Journal of Integrative Neuroscience

Magnetoencephalographic (MEG) recordings of the brain in Parkinson’s disease were obtained in order to look for possible effect of pico-Tesla transcranial magnetic stimulation (pT-TMS). We found a significant effect of an increase of frequencies in the range of 2–7 Hz across subjects. In addition, we observed the mean peak frequency difference within the 2–7 Hz band towards frequencies of less or equal to those frequencies of the alpha frequency range (8–13 Hz).

Calcium signaling is important for synaptic plasticity, generation of brain rhythms, regulating neuronal excitability, data processing and cognition. Impairment in calcium homeostasis contributed to the development of psychiatric disorders such as bipolar disorder (BP). MCU is the most important calcium transporter in mitochondria inner membrane responsible for influx of Ca${}^{2+}$. MICU1 is linked with MCU and has two canonical EF hands that are vital for its activity and regulates MCU-mediated Ca${}^{2+}$ influx. In the current study, we aimed to investigate the role of genetic alteration of EF hand calcium binding motifs of MICU1 on the development of BP. We examined patients with BP, first degree relatives of these patients and healthy volunteers for mutations and polymorphisms in EF hand calcium binding motifs of MICU1. The result showed no SNP/mutation in BP patients, in healthy subjects and in first degree relatives. Additionally, alignment of the EF hand calcium binding regions among species (Gallus-gallus, Canis-lupus-familiaris, Bos-taurus, Mus-musculus, Rattus-norvegicus, Pan-troglodytes, Homosapiens and Danio-rerio) showed exactly the same amino acids (DLNGDGEVDMEE and DCDGNGELSNKE) except in one of the calcium binding domain of Danio-rerio that there was only one difference; leucine instead of Methionine. Our results showed that the SNP on EF-hand Ca${}^{2+}$ binding domains of MICU1 gene had no effect in phenotypic characters of BP patients.

It was suggested that muscarinic, and nicotinic receptors increase free Ca${}^{2+}$ levels in the facial nerve nucleus via various channels following facial nerve injury. However, intracellular Ca${}^{2+}$ overload can trigger either necrotic or apoptotic cell death. It is assumed that, following facial nerve injury, the interactions of nicotinic and muscarinic acetylcholine receptors in facial nerve nucleus may negatively regulate free Ca${}^{2+}$ concentrations in the facial nerve nucleus, which provide important information for the repair and regeneration of the facial nerve. The present study investigated the regulatory effects of nicotine on muscarinic receptor-mediated free calcium ion level changes in the facial nucleus in a rat model of facial nerve injury at 7, 30, and 90 days following facial nerve injury using laser confocal microscopy. The dose-dependent regulation of nicotine on muscarinic receptor-mediated free calcium ion level changes in the facial nucleus may decrease the range of free Ca${}^{2+}$ increases following facial nerve injury, which is important for nerve cell regeneration. It is concluded that the negative effects of nicotine on muscarinic receptors are related to the ${\alpha }_4{\beta }_2$ subtype of nicotinic receptors.

This work purpose was to estimate the implication of suspected adrenal function deficiencies, which was influenced by oxidative stress (OS) that are generating brain plasticity, and reorganization of the functional control. This phenomenon was revealed in two-hemodialysis patients described in this paper. Blood oxygenation level dependent functional magnetic resonance imaging (BOLD-fMRI) revealed a significant activation of the motor cortex. Hemodialysis seems to originate an inflammatory state of the cerebral tissue reflected by increased OS, while expected to decrease since hemodialysis eliminates free radicals responsible for OS. Considering adrenal function deficiencies, sensitivity to OS and assessed hyponatremia and hypercalcemia, adrenal function deficiencies is strongly suspected in both patients. This probably contributes to amplify brain plasticity and a reorganization of functional control after hemodialysis that is compared to earlier reported studies. Brain plasticity and functional control reorganization was revealed by BOLD-fMRI with a remarkable sensitivity. Brain plastic changes are originated by elevated OS associating indices of adrenal function deficiencies. These results raise important issues about adrenal functional deficiencies impact on brain plasticity in chronic hemodialysis-patients. This motivates more global studies of plasticity induced factors in this category of patients including adrenal functional deficiencies and OS.

Doose and Lennox–Gastaut (syndromes) are rare generalized electroclinical affections of early infancy of variable prognosis which manifest with very diverse kinds of seizures. Very frequently, these types of epilepsy become drug resistant and finding reliable treatment results is very difficult. As a result of this, fighting against these syndromes becomes a long term (or endless) event for the little patient, the neurologist and the parents. A lot of Electroencephalographic (EEG) records are so accumulated during the child’s life in order to monitor evolution and correlate it with medications. So, given a bunch of EEG, three questions arise: (a) On which year was the child healthier (less affected by seizures)? (b) Which area of the brain has been the most affected? (c) What is the status of the child with respect to others (which also have a bunch of EEG, each)? Answering these interrogations by traditional scrutinizing of the whole database becomes subjective, if not impossible. We propose to answer these questions objectively by means of time series entropies. We start with our modified version of the Multiscale Entropy (MSE) in order to generalize it as a Bivariate MSE (BMSE) and from them, we compute two indices. All were tested in a series of patients and coincide with medical conclusions. As far as we are concerned, our contribution is new.

