mahmoudreza hadjighassem

Obsessive-compulsive disorder (OCD) is characterized by alterations in brain connectivity, particularly within the default mode network (DMN) and the salience network (SN). Investigating these connectivity differences can provide a deeper understanding of the neural mechanisms underlying OCD.

This cross-sectional study involved 58 patients diagnosed with OCD and 38 healthy control subjects, totaling 96 participants. Resting-state functional MRI (fMRI) data were acquired and analyzed using the CONN toolbox to examine functional connectivity within intrinsic resting-state networks. Graph theory metrics were applied to evaluate node connections and the overall network topology. Clinical symptoms were assessed using the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), and their correlations with connectivity patterns and graph-theory parameters were analyzed.

The OCD patients and healthy controls were matched in terms of age, gender, marital status, socioeconomic status, and handedness. However, OCD patients had significantly worse general health, quality of life, and higher levels of depression and anxiety. Network analyses revealed altered whole-brain connectivity in OCD patients, particularly within the DMN and the frontoparietal network. The most significant between-group connectivity differences were observed between the posterior parietal cortex (PPC) and the precuneus. Disruptions in the DMN, specifically altered connectivity between the medial prefrontal cortex and posterior cingulate cortex, and changes in the SN involving the anterior insula and anterior cingulate cortex, were significantly correlated with the severity of OCD symptoms.

The findings suggest that OCD is associated with distinct alterations in DMN connectivity, which may play a critical role in the disorder's pathophysiology. These disruptions offer potential targets for therapeutic intervention. Further research is needed to explore these connectivity changes in larger cohorts and at various stages of OCD to better understand their clinical significance.

Olfactory ensheathing cells (OECs) are widely used in transplantation studies. The high purification of this unique cell type is valuable for medical applications. Although recent improvements in OECs isolation procedures opened a new era in this field, the high purification efficacy and viability rate are still of concern. The most widely used OECs isolation techniques can be broadly classified based on adherence properties, particularly in olfactory bulb-derived OEC isolation. Considering the invasive nature of harvesting OECs from human olfactory bulbs, a highly efficient purification of these cells from olfactory mucosa can benefit clinical trials. In this study, we isolated OECs from rats’ olfactory bulbs and mucosa due to their differential adherence properties and compared them. 

Cell preparations were characterized by NGFR p75 and S100β antibodies, the specific markers for OECs, using immunocytochemistry and western blot analysis, respectively. OECs morphology and viability were monitored over time by microscopy and MTT (3-[4,5-dimethylthiazol2-yl]-2,5-diphenyltetrazolium bromide) assay. 

We found that OECs could be purified from the olfactory mucosa using our suggested method as efficiently as the olfactory bulb. Both derived OECs showed high levels of NGFR p75 and S100β expression, although the S100β expression was higher in olfactory mucosa-derived OECs preparations (P<0.05). Moreover, there was no significant difference between the two sources in cell viability in our suggested protocol. 

Due to the non-invasive harvesting method, olfactory mucosa-derived OECs are preferred from a clinical point of view in transplantation studies.

Spinal cord injury (SCI) is characterized by serious both motor and sensory disability of the limbs below the injured segment. It is the most traumatic disorder among central nervous system (CNS) conditions which not only leads to psychological and physical harm to patients but also results in a dramatic loss in the life quality. Many efforts have been developed to find a therapeutic approach for SCI; however, an effective treatment has not yet been found. The lack of effective treatment approach and rehabilitation of SCI underscores the need to identify novel approaches. Tissue engineering associated with stem cells has been recently introduced as an effective treatment approaches for traumatic SCI. Although, low survival rates, immune rejection, cell dedifferentiation, and tumorigenicity have been addressed for tissue engineering. Regenerative medicine is an interdisciplinary field developing and applying tissue engineering, stem cell (SC) therapy, and SC-derived extracellular vesicle therapy that aims to provide reliable and safe ways to replace injured tissues and organs. The application of mesenchymal stem cells-derived extracellular vesicles (MSC-EVs) has recently attracted attention to improve central nervous system dysfunction such as SCI, mainly by promoting neurogenesis and angiogenesis.

