting that it can differently affect resting brain function; in particular, the brain can hardly rest during mouth breathing, as opposed to conventional nasal breathing.

Introduction: The footprint of Neuregulin 1 (NRG1) / ERbB4 in the pathophysiology of some neurological disorders and TRPV1 regulation has been indicated. The alterations in NRG1 and ErbB4 as well as the TRPV1 signaling pathway were investigated during the development of absence epilepsy in the genetic animal model of absence epilepsy.

Methods: Male WAG/Rij and Wistar rats were divided into four experimental groups of two and six months of age. The protein levels of NRG1, ERbB4, and TRPV1 were measured in the somatosensory cortex and hippocampus.

Results: The cortical protein levels of NRG1 and ErbB4 in the 6-month-old WAG/Rij rats were lower than in Wistar rats. Protein levels of TRPV1 were lower in two- and six-month-old WAG/Rij rats compared to age-matched Wistar rats.Hippocampal protein levels of NRG1 in 6-month-old WAG/Rij rats were lower than two-month-old WAG/Rij rats. Low levels of ErbB4 protein in two-month-old and high levels in six-month-old WAG/Rij rats were found compared to Wistar rats. Protein levels of TRPV1 were lower in the two-month-old and higher in the six-month-old WAG/Rij rats compared to age-matched Wistar rats.Furthermore, a high correlation between NRG1/ERbB4 and TRPV1 expressions in the cortex and hippocampus was indicated. The expression of NRG1/ERbB4 and TRPV1 followed a similar pattern during the life span of Wistar and WAG/Rij rats.

Conclusion: Our findings indicated the potential role of the NRG1/ErbB4 pathway as well as TRPV1 in the pathogenesis of absence epilepsy. The regulatory effect of the ERbB4 receptor on the TRPV1 expression has been suggested following the similar pattern of expression.

Introduction: Fundamental notions of mapping hypothesis and canonicity were scrutinized in Persian-speaking aphasics.

Methods: To this end, the performance of four age-, education-, and gender matched Persian-speaking Broca's patients and eight matched healthy controls in diverse complex structures were compared via the conduction of two tasks of syntactic comprehension and grammaticality judgment.

Results: The tested structures included subject agentive, agentive passive, object experience, subject experience, subject cleft, and object cleft constructions. Our results, while corroborating the predictions of the mapping hypothesis, showed that in structures, in which linguistic elements were substituted and dislocated out of their canonical syntactic positions, namely, agentive passive, subject experiencer, object experiencer, and object cleft constructions, Broca's problems escalated. In contrast, in those structures whose constituent concatenations were aligned with canonical syntactic structures, namely subject agentive, and cleft structures, patients had above the chance performance. Ultimately, the theoretical and clinical implications of the study were discussed.

Conclusion: The number of predicates in a sentence, predicate types (psychological and agentive), as well as semantic heuristics and canonicity all by all could be regarded as the major culprits for aphasics' poor performance.

Introduction: Appropriate information about the ability of patients with Parkinson disease (PD) to perform cognitive instrumental activities of daily living (IADL) is necessary. The present study aimed to assess the psychometric properties of the Persian version of the Penn Parkinson daily activities questionnaire-15 (PDAQ-15).

Methods: A total of 165 knowledgeable informants of PD patients completed the PDAQ-15. The clinical dementia rating scale, Hoehn and Yahr staging, hospital anxiety and depression scale (HADS), and Lawton IADL scale were used in the study. Internal consistency and test-retest reliability were evaluated by the Cronbach α coefficient and intraclass correlation coefficient (ICC), respectively. To examine the dimensionality of the questionnaire, exploratory factor analysis was used. The construct validity was assessed using the Spearman rank correlation test. To assess the discriminative validity, PDAQ-15 scores were compared across cognitive stages.

Results: The PDAQ-15 showed strong internal consistency (the Cronbach α=0.99) and test-retest reliability (ICC= 0.99). Only one dimension was identified for the PDAQ-15 in the factor analysis. There was a strong correlation between PDAQ-15 with the depression domain of the HADS scale and the Lawton IADL scale (rs=|0.71-0.95|). The correlation of PDAQ-15 with the anxiety domain of the HADS scale was moderate (rs=0.66). Discriminative validity analysis showed that the PDAQ-15 has significant power to discriminate between PD patients across cognitive stages.

Conclusion: These results suggest that the PDAQ-15 is a valid and reliable PD-specific instrument and can be useful in clinical and research settings.

Introduction: Several neuropsychiatric disorders, such as addiction, have indicated variations in the levels of neurotrophic factors. As an extremely addictive stimulant, methamphetamine (METH) is associated with rising levels of abuse worldwide. We have recently demonstrated that repeated intracerebroventricular (ICV) of cannabidiol (CBD), the most important non-psychotomimetic compound, can lead to diminished impairing memory and hippocampal damage caused by chronic exposure to METH (CEM) in rats over the abstinence period. Furthermore, the results indicated a possible contribution of the neurotrophin signaling pathway (NSP) in regulating neurogenesis and survival. This study intends to evaluate whether these effects remained as measured in molecular pathways after the abstinence period.

