mohammad javad eslamizade

Non-invasive brain stimulation technologies are a group of powerful tools that are exploited in manipulating functional properties of the brain. These technologies have a relatively long history in cognitive enhancement and rehabilitation, as well as in treating stress and depression. Of these technologies are transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS). TMS technology works with producing magnetic fields emitted from a coil over the scalp to induce ion currents; however, in tDCS there is a direct connection of electrodes on the skin over the scalp to inject electrical currents yielding modulation in neural circuits.
In this review, we reviewed over the literature concerning applications of neurotechnologies, TMS and tDCS, in cognitive enhancement and rehabilitation.

Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders, which has much benefited from animal models to find the basics of its pathophysiology. In our previous work (Haghani, Shabani, Javan, Motamedi, & Janahmadi, 2012), a non-transgenic rat model of AD was used in electrophysiological studies. However, we did not investigate the histological aspects in the mentioned study. An AD model was developed through bilateral injection of amyloid-β peptides (Aβ) into the frontal cortices. Behavioral and histological methods were used to assess alterations in the memory and (ultra)structures. Furthermore, melatonin has been administered to assess its efficacy on this AD model. Passive avoidance showed a progressive decline in the memory following Aβ injection. Furthermore, Nissl staining showed that Aβ neurotoxicity caused shrinkage of the CA1 pyramidal neurons. Neurodegeneration was clearly evident from Fluoro-jade labeled neurons in Aβ treated rats. Moreover, higher NF-κB immunoreactive CA1 pyramidal neurons were remarkably observed in Aβ treated rats. Ultrastructural analysis using electron microscopy also showed the evidence of subcellular abnormalities. Melatonin treatment in this model of AD prevented Aβ- induced increased NF-κB from immunoreaction and neurodegeneration. This study suggests that injection of Aβ into the frontal cortices results in the memory decline and histochemical disturbances in CA1 pyramidal neurons. Furthermore, melatonin can prevent several histological changes induced by Aβ.

Resveratrol, a phytoalexin, has a wide range of desirable biological actions. Despite a growing body of evidence indicating that resveratrol induces changes in neuronal function, little effort, if any, has been made to investigate the cellular effect of resveratrol treatment on intrinsic neuronal properties. This experimental study was performed to examine the acute effects of resveratrol (100 μM) on the intrinsic evoked responses of rat Cornu Ammonis (CA1) pyramidal neurons in brain slices, using whole cell patch clamp recording under current clamp conditions. Findings showed that resveratrol treatment caused dramatic changes in evoked responses of pyramidal neurons. Its treatment induced a significant (P<0.05) increase in the after hyperpolarization amplitude of the first evoked action potential. Resveratrol-treated cells displayed a significantly broader action potential (AP) when compared with either control or vehicle-treated groups. In addition, the mean instantaneous firing frequency between the first two action potentials was significantly lower in resveratrol-treated neurons. It also caused a significant reduction in the time to maximum decay of AP. The rheobase current and the utilization time were both significantly greater following resveratrol treatment. Neurons exhibited a significantly depolarized voltage threshold when exposed to resveratrol. Results provide direct electrophysiological evidence for the inhibitory effects of resveratrol on pyramidal neurons, at least in part, by reducing the evoked neural activity.

Resveratrol (3,5,4-trihydroxystilbene) a non-flavonoid polyphenol found in some plants like grapes, peanuts and pomegranates, possesses a wide range of biological effects. Evidence indicates that resveratrol has beneficial effects on nervous system to induce neuroprotection. However, the cellular mechanisms of the effects are not fully determined. In the present study, the cellular actions of resveratrol on intrinsic electrophysiological properties of the rat hippocampal CA1 pyramidal neurons were examined. The spontaneous and evoked firing properties of CA1 pyramidal neurons in adult rats exposed to resveratrol (100 µM) were examined using whole cell patch clamp recording under current clamp condition and the results were compared with control and vehicle treated groups. Treatment with resveratrol caused changes in neuronal firing characteristics. Application of resveratrol shifted the resting membrane potential (RMP) toward hyperpolarizing voltage (from -58.62±0.89 mV in control to -67.06±0.89 mV after resveratrol). The after hyperpolarization potential (AHP) amplitude was significantly (P < 0.001) increased following extracellular application of resveratrol. In addition, resveratrol treatment caused changes in evoked responses of pyramidal neurons. Its treatment induced a significant (P<0.05) increase in the peak amplitude of action potential in response to 100-300pA depolarizing current pulses. Furthermore, resveratrol-treated neurons displayed a significantly (P<0.05) increased time to peak in response to 400 and 500 pA depolarizing currents, when compared with either control or vehicle-treated groups. In addition, rise time to half-amplitude, rise tau and decay tau of action potential were significantly (P<0.01, P<0.01 and P<0.01, respectively) increased following resveratrol application. Resveratrol treatment changes the action potential parameters, hyperpolarizes the RMP and reduces the neuronal excitability and probably thereby may induce neuroprotective effects.

Manipulating the function of neural cells via electrophysiology and pharmacological agents in neuroscience research have long been interesting in unraveling the function of neural circuits, behavior, and attributed disorders. The power of electrophysiology and pharmacologic methods in the manipulation of neural cells varies and therefore researchers have been attempting to enhance their knowledge in this field in recent two decades. Optogenetics has the advantage to take under control both the temporal and spatial resolution in manipulating desired neural cells. In optogenetics, control over the function of neural cells is possible through shining the light onto the cells that bear light sensitive molecules.
Optogenetics come to help the researchers to know how the neural cells, circuits, and systems work and there is an attempt to move toward the treatment of nervous system disorders by this technology. In this article, I reviewed optogenetics and its potential clinical applications.

Some lines of evidences demonstrate that opioids are involved in water and food intake. On the other hand the dopaminergic mesolimbic system that consists of ventral tegmental area (VTA), nucleus accumbens (NAc) and medial prefrontal cortex is considered to be crucial in the rewarding actions of opiates. There are also reports showing that this system has some roles in appetite and drinking behaviors. The aim of this study was to investigate the effects of morphine self- administration on food and water intake in rats.Male Wistar rats were first trained to receive small pellets of food by pressing active lever in self-administration apparatus. Rats were anaesthetized with ketamine and their jugular vein was cannulated. After recovery the animals were placed in self-administration apparatus and allowed to self-administer morphine (0.5 mg in 0.1 ml per infusion, in morphine group) or 0.1 ml saline (in saline group) during 10 consecutive days for 2 h /sessions. The amount of 24 h water and food intake during the last 3 days compared between saline and morphine groups. The results showed that water and food intake in morphine group in days 8, 9 and 10 was lower than saline group. This study indicates that morphine self - administration alters food intake and drinking water but the exact mechanism(s) need to be more investigated.