In this review article the latest information of SCI improvement using stem cell-derived extracellular vesicles published data in the Web of Science, Scopus, Science Direct and Pub Med databases were collected. 

The data collected show that MSC-EVs, including exosomes, alone or in combination with scaffolds can can regenerate the injured nerve in SCI.

This study summarizes the efficacy of MSC-EVs, including exosomes, alone or in combination with scaffolds in the treatment of SCI and then discusses the therapeutic outcomes observed in SCI experimental models following treatment with MSC-EVs alone or loaded on scaffolds in particular collagen-based scaffolds.

Spinal cord injury (SCI) is a critical neurological condition that may impair motor, sensory, and autonomic functions. Spinal cord injury severely affects the independence and quality of life of the injured person and his family. At the cellular level, inflammation, impaired axonal regeneration, and neuronal death are responsible for complications after SCI. Due to the high mortality rate and complications caused by SCI, there is a need for effective treatment. Despite the advances made in SCI repair, the optimal treatment for complete recovery after SCI has not yet been found. The goal of therapeutic interventions in spinal cord injury is to prevent the further expansion of the injury and repair the damaged tissue. At the functional level, existing treatments focus on techniques that aim to restore some degree of walking or motor activity. One of these techniques is learning to walk on a treadmill.

In this study, we have investigated the impact of treadmill training on the restoration of motor ability, as well as the myelination and repair of neurons in rats with a contusion model. The assessment involved two groups: the sham group (experiencing a lesion without movement rehabilitation) and the treatment group (undergoing a lesion followed by movement rehabilitation).

Motor rehabilitation with a treadmill improved the motor performance of animals compared to the sham group. However, it did not affect sensory function. The motor rehabilitation group showed a significant increase in the sucrose test compared to the sham group. The size of the spinal cord lesion cavity and nerve tissue repair showed a significant decrease in the rehabilitation group compared to the sham group.

The results of this study showed that motor neurorehabilitation contributes to the restoration and enhancement of cell function, affecting not only functional and behavioral functions but also the tissue and cellular recovery.

Mesenchymal stem cell (MSC) derived exosomes (MSC-DE) have been demonstrated to be potential candidates for the treatment of rat spinal cord injury (SCI). The effect of AD-MSC and AD-MSC-DE encapsulated into collagen and fibrin hydrogels on the treatment of SCI in a rat animal model was investigated for introducing a new effective SCI treatment method The AD-MSC-DE was isolated using ultra-centrifugation at 100,000×g for 120 min and characterized by different methods. Fibrin and collagen hydrogels were synthesized and then mixed with AD-MSC-DE suspension. the characterized AD-MSC-DE were encapsulated into collagen and fibrin hydrogels. eighteen adult male Wister rats were randomly classified into 3 equal groups (n=6): the control group (SCI rat without treatment), SCI rat treated with either AD-MSC-DE encapsulated in collagen hydrogel or encapsulated in fibrin hydrogel groups. the treatment approaches were evaluated using clinical, histological, and molecular assays. The AD-MSC-DE encapsulated into fibrin and collagen groups showed better clinical function than the control group. The AD-MSC-DE encapsulated into fibrin and collagen also improved SCI-induced polio and leuko-myelomalacia and leads to higher expression of NF protein than the control group. In the AD-MSC-DE encapsulated into collagen and fibrin leads to up-regulation the mean levels of NEFL (23.82 and 24.33, respectively), eNOS (24.31 and 24.53, respectively), and CK19 mRNAs (24.23 and 23.98, respectively) compared to the control group. The AD-MSC-DE encapsulated within ECM-based hydrogel scaffolds such as collagen and fibrin can regenerate the injured nerve in SCI rats and reduce spinal cord lesion-induced central neuropathic pain.

