Same old

Wednesday, 18 April 2007

NMDA and dev. seizures

Alterations of NR2B and PSD-95 expression after early-life epileptiform discharges in developing neurons.

Alterations of NR2B and PSD-95 expression after early-life epileptiform discharges in developing neurons.

Int J Dev Neurosci. 2007 Feb 21;

Authors: Jiang Q, Wang J, Wu X, Jiang Y

As an extreme form of abnormally synchronized activity, epilepsy may modify patterns of organization in the nervous system. It is clear that enhanced glutamatergic excitatory synaptic transmission with alterations in the expression of ionotropic glutamate receptors is a mechanism critical for seizure susceptibility and excitotoxicity. However, the exact quomodo and the roles of regulated N-methyl-d-aspartate receptor (NMDAR) composition and expression of a major postsynaptic density (PSD) scaffolding molecule, PSD-95, are as yet unclear. To study protein expression changes after epileptiform discharges in cultured immature rat cortical neurons, we divided cells into three groups which were transiently exposed to regular Neurobasal/B27 (control group), physiological solution (PS group) and magnesium-free physiological solution (MGF group) at cultured day 6. Neurons at three different culture ages (DIV7, DIV12 and DIV17) were collected for immunoblotting analysis. We found a decrease in expression of NR2B NMDAR subunit and PSD-95 (P<0.05) shortly after insult (within 24h), which may show that brief magnesium-free media treatment of primary cultured rat cortical neurons, an in vitro model of seizure brain injury, has a major influence on the expression of NR2B subunit and PSD-95.

PMID: 17428633 [PubMed - as supplied by publisher]

Interesting hypothalamic e-phys

Pharmacological and molecular characterization of ATP-sensitive K(+) conductances in CART and NPY/AgRP expressing neurons of the hypothalamic arcuate nucleus.

Pharmacological and molecular characterization of ATP-sensitive K(+) conductances in CART and NPY/AgRP expressing neurons of the hypothalamic arcuate nucleus.

Neuroscience. 2007 Feb 9;144(3):815-24

Authors: van den Top M, Lyons DJ, Lee K, Coderre E, Renaud LP, Spanswick D

The role of hypothalamic ATP-sensitive potassium channels in the maintenance of energy homeostasis has been extensively explored. However, how these channels are incorporated into the neuronal networks of the arcuate nucleus remains unclear. Whole-cell patch-clamp recordings from rat arcuate nucleus neurons in hypothalamic slice preparations revealed widespread expression of functional ATP-sensitive potassium channels within the nucleus. ATP-sensitive potassium channels were expressed in orexigenic neuropeptide Y/agouti-related protein (NPY/AgRP) and ghrelin-sensitive neurons and in anorexigenic cocaine-and-amphetamine regulated transcript (CART) neurons. In 70% of the arcuate nucleus neurons recorded, exposure to glucose-free bathing medium induced inhibition of electrical excitability, the response being characterized by membrane hyperpolarization, a reduction in neuronal input resistance and a reversal potential consistent with opening of potassium channels. These effects were reversible upon re-introduction of glucose to the bathing medium or upon exposure to the ATP-sensitive potassium channel blockers tolbutamide or glibenclamide. The potassium channel opener diazoxide, but not pinacidil, also induced a tolbutamide and glibenclamide-sensitive inhibition of electrical excitability. Single-cell reverse transcription-polymerase chain reaction revealed expression of mRNA for sulfonylurea receptor 1 but not sulfonylurea receptor 2 subunits of ATP-sensitive potassium channels. Thus, rat arcuate nucleus neurons, including those involved in functionally antagonistic orexigenic and anorexigenic pathways express functional ATP-sensitive potassium channels which include sulfonylurea receptor 1 subunits. These data indicate a crucial role for these ion channels in central sensing of metabolic and energy status. However, further studies are needed to clarify the differential roles of these channels, the organization of signaling pathways that regulate them and how they operate in functionally opposing cell types.

PMID: 17137725 [PubMed - indexed for MEDLINE]

Lovely....

Olfactory lateralization in homing pigeons: initial orientation of birds receiving a unilateral olfactory input.

Olfactory lateralization in homing pigeons: initial orientation of birds receiving a unilateral olfactory input.

Eur J Neurosci. 2007 Mar;25(5):1511-6

Authors: Gagliardo A, Pecchia T, Savini M, Odetti F, Ioalè P, Vallortigara G

It has been shown that homing pigeons (Columba livia) rely on olfactory cues to navigate from unfamiliar locations. In fact, the integrity of the olfactory system, from the olfactory mucosa to the piriform cortex, is required for pigeons to navigate over unfamiliar areas. Recently it has been shown that there is a functional asymmetry in the piriform cortex, with the left piriform cortex more involved in the use of the olfactory navigational map than the right piriform cortex. To investigate further the lateralization of the olfactory system in relation to navigational processes in carrier pigeons, we compared their homing performance after either their left or the right nostril was plugged. Contrary to our expectations, we observed an impairment in the initial orientation of the pigeons with their right nostril plugged. However, both groups released with one nostril plugged tended to be poorer than control pigeons in their homing performance. The observed asymmetry in favour of the right nostril might be due to projections from the olfactory bulbs to the contralateral globus pallidum, a structure involved in motor responses.

