Inhibition of the NMDA Currents by Probenecid in Amygdaloid Kindling Epilepsy Model.

Epilepsy is characterized by a sustained depolarization and repeated discharge of neurons, attributed to overstimulation of N-methyl-D-aspartate receptors (NMDAr). Herein, we propose that probenecid (PROB), an inhibitor of the activity of some ATP binding-cassette transporters (ABC-transporters) can modify NMDAr activity and expression in amygdaloid kindled model. Some studies have suggested that NMDAr expression could be regulated by inhibiting the activity of P-glycoprotein (MDR1) and drug resistance protein-1 (MRP1).

Accurate Neurosurgery for the Establishment of the Electric Kindling Model of Epilepsy in Mice.

This article describes in detail the essential stereotaxic neurosurgery to develop the electric experimental kindling model in mice. To date, available literature describing the methodology of the kindling model is very poor and usually neglects many relevant details about the neurosurgery, such as the manufacture of the electrodes, accurate stereotaxic coordinates of the amygdala nuclei, and the general surgery procedures (e.g.

Neuronal Excitability in Epileptogenic Zones Regulated by the Wnt/ Β-Catenin Pathway.

Epilepsy is a neurological disorder that involves abnormal and recurrent neuronal discharges, producing epileptic seizures. Recently, it has been proposed that the Wnt signaling pathway is essential for the central nervous system development and function because it modulates important processes such as hippocampal neurogenesis, synaptic clefting, and mitochondrial regulation. Wnt/β- catenin signaling regulates changes induced by epileptic seizures, including neuronal death.

Prenatal Ozone Exposure Induces Memory Deficiencies in Newborns Rats.

Air pollution is fully acknowledged to represent a major public health issue. Toxic environmental substances, such as ozone, interfere with prenatal development. Animals exposed to ozone (O) develop biochemical and morphological alterations.

Activation of the Extrinsic and Intrinsic Apoptotic Pathways in Cerebellum of Kindled Rats.

The purpose of this study is to determine the activation of the extrinsic and intrinsic apoptotic pathways in the cerebellum of rats exposed to amygdaloid electrical kindling. Western blot analyses were carried out for caspase-8 and caspase-9, Bid, Bax, and Bcl-2 in the cerebellum and immunohistochemistry of Bid, Bax, cytochrome C, and VDAC (voltage-dependent anion channels) in the cerebellar cortex of Wistar male rats with 0, 15, and 45 kindling stimulations. In the experimental group of 45 stimuli, we observed an increase in protein activation of caspase-9 and truncated Bid and Bax, in addition to a decrease in expression of pro-caspase-8 and the anti-apoptotic protein Bcl-2, determined by Western blot.

Increase Signaling of Wnt/β-Catenin Pathway and Presence of Apoptosis in Cerebellum of Kindled Rats.

Background: Epilepsy is one of the most common neurological disorders in humans, and the role of the cerebellum in its physiopathology remains the subject of study. The Purkinje cells (PC), whose axons target the dentate and interpositus nuclei, form the main cerebellar output to forebrain structures involved in epilepsy. Cerebellar atrophy related to loss of PC has been reported in chronic epilepsy although its mechanism remains unclear.

Participation of the dentate-rubral pathway in the kindling model of epilepsy.

Lesions of the cerebellar dentate nucleus (DN) reduce the after-discharge duration induced by repetitive kindling stimulation and decrease seizures to a lower rank according to Racine's scale. The DN sends cholinergic and glutamatergic fibers to the red nucleus (RN), which is composed of glutamatergic and GABAergic cells. To test the participation of these neurotransmitters in seizures, we compared the levels of glutamate and gamma-aminobutyric acid (GABA) at the RN in a control condition, a kindled stage, and a kindled stage followed by DN lesions.

Decreased Expression of Sox-1 in Cerebellum of Rat with Generalized Seizures Induced by Kindling Model.

The single feature of all malformations in cortical development is the clinical association with epilepsy. It has been proven that Sox-1 expression is essential during neurodevelopment and it is reported that Sox-1 knockout mice present spontaneous generalized seizures. Particularly in cerebellum, Sox-1 plays a key role in the Bergmann´s glia (BG) function, which allows the correct function of the Purkinje cells (PC).

Exposure to ozone induces a systemic inflammatory response: possible source of the neurological alterations induced by this gas.