The precise identification of attention deficit-hyperactivity disorder (ADHD) is one of the challenging clinical processes. Disorganizations in functional neural networks revealed via functional magnetic resonance imaging have recently been contributing. Machine learning approaches, particularly classification methods, have commonly been employed as a framework for diverse data analysis, indicating promisingmedical diagnosis results. However, as the neuroimaging data are high-dimensional with a low sample size (the current dataset), this study aimed to evaluate the classification performance of the models by considering the specific contribution of the sparsity of data matrices.

This cross-sectional study analyzed the preprocessed data from the 2011 ADHD-200 Global Competition. A total of 768 and 171 data items were considered training and test, respectively. The diagnosis status was used as a response variable. Age, gender, hand dominance, and activity relationship between 116 brain regions derived from inverse covariance matrix and inverse sparse covariance matrix were used as predictive variables. Accordingly, this study compared the performance of three models, namely support vectormachine(SVM), distance-weighted discrimination (DWD),anddatamaximumdispersion classifier(DMDC)forADHD categorization.

The highest value for the total accuracy was reported for the SVM model on the sparse covariance matrix. Moreover, the highest values for the balanced classification rate (BCR) (59%) and sensitivity (64%) were reported forDMDCon the sparse covariance matrix. The best level of specificity (99%) was obtained fromDWDusing the sparse covariance matrix. The highest levels of the values (i.e., total accuracy and BCR) were achieved through the model fitting on the sparse matrices. Among the six models, the DMDC model on sparse covariance matrix was the most optimal algorithm due to the superiority of the two indices (i.e., accuracy: 60% and BCR: 60%) and the favorable balance between sensitivity and specificity values.

Amongthe current studied three models,DMDC performance, applying the sparse data, remarkably improved the results of classification processes. Based on the present findings, the neuronal connectivity among subcortical structures comprising parts of the basal ganglia and cerebellum provides a distinction between ADHD subjects and healthy controls.

Spinal cord injury (SCI) is a severe neurological disease leading to poor quality of life.

The regenerative effect of adipose-derived mesenchymal stem cells (AD-MSCs) encapsulated into fibrin, and collagen hydrogel scaffolds on a rat model of SCI was investigated using clinical and histopathological examinations.

A total of 18 adult male Wistar rats (250 - 300 g) were prepared and randomly divided into three equal groups, each with six rats, including the control or SCI group (SCI contusion model without treatment), SCI contusion model treated with AD-MSCs encapsulated in fibrin hydrogel, and SCI contusion model treated with AD-MSCs encapsulated in collagen hydrogel groups. Clinically, functional recovery or hindlimb locomotor activity was assessed using Basso, Beattie, and Bresnahan's (BBB) scoring system four weeks post-treatment. The rats were sacrificed at week four post-treatment, and their spinal cords were examined histopathologically.

Faster functional recovery indicated with hindlimb locomotor activity was seen in both treatment groups compared to the control group. Severe polio and leuko-myelomalacia associated with disruption of spinal cord structure were identified in the control group. Mild polio and leuko-myelomalacia associated with mild to moderate disruption of spinal cord structure were seen in the collagen hydrogel + AD-MSCs and fibrin hydrogel + AD-MSCs groups.

AD-MSCs encapsulated into fibrin and collagen hydrogels, as two of the most promising ECM-based or natural scaffolds have the potential to be developed in neural tissue engineering (NTE), such as for the treatment of SCI.

Animal spinal cord injury (SCI) models have provided a better perception of the mechanisms related to traumatic SCI and evaluation of the effectiveness of experimental therapeutic interventions.

The aim of this study is to develop a cost-effective modified Allen's device to induce contusive spinal cord injury.

