Excitotoxic insults to the optic nerve alter visual evoked potentials

Soto, Adriana; Pérez-Samartı́n, Alberto; Etxebarria, Estibaliz; Matute, Carlos

doi:10.1016/j.neuroscience.2003.09.009

Cited by 8 publications

(3 citation statements)

References 21 publications

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“…Cryostat sections (10 lm thick) of optic nerves were processed for conventional immunoperoxidase staining (for details, see Soto et al, 2004) using antibodies to myelin basic protein (MBP, 0.8 lm/ml; Boehringer Mannheim, Germany), to dephosphorylated heavy-chain neurofilament (SMI 32, 1:500; Sternberger Monoclonals, Lutherville, MD), glial fibrillary acidic protein (GFAP, 10 lg/ml; Dako, Glostrup, Denmark), and to adenomatous polyposis sporadic colorectal cancer (APC, 1 lg/ml; Oncogene Research Products, Cambridge, MA). Microglia was labeled with biotinylated Bandeira simplicifolia B 4 -isolectin (IB 4 , 20 lg/ml; Sigma) as previously described (Gottlieb and Matute, 1997).…”

Section: Rabbit Optic Nerve Surgery and Drug Applicationmentioning

confidence: 99%

Excitotoxic oligodendrocyte death and axonal damage induced by glutamate transporter inhibition

Domercq

Etxebarria

Pérez-Samartı́n

et al. 2005

Glia

105

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Glutamate uptake is crucial to terminate glutamate signaling and to prevent excitotoxicity. The present study describes the expression of functional glutamate transporters GLAST and GLT-1 in oligodendrocytes by means of electrophysiology, uptake assays, and immunocytochemistry. Inhibition of glutamate uptake, both in oligodendrocyte cultures and in isolated optic nerves, increases glutamate levels and causes oligodendrocyte excitotoxicity, which is prevented by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainate receptor antagonists. Furthermore, glutamate transporter inhibitors or antisense oligonucleotides applied onto the optic nerve in vivo lead to oligodendroglial loss, massive demyelination, and severe axonal damage. Overall, these results demonstrate that the integrity of oligodendrocytes and white matter depends on proper glutamate transporter function. Deregulated transporter activity may contribute to acute and chronic white matter damage.

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Section: Rabbit Optic Nerve Surgery and Drug Applicationmentioning

confidence: 99%

Excitotoxic oligodendrocyte death and axonal damage induced by glutamate transporter inhibition

Domercq

Etxebarria

Pérez-Samartı́n

et al. 2005

Glia

105

View full text Add to dashboard Cite

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“…Because of the relevance of the information offered by this technique and its relative simplicity, it is nowadays considered one of the most powerful tools in clinical diagnostics, clinical investigation 10,11 and animal biological research. 3,20 For a review of the biological background of the generation of VEPs, the reader can refer to the reviews by Schlag 19 and Kriss. 13 The purpose of our work was to study the persistence properties of the neuronal activity of the visual area of the rabbit brain evoked by light stimulation.…”

Section: Introductionmentioning

confidence: 99%

Long-Range Correlations in Rabbit Brain Neural Activity

et al. 2006

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We have analyzed the presence of persistence properties in rabbit brain electrical signals by means of non-equilibrium statistical physics tools. To measure long-memory properties of these experimental signals, we have first determined whether the data are fractional Gaussian noise (fGn) or fractional Brownian motion (fBm) by calculating the slope of the power spectral density plot of the series. The results show that the series correspond to fBm. Then, the data were studied by means of the bridge detrended scaled windowed variance analysis, detecting long-term correlation. Three different types of experimental signals have been studied: neural basal activity without stimulation, the response induced by a single flash light stimulus and the average of the activity evoked by 200 flash light stimulations. Analysis of the series revealed the existence of persistent behavior in all cases. Moreover, the results also exhibited an increasing correlation in the level of long-term memory from recordings without stimulation, to one sweep recording or 200 sweeps averaged recordings. Thus, brain neural electrical activity is affected not only by its most recent states, but also by previous states much more distant in the past.

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“…VEP is a reliable test for diagnosing demyelination in an animal model that presents with an insult to the optic nerves and chiasm [3,36,47]. Histological assessment after a VEP recording has confirmed the validity of VEP data on demyelination and remyelination of the optic nerves and chiasm [47,58].…”

Section: Introductionmentioning

confidence: 82%

Castration Attenuates Myelin Repair Following Lysolecithin Induced Demyelination in Rat Optic Chiasm: An Evaluation Using Visual Evoked Potential, Marker Genes Expression and Myelin Staining

et al. 2011

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Multiple sclerosis (MS) is a demyelinating disease that affects the central nervous system. MS is the most common neurological disorder in young adults with a greater incidence among females. Male gonadal hormones have a protective effect on neural system development and myelin maturation. In this study, we investigate the effect of castration on lysolecithin-induced demyelination and remyelination processes using visual evoked potentials, in addition to measuring the expressions of Olig2, MBP, Nogo-A and GFAP mRNAs as oligodendrocyte or astrocyte markers; and histological assessments by myelin-specific staining. We observed more expanded demyelination with delayed repair process in castrated rats. Expression levels of the aforementioned marker genes confirmed histological and electrophysiological observations. Our results showed a pivotal role for endogenous male hormones in the context of demyelinating insults. It may also account for the different prognosis of MS between male and female genders and provide new insights for therapeutic treatments.

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Excitotoxic insults to the optic nerve alter visual evoked potentials

Cited by 8 publications

References 21 publications

Excitotoxic oligodendrocyte death and axonal damage induced by glutamate transporter inhibition

Excitotoxic oligodendrocyte death and axonal damage induced by glutamate transporter inhibition

Long-Range Correlations in Rabbit Brain Neural Activity

Castration Attenuates Myelin Repair Following Lysolecithin Induced Demyelination in Rat Optic Chiasm: An Evaluation Using Visual Evoked Potential, Marker Genes Expression and Myelin Staining

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