The complex nature of neuronal interactions of the human brain has posed many challenges to the research community. To explore the underlying mechanisms of neuronal activity of cohesive brain regions during different cognitive activities, many innovative mathematical and computational models are required. This paper presents a novel Common Functional Pattern Mining approach to demonstrate the similar patterns of interactions due to common behavior of certain brain regions. The electrode sites of EEG-based functional brain network are modeled as a set of transactions and node-based complex network measures as itemsets. These itemsets are transformed into a graph data structure called Functional Pattern Graph. By mining this Functional Pattern Graph, the common functional patterns due to specific brain functioning can be identified. The empirical analyses show the efficiency of the proposed approach in identifying the extent to which the electrode sites (transactions) are similar during various cognitive load states.

Aggregation of amyloid $\beta$ protein (A$\beta )$ and progressive loss of memory are the main characteristics of Alzheimer’s disease (AD). It is noteworthy that approximately 40% of AD patients have depressive symptom. The close correlation between cognitive deficits and mental depression suggests a possibility that antidepression treatment might be beneficial to cognitive improvement in AD. The present study, by using tail-suspension test (TST), forced swimming, alternative electro-stimulus Y maze test and immunohistochemistry, examined the neuroprotective effects of desipramine, a newer generation tricyclic antidepressants (TCA), and investigated its possible molecular mechanism. The results showed that: (1) intra-hippocampal injection of A${\beta }_{1-42}$ induced depression-like behavior and associative learning deficits in mice, with an increased mean immobility time in tail-suspension and forced swimming test and an increased mean error times in Y maze test; (2) after treatment with desipramine (10mg/kg, i.p.), the average immobility time significantly decreased, from $101.60\pm 8.37$s in A${\beta }_{1-42}$ group to $57.7\pm 9.31$s in A${\beta }_{1-42}$ plus desipramine group ($n=10,p<0.05$) in TST and from $184.70\pm 6.52$s to $144.13\pm 8.63$s ($n=8$ or 9, $p<0.05$) in forced swimming test, respectively;the mean error times of mice in Y maze test also significantly decreased, from $6.50\pm 2.95$ in A${\beta }_{1-42}$ group to $4.90\pm 3.11$ in A${\beta }_{1-42}$ plus desipramine group ($n=10$, $p<0.05$); (3) desipramine administration significantly prevented against A${\beta }_{1-42}$-induced down-regulation of phosphorylated cAMP response element binding protein (p-CREB) in the hippocampus. These results indicate that A${\beta }_{1-42}$ could concurrently mimic the depression-like behavior and working memory disorder in mice, while desipramine could effectively reverse both the deficits induced by A${\beta }_{1-42}$. The neuroprotection of desipramine may be involved in the up-regulation of p-CREB level in the hippocampus of mice.

The present study investigates action potential abnormalities in previously simulated cases of amyotrophic lateral sclerosis, termed as ALS1, ALS2 and ALS3, respectively, when the temperature is changed from 20${}^{\circ }$C to 42${}^{\circ }$C. These ALS cases are modeled as three progressively severe axonal abnormalities. The effects of temperature on the kinetics of currents, defining action potentials in the normal and abnormal cases, are also given and discussed. These computations use our temperature-dependent multi-layered model of human motor nerve fibers. The results show that the classical “transient” sodium current ($I_{\mathrm{\text{Na}}}$) contributes mainly to the nodal action potential generation in the normal and abnormal cases for the temperature range of 20–39${}^{\circ }$C, as the contribution of fast and slow potassium currents ($I_{\mathrm{\text{Kf}}}$ and $I_{\mathrm{\text{Ks}}}$) to the total ionic current ($I_i$) is negligible. However, the contribution of $I_{\mathrm{\text{Ks}}}$ and $I_{\mathrm{\text{Kf}}}$ to the membrane repolarization is enhanced at temperatures higher than 39${}^{\circ }$C, especially at 42${}^{\circ }$C, and the after-potentials are hyperpolarized in the normal and ALS1 cases, while, they are re-depolarized in the ALS2 and ALS3 cases. The ionic channels beneath the myelin sheath are insensitive to the short-lasting current stimuli and do not contribute to the internodal action potential generation for the normal and abnormal cases in the whole investigated temperature range. Nevertheless that the uniform axonal dysfunction progressively increases in the nodal and internodal segments of each next simulated ALS case, the action potentials cannot be regarded as definitive indicators for the progressive degrees of this disease, when the temperature is changed from 20${}^{\circ }$C to 42${}^{\circ }$C. However, the results are essential for the interpretation of mechanisms of action potential measurements in ALS patients with symptoms of cooling, warming and fever, which can result from alteration in body temperature. Our results also suggest that the conducting processes in patients with ALS are in higher risk during hyperthermia ($\ge 40^{\circ }$C) than hypothermia ($\le 25^{\circ }$C).