Adult male Wistar rats were subjected to contusive spinal cord injury using a customized weight drop model through 10-g weights delivered from a 25-mm height onto an exposed spinal cord. Locomotor and sensory function during 28 days were assessed. Moreover, histopathological changes were assessed at one week and 28 days post SCI.

All the SCI rats showed hind limb paralysis up to 48 h post SCI and neuropathic pain after injury. Histological changes similar to the previous reports for contusion model were observed.

According to our findings, little variability was observed in the BBB score of individual rats at 28 days after injury. Our customized device to induce spinal cord injury is a simple and inexpensive alternative method to the highly sophisticated contusion device commonly used to induce SCI.

Spreading depolarization is associated with the extension of lesion size and complications in some important neurological diseases such as stroke, epilepsy, migraine, and traumatic brain injury.

This study aimed to reveal some molecular aspects of spreading depolarization and suggesting new therapeutic targets for its control by changing the function of different astrocytic and neuronal ion channels.

The effects of nortriptyline on spreading depolarization in cortical and hippocampal tissues and on the electrophysiological properties of CA1 hippocampal pyramidal neurons were assessed by extra- and intracellular recording, following washing rat brain slices by the drug.

Nortriptyline made a significant increase in the amplitude of spreading depolarization in cortical and hippocampal tissues relative to control but did not change the duration significantly in each of the tissues. No significant difference was found in the effects of spreading depolarization on the electrophysiological properties of the CA1 pyramidal neurons between nortriptyline and control groups.

The stimulating effect of nortriptyline on spreading depolarization is probably related to the augmentation of extracellular potassium collection in the cortex and hippocampus due to inhibition of astrocytic potassium scavenging function. This change can make more neurons prone to depolarization and increase the overall amplitude of spreading depolarization waves. Further studies should assess the effect of enhancing the clearance function of astrocyte-specific inwardly rectifying potassium channels, Kir4.1, or preventing other factors contributing to spreading depolarization on control of the process.

Cell culture is an important technique in cellular and molecular biology. There are two basic systems for culturing cells, adherent (monolayer) culture and suspension culture. In adherent cell culture, cellular adhesion molecules play a vital role in many physiological processes. Many cells, especially primary-obtained cells, hardly attach to plates, so coating agents are used for cell attachment and growth. There is no striking report on whether all cells need coated plates.

We investigated whether a coating plate is essential for primary spinal cord-obtained neuron culture.

Cells were separated and seeded in tissue culture plates coated with either Poly(L-lysine) or Poly(D-lysine), as well as without coating containing DMEM-F12 media with 10% FBS.

Interestingly, we found that neuron cells more potently attached to coating free plates.

These results provide strong evidence helping the researchers to optimize primary spinal cord cultures.

Plant extracts contain useful components that could be considered in pharmacotherapy. Due to containing anticancer components such as phenol, cyclotide, and anthocyanins, Viola odorata (sweet violet) is one of the most important components used in cancer therapy. The current study aimed at examining antitumor activity and related mechanisms to V. odorata on primary culture of human glioblastoma multiforme (GBM). It was observed that survival rate of the obtained astrocytes from human GBM tumor decreased with V. odorata hydroalcoholic extract (10 - 500 µg/mL) in a dose- and time-dependent manner and DNA fragmentation happened in concentrations above 100 µg/mL of this extract. Further observations revealed that induced apoptosis activates mitochondrial death pathway, release cytochorome C, and activates caspase-3. The current study findings revealed the effect mechanism of V. odorata extract and suggested its potential application in cancer therapy.

