● There are several animal models of absence epilepsy.
● It seems that genetic models are more valid than chemical models.
● WAG/Rij rats as one of genetic model of absence epilepsy have most similarity to human absence epilepsy.

Plain Language Summary 
We studied arious laboratory models of absent epilepsy. Typical absence seizures are defined behaviorally by a paroxysmal loss of consciousness without aura or postictal mood and accompanied with bilateral synchronous spike and wave discharges (SWDs). This study helps young students and researchers to select a suitable model for their research by reviewing and validating the models that we have discussed in this article.

● The arcuate nucleus inhibition increased thermal nociception.
● Administrating insulin within the arcuate nucleus decreased the acute thermal pain perception.
● Streptomycin-induced diabetes makes thermal hypoalgesia.
● Pain response latency progressively increased over time after induction of diabetes.
● Intra-arcuate injection of insulin reduced the latency of thermal nociception in streptomycin-induced diabetes. 

Plain Language Summary 
The arcuate nucleus is a part of the ventral hypothalamus. It secrets endogenous opioids and projects to several parts of the brain involved in pain perception. The arcuate nucleus contains insulin receptors, and it seems that insulin can excite its neuron to secret the endogenous opioids. In type 1 diabetes, insulin secretion decreases. Accordingly, it appears that the arcuate nucleus excitation decreases because of insulin reduction. The present study illustrated that the arcuate nucleus inhibition by lidocaine increases pain feeling, so this nucleus is a pivotal part of pain sensation. Insulin injection inside the arcuate nucleus reduces pain sensation in healthy rats. Also, type 1 diabetes decreases pain sensation, but insulin injection within the arcuate nucleus increases it. This phenomenon is contrary to the results observed in healthy rats. Therefore, it seems that different mechanisms affect arcuate nucleus neurons in healthy and diabetic rats.

● Respiration and heartbeat as physiological functions affect the spinal cord functional Magnetic Resonance Imaging (fMRI) data.
● Physiological noise correction in spinal fMRI increases the activated voxels in the spinal cord as true positive, and decreases the activated voxels in cerebrospinal fluid and surrounded tissues.
● Respiration function correction has a significant role in the reduction of physiological noise in thoracolumbar spinal cord fMRI, compared to cardiac function
effect correction.

Plain Language Summary 
During the last decades, functional MRI has become a powerful tool in discovering complicated cognitive functions and diagnosing neurological problems. Recently, spinal cord fMRI is introduced to investigate sensory and motor pathways to detect functions of the central nervous system. As it has several confounding factors, including the physiological noise, spinal cord fMRI is encountered as a challenging methodology. Two of the main sources of noise in spinal cord fMRI, which affect the activation map, are respiration and heartbeat. In this study, we assessed the effects of each of these noise sources, separately. We also integrated them in thoracolumbar and lumbar regions, where most of the noise effects exist. Our results suggest that correction of the heartbeat would result in a greater effect on the activated voxels in the spinal cord, comparing with respiration noise correction. Also, we have shown that integration between these two corrections may increase the precision of fMRI activation maps. It is worth mentioning that this study is the first of its kind to investigate the effect of different noises in thoracolumbar and lumbar regions.

● We report on the effect of pelvic floor muscles biofeedback in the treatment of coccydynia for the first time. 
● Coccydynia significantly affects patients’ function and quality of life without any accepted treatment.
● According to the reputable theory of pelvic floor muscle dysfunction as one of the most important etiologies of coccydynia, manual therapies have been proposed as the first line of treatment. 
● Pelvic floor muscles biofeedback would be a new and safe treatment option in this area.
● The paper should be of interest to readers in the areas of the importance of the issue and the novelty of the treatment approach.

Plain Language Summary 
Coccydynia is a painful condition that is felt in the coccyx area. Its prevalence in women is five times more than in men. The most common type of trauma is falling back in a sitting position. Repeated minor trauma for example due to prolonged sitting in an inappropriate position is also mentioned as an important cause of coccydynia. Biofeedback is a method of gaining control and strengthening the muscles. In this study, we aimed to investigate the effect of adding pelvic floor biofeedback to topical anti-inflammatory drug injection plus pelvic floor muscle exercises in patients with coccydynia. In the end, we have concluded that adding biofeedback to pelvic floor muscles exercises did not lead to any further improvement in pain and quality of life in patients with chronic coccydynia.

● CoQ10 deficiency plays a role in the pathogenesis of Epileptic Seizure (ES). 
● Decrement of CoQ10 level in ES may be contributed to an increase in the frequency and duration of the seizure.
● There is no association between the type of seizure and CoQ10 levels in epileptic patients. 

