Changes in local cerebral glucose utilization induced by convulsants

Pazdernik, Thomas L.; Cross, Robert S.; Giesler, M.; Samson, Frederick E.; NelsonP, S.R.

doi:10.1016/0306-4522(85)90146-0

Cited by 70 publications

(17 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, we confirmed the findings of others that the entire SNR was metabolically active during the ictal period (Ben-Ari et al, 1981;Engel et al, 1978;Nehlig et al, 1992;Pazdernik et al, 1985). We also investigated the possibility that GPe and GPi (endopeduncular nucleus) act differentially because they may have opposing effects on movement (DeLong, 1990;Gerfen et al, 1990).…”

Section: Discussionsupporting

confidence: 86%

Regional neural activity within the substantia nigra during peri-ictal flurothyl generalized seizure stages

Velı́šková

Miller

Nunes

et al. 2005

Neurobiology of Disease

View full text Add to dashboard Cite

Structures responsible for the onset, propagation, and cessation of generalized seizures are not known. Lesion and microinfusion studies suggest that the substantia nigra pars reticulata (SNR) seizurecontrolling network could play a key role. However, the expression of neural activity within the SNR and its targets during discrete pre-and postictal periods has not been investigated. In rats, we used flurothyl to induce generalized seizures over a controlled time period and 2-deoxyglucose autoradiography mapping technique. Changes in neural activity within the SNR were region-specific. The SNR posterior was selectively active during the pre-clonic period and may represent an early gateway to seizure propagation. The SNR anterior and superior colliculus changed their activity during progression to tonic-clonic seizure, suggesting the involvement in coordinated regional activity that results in inhibitory effects on seizures. The postictal suppression state was correlated with changes in the SNR projection targets, specifically the pedunculopontine tegmental nucleus and superior colliculus.

show abstract

Section: Discussionsupporting

confidence: 86%

Regional neural activity within the substantia nigra during peri-ictal flurothyl generalized seizure stages

Velı́šková

Miller

Nunes

et al. 2005

Neurobiology of Disease

View full text Add to dashboard Cite

show abstract

“…Other effects after severe acute intoxication (e.g. on brain glucose) are secondary to seizures [40]. An additional important effect of anticholinesterases is that they increase the permeability of the bloodbrain barrier (BBB) [41].…”

Section: Discussionmentioning

confidence: 99%

Toxicogenomic Studies of the Rat Brain at an Early Time Point Following Acute Sarin Exposure

et al. 2006

View full text Add to dashboard Cite

We have studied sarin-induced global gene expression patterns at an early time point (2 h: 0.5 x LD50) using Affymetrix Rat Neurobiology U34 chips and male Sprague-Dawley rats. A total of 46 genes showed statistically significant alterations from control levels. Three gene categories contained more of the altered genes than any other groups: ion channel (8 genes) and calcium channel and binding proteins (6 genes). Alterations were also found in the following gene groups: ATPases and ATP-based transporters (4), growth factors (4), G-protein-coupled receptor pathway-related molecules (3), neurotransmission and neurotransmitter transporters (3), cytoskeletal and cell adhesion molecules (2), hormones (2), mitochondria-associated proteins (2), myelin proteins (2), stress-activated molecules (2), cytokine (1), caspase (1), GABAnergic (1), glutamergic (1), immediate early gene (1), prostaglandin (1), transcription factor (1), and tyrosine phosphorylation molecule (1). Persistent alteration of the following genes also were noted: Arrb1, CaMKIIa, CaMKIId, Clcn5, IL-10, c-Kit, and Plp1, suggesting altered GPCR, kinase, channel, and cytokine pathways. Selected genes from the microarray data were further validated using relative RT-PCR. Some of those genes (GFAP, NF-H, CaMKIIa, Calm, and MBP) have been shown by other laboratories and ours, to be involved in the pathogenesis of sarin-induced pathology and organophosphate-induced delayed neurotoxicity (OPIDN). Induction of both proapoptotic (Bcl2l11, Casp6) and antiapoptotic (Bcl-X) genes, besides suppression of p21, suggest complex cell death/protection-related mechanisms operating early on. Principal component analysis (PCA) of the expression data confirmed that the changes in gene expression are a function of sarin exposure, since the control and treatment groups separated clearly. Our model (based on current and previous studies) indicates that both degenerative and regenerative pathways are activated early and contribute to the level of neurodegeneration at a later time, leading to neuro-pathological alterations.

show abstract

“…When administered at near the LDso dose, it induces central symptoms including overt clonic convulsions and tremors, as well as peripheral symptoms of salivation and muscle fasciculation (11,13,34,35,43). These clinical signs are accompanied by central nervous system (CNS) and myocardial morphologic lesions (4,5,9,11,12,14,24,27,31,33,36,38,39,54).…”

Section: Introductionmentioning

confidence: 99%

Early Histopathologic and Ultrastructural Changes in the Heart of Sprague-Dawley Rats Following Administration of Soman

Tryphonas

Veinot

Clement³

1996

Toxicol Pathol

View full text Add to dashboard Cite

Male Sprague-Dawley rats were given atropine methylnitrate (20 mg/kg) and HI-6 (125 mg/kg) ip 10 min before a single injection of 130 micrograms soman/kg sc, and the heart was examined by light and electron microscopy 10, 25, 45, 90, and 180 min after the onset of seizures. Seizures appeared within 6-11 min after treatment. Control rats were given saline sc in place of soman. Early myocardial lesions consisting of hypercontraction and hyperextension of sarcomeres, focal myocytolysis, and contraction bands were detected in individual or groups of myocardial fibers. Hypercontraction was characterized by shortening of the sarcomere length, disappearance of the I and H bands, and thickening of the Z line. In contrast, hyperextended sarcomeres had thickened I and H bands. Myocytolysis was characterized by a progressively severe focal dissolution of myofilaments and edema of the affected sarcoplasmic area. Contraction bands appeared to result from the breakdown of markedly hypercontracted myofibril bundles. Due to the presence of a number of surviving myofilaments and the preservation of the sarcolemmal tube, distortion of the overall myocytic structure was minimal. Changes in the mitochondria and other intracellular organelles were also minimal and nonspecific. The close resemblance of morphologic findings to those induced by catecholamines supports the view that soman-induced myocardial damage is secondary to a treatment-related release of unphysiologic amounts of endogenous catecholamines.

show abstract

Changes in local cerebral glucose utilization induced by convulsants

Cited by 70 publications

References 33 publications

Regional neural activity within the substantia nigra during peri-ictal flurothyl generalized seizure stages

Regional neural activity within the substantia nigra during peri-ictal flurothyl generalized seizure stages

Toxicogenomic Studies of the Rat Brain at an Early Time Point Following Acute Sarin Exposure

Early Histopathologic and Ultrastructural Changes in the Heart of Sprague-Dawley Rats Following Administration of Soman

Contact Info

Product

Resources

About