Olfactory ensheathing cells-based therapy for spinal cord injury (SCI) repair has been a possible treatment for clinical study because of their safety in autologous transplantation and potential regenerative capability. However, there are contradictory reports on the results after transplantation in animal models. The purpose of this research was to investigate the effect of acute transplantation of human mucosa-derived olfactory ensheathing cells (OECs) on the repair of the spinal cord. Human olfactory ensheathing cells were isolated from the human mucosa and cultured under supplemented neuronal cell culture medium. They were characterized by immunocytochemistry for olfactory ensheathing cell markers. We induced spinal cord injury at T8-T9 of rats by aneurysm clips and simultaneously injected two million OECs into subarachnoid space of spinal cord. Sensory and motor behaviors were recorded by tail-flick reflex (TFR) and BBB scores, respectively every week for seven weeks after injury. Morphology and S100-beta antigen expression in olfactory ensheathing cells of the human olfactory mucosa was confirmed by immunostaining. OECs transplantation did not recover inflammation, neuronal vacuolation, hemorrhage, and cyst formation. These findings suggest that OECs transplantation in this experimental setting did not lead to tissue regeneration to enhance locomotion. These results broaden current knowledge and are additions to the science and literature.

Many recent epidemiological studies have shown that epileptic patients are more likely suffer from depression, anxiety, and irritability. However, the cellular mechanisms of epilepsy-induced psychotic behaviors are not fully elucidated. Neurotrophin receptors have been suggested to be involved in epilepsy and also in psychiatric disorders. Up-regulation of p75NTR expression and activation of p75NTR signalling cascades after the seizure have been shown, but the role of the p75 receptor in epilepsy-induced psychotic behaviors has not been documented so far. Therefore, the present work aimed to investigate the effect of p75 receptor blockade on seizure activity, irritability, and anxiety-like behaviors in a rat model of status epilepticus.
Rats were injected with pilocarpine (350 mg/ kg, i.p.) to induce status epilepticus. Then various behavioral tests were performed after the blockade of p75NTR alone or in combination with p75 antagonist and phenobarbital. Molecular analysis by PCR was performed to investigate the expression of p75 and pro-NGF.
Molecular findings indicated a high level of mRNA expression for both p75 receptors and pro-NGF in the epileptic model group. Results also showed that the administration of p75 antagonist alone or in combination with phenobarbital was able to significantly influence the behavioral responses. Furthermore, 20-hours video monitoring showed a decrease in the frequency and duration of seizures in the rat group receiving p75 antagonist.
Taken together, the present study suggests that the blockade of the p75 receptor may affect the irritability and anxiety-related behavior in a rat model of status epilepticus.

Despite the infectiveness of conventional anti-epileptic drugs (AEDs) in refractory focal epilepsy, surgery along with medications, as the only treatment, was not successful in 30% of the cases. Recently, cysto- and histo-physiological investigations revealed the role of gamma-aminobutyric acid (GABA)-ergic system in etiopathology of temporal lobe epilepsy (TLE). Studies reported that the inhibitory action of GABA neurotransmitter due to elevated intracellular Cl-concentration through abnormal expression of Na-K-Cl cotransporter (NKCC)-1 became excessive in recurrent seizures. These primary results were confirmed in the brain tissue obtained from patients with TLE. Based on the evidence, the current study suggested the administration of bumetanide, an NKCC1 inhibitor, as a potential candidate for the treatment of intractable TLE. The previous study by authors showed a significant reduction in seizural activity of 2 out of 3 patients with TLE following the administration of bumetanide. However, result of the current study showed the control of seizure in the 3rd case of previous study by the administration of bumetanide as an adjuvant to AEDs. Moreover, his AEDs dosage after discontinuation of Bumetanide tapered without any relapse.