Plain Language Summary 
Decreasing antioxidants plays an important role in the pathogenesis of epilepsy. Coenzyme Q10 (CoQ10) is a strong endogenous antioxidant that protects the body against several diseases; however, the impact of CoQ10 in epilepsy is unclear. We evaluated the serum concentration of CoQ10 to test if there is any relationship between CoQ10 levels and clinical manifestation of seizure. We found that the levels of CoQ10 in epileptic patients were significantly lower compared to healthy volunteers. We also found that the clinical manifestation of the seizure (duration of epilepsy and seizure frequency) were negatively correlated with serum CoQ10 levels.

● The ventral tegmental area participates in the control of regular feeding.
● Microinjection of SKF38393 in the ventral tegmental area increases regular food intake.
● Ventral tegmental area D1-like and or serotonergic receptors may be involved in regulatory pathways.

Plain Language Summary 
The Ventral Tegmental Area (VTA) has an essential role in food reward. For the first time, we showed that SKF38393 (a D1-like dopamine or serotonergic receptors agonist) increases regular food intake in a dose-dependent manner. Also, it does not affect locomotor activities. Our results suggest that VTA dopaminergic or serotonergic pathways may be involved in the homeostatic regulation of food intake. Based on the present findings, it is essential to understand the VTA mechanisms involved in regular food intake and its possible use in treating eating disorders.

● Short-term memory impairment and retrieval deficit in combination with anxiety-like behavior were observed 8 weeks after the onset of diabetes.
● Biochemical changes of impaired glycosylated hemoglobin (HgbA1c) and serum insulin level were observed in diabetic rats.
● Cellular changes in decreased mitochondrial membrane potential in the hippocampus were observed in diabetic rats.
● Molecular changes of increased kinesin (KIF5b) gene expression levels in the hippocampus were observed in diabetic rats.
● After 8 weeks of insulin injection, KIF5b gene expression levels were reversed.

Plain Language Summary 
Diabetes Mellitus (DM) is strongly associated with degenerative and functional disorders in the Central Nervous System (CNS). One of the most chronic complications of DM in CNS is “diabetic encephalopathy.” According to the definition, any cognitive impairment affected by diabetes is called diabetic encephalopathy and or type 3 diabetes mellitus (T3DM). Several studies show mitochondrial dysfunction in different regions of the brain. Also, mitochondrial movement and transport are disrupted in diabetic condition. The mechanisms underlying those impairments are still unknown. In this work, we evaluated the effect of diabetic encephalopathy on mitochondrial function and transport by studying the proteins (KIF5b & dynein) that are involved in axonal transport of mitochondria in male rats. After 8 weeks of induction of diabetes (by a single dose of STZ), the animals were monitored by behavioral test (elevated plus maze, Y-maze, and passive avoidance learning), biochemical parameters (HgbA1c and insulin), and mitochondrial function and transport using rhodamine 123 staining and real-time PCR. We showed that diabetic encephalopathy resulted in cognitive decline and mitochondrial dysfunction by decreased Mitochondrial Membrane Potential (MMP) and kinesin gene overexpression. We suggested that abnormal translocation of mitochondria and its malfunction induced by kinesin gene overexpression possibly resulted in cognitive and memory impairment in diabetic encephalopathy.

● Treatment with dalteparin improved the cognitive dysfunctions and symptoms of Alzheimer’s disease in STZ-induced diabetic.
● This is applicable by appropriately modulating and reducing oxidative stress and neuroinflammation. 
● This may promote the existing knowledge of therapeutics to reduce cognitive impairment in diabetes and may be a proper substitute to insulin therapy.

Plain Language Summary 
Hepcidin is the principal modulator of systemic iron metabolism, and its role in the brain has been clarified recently. Studies have shown hepcidin plays a twofold role for in neuronal iron load and inflammation. The findings indicated that treatment with dalteparin (anti-hepcidin) improved the cognitive dysfunctions in STZ-induced diabetic rats by appropriately modulating and reducing oxidative stress and neuroinflammation. This may include therapeutics to reduce cognitive impairment in diabetes and maybe a proper substitute for insulin therapy.

● Ischemic and hemorrhagic stroke differ by the temporal dynamics of cell-free DNA (cfDNA) accumulation. 
● In hemorrhagic stroke, an initial increase in cfDNA, most likely reflects an extent of the tissue damage
● In ischemic patients, the apoptotic cfDNA increase in parallel with the damage caused by hypoxia and subsequent compensatory reperfusion. 
● An optimal assessment windows with maximum differentiating power for stroke outcomes is 24-48 hours post-event for ischemic stroke, and as close as possible to the moment of hospital admission for hemorrhagic stroke.