The World Health Organization identified urban outdoor air pollution as the eighth highest mortality risk factor in high-income countries. Exposure to ambient pollutants such as ozone (O3) increases the number of hospital admissions. O3 is a highly reactive gas that reacts with cells lining the airways, producing the formation of reactive oxygen species and inflammation.

Whole-brain irradiation increases NREM sleep and hypothalamic expression of IL-1β in rats.

Purpose: Although it has mainly been described qualitatively, whole brain irradiation induces somnolence in patients with malignant diseases. Therefore, we used a rat model to quantify the effects of irradiation of healthy brain tissue on both sleep-wake patterns and the expression of the pro-inflammatory cytokine interleukin-1β (IL-1β), which is known to induce sleep.

Materials And Methods: Different groups were examined at three time points after irradiation (1 day, 30 days and 60 days).

The effects of ozone exposure and associated injury mechanisms on the central nervous system.

Ozone (O3) is a component of photochemical smog, which is a major air pollutant and demonstrates properties that are harmful to health because of the toxic properties that are inherent to its powerful oxidizing capabilities. Environmental O3 exposure is associated with many symptoms related to respiratory disorders, which include loss of lung function, exacerbation of asthma, airway damage, and lung inflammation. The effects of O3 are not restricted to the respiratory system or function - adverse effects within the central nervous system (CNS) such as decreased cognitive response, decrease in motor activity, headaches, disturbances in the sleep-wake cycle, neuronal dysfunctions, cell degeneration, and neurochemical alterations have also been described; furthermore, it has also been proposed that O3 could have epigenetic effects.

[Major neurotransmitters involved in the regulation of sleep-wake cycle].

Neuronal activity in the central nervous system undergoes a variety of electrophysiological changes along the sleep-wake cycle. These changes are modulated by a complex interaction between different neurochemical systems located throughout the brain. Within brainstem and hypothalamus there are a number of neuronal populations that promote wakefulness through the action of different neurotransmitters like noradrenaline, serotonin, histamine and orexin.

Plasma levels of clozapine and norclozapine in Mexican schizophrenia patients.

The aim of the present study was to determine the prescribing practice for clozapine (CAS 5786-21-0) as well as the plasma levels of clozapine and its main metabolite norclozapine (CAS 6104-71-8) in Mexican patients. A prospective study was performed in 69 in and out psychotic patients taking clozapine. Blood samples were taken at steady state.

Brain noradrenaline changes in rats prenatally exposed to ozone.

In the present study we considered the possible impairment of developmental noradrenergic maturity of the cerebellum, cerebral cortex and pons at 10-, 20- and 30-day-old rats arising from mothers subjected to 1ppm ozone concentration during pregnancy. The noradrenaline concentration was found to be significantly reduced in the cerebellum during the study, while in the cerebral cortex and the pons it was found to be reduced at days 10 and 30 respectively as compared to controls. We concluded that prenatal exposure of 1.

Effects of kainic acid lesions of the cerebellar interpositus and dentate nuclei on amygdaloid kindling in rats.

Some neurophysiological studies suggest that the cerebellum could participate in epileptic activity. Therefore, to study the participation of the main efferent projections from the cerebellum to the forebrain, we injected small doses of kainic acid (KA) into the deep cerebellar nuclei to selectively injure neighboring cells while avoiding fiber lesions. Uninjured fibers were confirmed using histological findings and by assessing the number of cells in the main cerebellar afferents, compared with controls.

In vivo experimental models of epilepsy.

This study reviews the different in vivo experimental models that have been used for the study of epileptogenesis. In this review we will focus on how to replicate the different models that have led to the study of partial seizures, as well as generalized seizures and the status epilepticus. The main characteristics that participate in the processes that generate and modulate the manifestations of different models of epileptogenesis are described.

Stimulation of the superior cerebellar peduncle during the development of amygdaloid kindling in rats.

Cerebellar manipulations have been used successfully in some intractable epileptic patients, however, their intrinsic mechanisms are not fully understood. To further clarify the cerebellar participation in epilepsy, we stimulated 10 rats with 100 Hz, 20 microA at the superior cerebellar peduncle (SCP) during amygdaloid kindling. Results were compared to 10 rats with an electrode placed at the SCP without stimulation and 10 rats without electrodes at the SCP used as control.