The mechanism of putative cytotoxicity of 4-[3-(cyclopentyloxy)-4-methoxyphenyl]-2-pyrrolidone (rolipram), a specific phosphodiesterase-4 (PDE4) inhibitor, on glioblastoma multiforme (GBM) is almost unknown. This study aimed to investigate the role of protein kinase B (Akt) pathway in the cytotoxic effect of rolipram on human GBM U87 MG cell line and tumor-initiating cells (TICs) isolated from patient's GBM specimen.
TICs were characterized by using flow cytometry and quantitative real-time PCR. The cells were treated with rolipram at inhibitory concentration of 50% (IC50) in the presence or absence of SC79 (4µg/mL), a specific AKT activator, for 48 hours. The cell viability and apoptosis were measured by MTT assay and TUNEL staining, respectively. The relative expression of Phospho-Akt (Ser473), matrix metalloproteinase 2 (MMP2), and vascular endothelial growth factor A (VEGFA) were detected using Western blotting.
The findings showed that rolipram could suppress cell viability in both U87MG and TICs, dose-dependently. Interestingly, the rolipram-induced cytotoxicity was significantly reduced in the presence of SC79. Nevertheless, in rolipram-treated cells, the pretreatment with SC79 significantly led to increase in U87 MG cells and TICs apoptosis and decrease in viability of U87 MG cells but not TICs relative to corresponding control. In U87 MG and TICs, rolipram-induced reduction of Phospho-Akt (Ser473) and MMP2 levels were significantly suppressed by SC79.
There is a cell type-specific mechanism of anti-proliferative action of rolipram on GBM cells. The reduction of intracellular level of MMP2 but not VEGFA by rolipram is conducted through the inhibition of Akt signal. Rolipram-induced apoptosis is mediated via Akt dependent/independent mechanisms.

Although the etiology of schizophrenia is unknown, it has a significant genetic component. ýA number of studies have indicated that neuregulin-1 (NRG1) gene may play a role in the ýpathogenesis of schizophrenia. In this study, we examined whether the rs2439272 of NRG1 ýis associated with schizophrenia and its negative symptoms in an Iranian population.ý
Rs2439272 was genotyped in 469 participants including 276 unrelated patients with schizophrenia and 193 healthy controls. The association of genetic risk with PANSS, and negative ýsymptoms was examined in the total, male and female samples. COCAPHASE and ýCLUMP22 programs were used to compare the allele and genotype frequencies, and ýgeneral linear regression was used to analyze the quantitative dependent variables by the ýselected variant.ý
In this study, it was revealed that the G allele of rs2439272 might be an allele with the ýincreased risk of developing schizophrenia, especially in the male participants. In addition, ýsignificant differences were found between the G allele and GG genotype frequencies and ýPANSS, and negative symptoms in the total and male participants.ý
Our results supported the association between rs2439272 in NRG1 gene and risk of ýschizophrenia and its negative symptoms in an Iranian population.

Transforming Growth Factor-Beta 1 (TGF-β1) is a pleiotropic cytokine with potent anti-inflammatory property, which has been considered as an essential risk factor in the inflammatory process of Ischemic Stroke (IS), by involving in the pathophysiological progression of hypertension, atherosclerosis, and lipid metabolisms. -509C/T TGF-β1 gene polymorphism has been found to be associated with the risk of IS. The aim of this meta-analysis was to provide a relatively comprehensive account of the relation between -509C/T gene polymorphisms of TGF-β1 and susceptibility to IS.
Male Wistar rats were divided into sham (receiving phosphate buffered saline within dorsal hippocampus), pilocarpine (epileptic model of TLE), single injection BDNF (epileptic rats which received single high dose of BDBF within dorsal hippocampus), and multiple injections BDNF (epileptic rats which received BDNF in days 10, 11, 12, and 13 after induction of TLE) groups. Their electrocorticogram was recorded and amplitude, frequency, and duration of spikes were evaluated.
Amplitude and frequency of epileptiform burst discharges were significantly decreased in animals treated with BDNF compared to pilocarpine group.
Our findings suggested that BDNF may modulate the epileptic activity in the animal model of TLE. In addition, it may have therapeutic effect for epilepsy. More studies are necessary to clarify the exact mechanisms of BDNF effects.