Plain Language Summary 
Acute cerebrovascular accidents are a prominent cause of death worldwide and are the leading cause of long-term disability. Stroke is a phenotypically, various disease. The outcome of acute cerebrovascular accidents is largely determined by the timeliness and adequacy of treatment, which is fundamentally different in patients with ischemic and hemorrhagic stroke. Cell-free DNA is released from apoptotic and necrotic cells, and its fragments circulate in the blood until cleared by DNA hydrolyzing enzymes. In plasma, cell-free DNA is represented by fragments of various sizes, with the most common fragment length corresponding to the nucleosome's size and reflecting its apoptotic origin. LmwDNA samples were isolated from plasma and cerebrospinal fluid by phenol deproteinization; they were analyzed by gradient polyacrylamide electrophoresis and were quantified by spectrophotometry. Two common types of stroke, ischemic and hemorrhagic, differ by the temporal dynamics of cell-free DNA accumulation. In hemorrhagic stroke, an initial increase in lmwDNA levels most likely reflects an extent of the tissue damage. In contrast, in ischemic patients, the lmwDNA levels increase in parallel with the damage caused by hypoxia and subsequent compensatory reperfusion. These time-course data specify optimal assessment windows with maximum differentiating power for stroke outcomes: 24-48 hours post-event for ischemic stroke, and as close as possible to the moment of hospital admission for hemorrhagic stroke. These data also indicate the role of apoptosis in the formation of ischemic focus.

● ABR thresholds rose after common carotid arteries occlusion.
● Abnormal electrocochleography results were observed in the first few days.
● Biochemical results confirmed the electrophysiological finding.

Plain Language Summary 
This study showed that the auditory threshold (auditory brainstem thresholds) significantly increased after common carotid arteries occlusion on the first, fourth, and seventh days after surgery. The electrocochleography test showed the hydrops in cochlea were abnormal at 75%, 70%, and 85% on the first, fourth, and seventh days after surgery, respectively. Biochemical results also confirmed these results. This study showed that bilateral common carotid artery occlusion increases cochlear oxidative stress and induces a hearing loss in rats.

● Hippocampal rapid kindling decreased seizure latency and increased seizure duration of stages 4 and 5.
● The latency time of stages 4 and 5 seizure increased after the application of sodium valproate combined with low-frequency electrical stimulation.
● The seizure duration of stages 4 and 5 seizure declined after the application of sodium valproate with low-frequency electrical stimulation.

Plain Language Summary 
Some patients do not successfully respond to the antiepileptic drugs in refractory epilepsy. The interaction between antiepileptic drugs and brain electrical stimulation is a potential therapy to control seizures in patients with pharmacoresistance to drugs. Our findings demonstrated that the application of sodium valproate with low-frequency electrical stimulation may have a critical role in the antiepileptic effects of sodium valproate.

● Second Language (L2) proficiency significantly affects the first language (L1)-like processing of L2 violations.
● Components close to N400 showed conscious syntactic processing in low proficiency. 
● Components close to P600 showed automatic syntactic processing in high proficiency.
● L2 semantic violations activate similar areas as L1 in low proficiency. 
● L2 semantic violations activate different areas from L1 in high proficiency.  

Plain Language Summary 
This study examined the underlying brain mechanisms responsible for the first language (L1) and second language (L2) syntactic and semantic processing. Proficiency level, age of acquisition, and type of learning/context are three significant factors accounting for the differences between L1 and L2 processing. According to the declarative/procedural (DP) memory model, drawing on the procedural memory system, syntactic processing in L1 is automatic and unconscious. Aspects of L1 semantics related to the facts and meaning of words are processed in an explicit conscious manner through the declarative memory system. However, in L2, the syntax is initially processed consciously as rules are just learned. Practice and increased proficiency lead to automatic and less conscious L2 syntax processing.  Adult Persian-English bilinguals of high and low proficiency levels in English as their L2 were compared based on the components extracted from their processing of syntactic and semantic violations. Unlike native speakers, low proficient subjects relied on their declarative memory for processing L2 syntax as they needed more practice to process automatically. Several brain areas, similar to those observed for L1, were activated during L2 syntactic processing in high-proficient subjects addressing their reliance on the procedural memory system for automatic processing. Findings were opposite for the semantic processing. This finding shows that L2 learners initially draw on the concepts and semantic processing mechanism of their L1. With an increase in their L2 proficiency, diverging areas are activated as an independent meaning system is built for the L2.