PMID: 17425577 [PubMed - in process]

CB changes in epilepsy

Status epilepticus causes a long-lasting redistribution of hippocampal cannabinoid type 1 receptor expression and function in the rat pilocarpine model of acquired epilepsy.

Status epilepticus causes a long-lasting redistribution of hippocampal cannabinoid type 1 receptor expression and function in the rat pilocarpine model of acquired epilepsy.

Neuroscience. 2007 Apr 11;

Authors: Falenski KW, Blair RE, Sim-Selley LJ, Martin BR, Delorenzo RJ

Activation of the cannabinoid type 1 (CB1) receptor, a major G-protein-coupled receptor in brain, acts to regulate neuronal excitability and has been shown to mediate the anticonvulsant effects of cannabinoids in several animal models of seizure, including the rat pilocarpine model of acquired epilepsy. However, the long-term effects of status epilepticus on the expression and function of the CB1 receptor have not been described. Therefore, this study was initiated to evaluate the effect of status epilepticus on CB1 receptor expression, binding, and G-protein activation in the rat pilocarpine model of acquired epilepsy. Using immunohistochemistry, we demonstrated that status epilepticus causes a unique "redistribution" of hippocampal CB1 receptors, consisting of specific decreases in CB1 immunoreactivity in the dense pyramidal cell layer neuropil and dentate gyrus inner molecular layer, and increases in staining in the CA1-3 strata oriens and radiatum. In addition, this study demonstrates that the redistribution of CB1 receptor expression results in corresponding functional changes in CB1 receptor binding and G-protein activation using [(3)H] R(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazin-yl](1-napthalen-yl)methanone mesylate (WIN55,212-2) and agonist-stimulated [(35)S]GTPgammaS autoradiography, respectively. The redistribution of CB1 receptor-mediated [(35)S]GTPgammaS binding was 1) attributed to an altered maximal effect (E(max)) of WIN55,212-2 to stimulate [(35)S]GTPgammaS binding, 2) reversed by the CB1 receptor antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride (SR141716A), 3) confirmed by the use of other CB1 receptor agonists, and 4) not reproduced in other G-protein-coupled receptor systems examined. These results demonstrate that status epilepticus causes a unique and selective reorganization of the CB1 receptor system that persists as a permanent hippocampal neuronal plasticity change associated with the development of acquired epilepsy.

PMID: 17433556 [PubMed - as supplied by publisher]

Very interesting....Ca channels, network-level excitability etc.

Density is destiny--on [corrected] the relation between quantity of T-type Ca2+ channels and neuronal electrical behavior.

Density is destiny--on [corrected] the relation between quantity of T-type Ca2+ channels and neuronal electrical behavior.

CNS Neurol Disord Drug Targets. 2006 Dec;5(6):655-62

Authors: Chorev E, Manor Y, Yarom Y

The electroresponsiveness fingerprint of a neuron reflects the types and distributions of the ionic channels that are embedded in the neuronal membrane as well as its morphology. Theoretical analysis shows that subtle changes in the density of channels can contribute substantially to the electroresponsive fingerprints of neurons. We have confirmed these predictions, using the dynamic clamp approach to emulate changes in channels' densities in neurons from the inferior olive. We demonstrate how the density of T-type channels determines the behavioral destiny of neurons. We argue that regulation of channel densities could be an efficient mechanism for controlling the electrical activity of single cells, as well as the output of neuronal networks.

PMID: 17168749 [PubMed - indexed for MEDLINE]

Thursday, 12 April 2007

Ictogenesis and non-linear analyses

Epilepsia. 2003;44 Suppl 12:30-43. Links Toward a neurodynamical understanding of ictogenesis. * Le Van Quyen M, * Navarro V, * Martinerie J, * Baulac M, * Varela FJ. LENA (Laboratoire de Neurosciences Cognitives et Imagerie Cerebrale), CNRS UPR 640, Hopital de la Pitie-Salpetriere, 47 Boulevard de l'Hopital, 75651 Paris cedex 13, France. Although considerable information on cellular and network mechanisms of epilepsy exists, it is still not understood why, how, and when the transition from interictal to ictal state takes place. The authors review their work on nonlinear EEG analysis and provide consistent evidences that dynamical changes in the neural activity allows the characterization of a preictal state several minutes before seizure onset. This new neurodynamical approach of ictogenesis opens new perspectives for studying the basic mechanisms in epilepsy as well as for possible therapeutic interventions. PMID: 14641559 [PubMed - indexed for MEDLINE]

Entrez PubMed

Blogged with Flock

Ictogenesis and models

C R Biol. 2005 Feb;328(2):187-98. Links Anticipating epileptic seizures: from mathematics to clinical applications. * Le Van Quyen M. Laboratoire de Neurosciences Cognitives et Imagerie Cerebrale, LENA, CNRS UPR 640, Hopital de la Pitie-Salpetriere, 47, bd de l'Hopital, 75651 Paris, France. lenalm@ext.jussieu.fr The study of dynamical changes in the neural activity preceding an epileptic seizure allows the characterization of a preictal state several minutes prior to seizure onset. This opens new perspectives for studying the mechanisms of ictogenesis as well as for possible therapeutic interventions that represent a major breakthrough. In this review we present and discuss the results from our group in this domain using nonlinear analysis of brain signals, as well as its limitation and open questions. PMID: 15771005 [PubMed - indexed for MEDLINE]