Methods: The animals were given 2mg/kg METH twice a day for 10 days. Then, we adopted real-time polymerase chain reaction (PCR) throughout the 10-day abstinence period to assess the CBD's effect (10 and 50μg/5μL) on the levels of the mRNA expression of the NSP.

Results: The findings suggested that CEM, when compared to the control group in the hippocampus, downregulated mRNA expression of NSP. Moreover, a dosage of 50 μg/5μL CBD may possibly enhance the mRNA expression level of BDNF/TrkB and NGF/TrkA in the hippocampus. Besides, the expression of RAF-1 mRNA level could be reversed significantly by both doses of CBD.

Conclusion: According to our results, CBD may partly bring about neuroprotective effects by modulating the NSP. These findings set forth solid evidence demonstrating that CBD is a protective factor attributed to neuropsychiatric disorders, such as METH addiction.

Introduction: Memantine (MEM) is a noncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonist clinically used for the treatment of Alzheimer disease (AD) in mild to severe conditions. The present study was conducted to investigate the effects of memantine on the spontaneous firing frequency of CA1 pyramidal neurons in rats caused by an electrical lesion of Nucleus Basalis Magnocellularis (NBM). Then, this model of AD rats was compared with the intact adult male rats.

Methods: In this study, adult male rats were divided into two groups. Group I (lesion of NBM, n=53) includes the following subgroups: lesion+saline, sham+saline, lesion+MEM 5 mg/kg, lesion+MEM 10 mg/kg, and lesion+MEM 20mg/kg. Group II (intact, n=48) includes the following subgroups: intact+saline, intact+MEM 3mg/kg, intact+MEM 5mg/kg, and intact+MEM 10mg/kg. Extracellular single-unit recording (15 min baseline+105 min after MEM or saline) was performed under urethane-anesthetized rats.

Results: The results showed that the mean frequency of CA1 pyramidal neurons after saline in the lesion+saline (P<0.001) group significantly decreases compared with the intact+saline and sham+saline groups. In addition, after saline and memantine, the mean frequency of CA1 pyramidal neurons in the lesion+MEM 10 mg/kg (P<0.01) and lesion+MEM 20 mg/kg (P<0.001) groups significantly increased compared with the lesion+saline group. Also, the mean frequencies of CA1 pyramidal neurons in the intact+MEM 10 mg/kg (P<0.001) group significantly decreased compared with the intact+saline group.

Conclusion: Results showed that memantine increases the electrical activity of CA1 pyramidal neurons in a rat model of AD. Furthermore, in the intact adult male rats, the low-dose memantine, contrary to high dose, does not decrease the electrical activity of CA1 pyramidal neurons.

Introduction: Electrical impedance tomography (EIT) is a non-invasive technique utilized in various medical applications, including brain imaging and other neurological diseases. Recognizing the physiological and anatomical characteristics of organs based on their electrical properties is one of the main applications of EIT, as each variety of tissue structure has its own electrical characteristics. The high potential of brain EIT is established in real-time supervision and early recognition of cerebral brain infarction, hemorrhage, and other diseases. In this paper, we review the studies on the neurological applications of EIT.

Methods: EIT calculates the internal electrical conductivity distribution of an organ by measuring its surface impedance. A series of electrodes are placed on the surface of the target tissue, and small alternating currents are injected. The related voltages are then observed and analyzed. The electrical permittivity and conductivity distributions inside the tissue are reconstructed by measuring the electrode voltages.

Results: The electrical characteristic of biological tissues is remarkably dependent on their structures. Some tissues are better electrical conductors than the others since they have more ions that can carry the electrical charges. This difference is attributed to changes in cellular water content, membrane properties, and destruction of tight junctions within cell membranes.

Conclusion: EIT is an extremely practical device for brain imaging, capturing fast electrical activities in the brain, imaging epileptic seizures, detecting intracranial bleeding, detecting cerebral edema, and diagnosing stroke.

Introduction: Natural rewards are essential for survival. However, drug-seeking behaviors can be maladaptive and endanger survival. The present study was conducted to enhance our understanding of how animals respond to food and morphine as natural and drug rewards, respectively, in a conditioned place preference (CPP) paradigm.

Methods: We designed a protocol to induce food CPP and compare it as a natural reward with morphine CPP in rats. The protocol for reward induction in both groups (foods and morphine) consisted of three phases: pre-test, conditioning, and post-test. In morphine groups, we injected morphine as a reward (5 mg/kg, SC). To induce natural reward, we used two different protocols. In the first one, the rats were deprived of food for 24 h. In the other method, the rats were restricted to food for 14 days. During the conditioning period, the animals received daily chow, biscuits, or popcorn as a reward inducer.

Results: Results revealed that CPP was not induced in food-deprived rats. A combination of food restriction (as a facilitator) and a biscuit or popcorn-induced reward using CPP. In contrast, food deprivation did not facilitate food CPP in response to regular food. Interestingly the CPP score of the group which received biscuits during a 7-day conditioning period was more than that of the morphine group.

Conclusion: In conclusion, food restriction could be a better protocol than food deprivation to facilitate food reward.