Malignant astrocytic gliomas are the most common and lethal brain malignancies due to their refractory to the current therapies. Nowadays, molecular targeted therapy has attracted great attention in treatment of glioma. Connexin 43 (Cx43) and micro ribonucleic acid- 21(miR-21) are among molecules that are involved in glioma development and progression. These molecules showed potential to be as target molecules with regard to glioma. Some studies have reported that cyclic adenosine monophosphate (cAMP) signaling could be effective on Cx43 and miR-21 in tissues other than in brain. We investigate possible relationship between β-adrenergic receptor and its newly described downstream, exchange protein directly activated by cAMP (Epac) signaling pathway and expression of Cx43 and miR-21 in low (1321N1) and high grade (U87MG) glioma cell lines. We treated cells with β-adrenergic agonist and Epac activator with and without adenyl cyclase inhibitor. Cx43 and miR-21 expression were measured with real-time PCR. Our data showed that in 1321N1 cells, β-adrenergic-Epac pathway stimulation up and down-regulated Cx43 and miR-21 expression respectively. Whereas, in U87MG cells these interventions had no effect on Cx43 and miR-21 expression. These findings demonstrate that low grade astrocytoma cells have better response to our pharmacological interventions.

Recent studies have shown that astrocytes play major roles in normal and disease condition of the central nervous system including multiple sclerosis (MS). Molecular target therapy studies in MS have revealed that connexin-43 (Cx43) and Aquaporin-4 (AQP4) contents of astrocytes undergo expression alteration. Fluoxetine had some effects in MS patients unrelated to its known antidepressant effects. Some of fluoxetine effects were attributed to its capability of cAMP signaling pathway stimulation. This study aimed to investigate possible acute effects of fluoxetine on Cx43 and AQP4 expression in astrocyte. Astrocytoma cells were treated for 24 hours with fluoxetine (10 and 20 μg/ml) with or without adenyl cyclase (AC) and protein kinase A (PKA) inhibition. Cx43 expression at both mRNA and protein levels and AQP4 expression at mRNA level were evaluated. Acquired results showed that fluoxetine with and without AC and PKA inhibition resulted in Cx43 up-regulation both in mRNA and protein levels, whereas AQP4 expression have not changed. In conclusion, data showed that fluoxetine alone and in the absence of serotonin acutely up-regulated Cx43 expression in astrocytes that can be assumed in molecular target therapy of MS patients. It seems that cAMP involvement in fluoxetine effects need more researches.

Transient receptor potential vanilloid 1 (TRPV1) belongs to a family of ligand gated ion channels. This non-selective cation channel is permeable to Na, K and highly to Ca2 ions. It acts as a trigger for Ca2 mediated cell signaling. Although this channel has been previously found highly expressed in dorsal root ganglion, there is a line of evidence indicating the remarkable expression of TRPV1 channels in other parts of the central nervous system.
There is evidence to suggest that TRPV1 channels in the brain contribute in many basic neuronal functions, including neurotransmitter release and synaptic plasticity.

Context: Parkinson''s disease (PD) is one of the common neurodegenerative disorders, characterized by the gradual loss of dopamine (DA) containing neurons in the substantia nigra. It is currently treated by L-DOPA and DAergic drugs. Although these treatments are very effective in the beginning of the disease, but they are not curative and have side effects in chronic use.. Evidence Acquisitions: The aim of cell replacement therapies for PD is looking for a long-lasting relief of patients’ symptoms. Different sources of stem cells are recruited to establish a long lasting treatment for PD. We have categorized them into embryonic stem cells from the fertilized egg, neural stem cells from the embryonic or adult brain, mesenchymal stem cell, and stem cells from other tissues. In this review we used three key words «Parkinson''s disease, stem cells and neostriatum transplantation» to search in «PubMed» search engine. We found more than hundreds of publications but limitation for citation led us to select only those that were more innovative.. Cell replacement therapies in PD aim to provide greater long-lasting relief of patients’ symptoms. Although the transplants survive, reinnervate the striatum, and generate adequate symptomatic relief in some patients yet side effects are still major concern.. This article reviewed different sources of cell used in transplantation and focused on their advantages and disadvantages in transplantation studies..