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Page 1 od 25 rezultati
Properties of depolarizing plateau potentials in aminopyridine-induced ictal seizure foci of cat motor cortex.
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The mechanisms of generation of self-sustained depolarizing plateau potentials (DPs) were studied in intracellular recordings in aminopyridine-induced ictal seizure foci in the motor cortex of the cat. In some experiments single-electrode voltage clamp techniques were used and intracellular pressure
The effect of acute and chronic electroconvulsive shock on [3H]phorbol-dibutyrate binding to rat brain membranes.
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The present study investigated the effect of single and repeated electroconvulsive shock (ECS) on proteinkinase C in rat cerebral cortex, cerebellum, hippocampus and striatum using [3H]Phorbol-12,13-butyrate binding. In the postictal period and 24 hr after a single ECS there was no alteration in any
The protein kinase C activators, phorbol 12-myristate,13-acetate and phorbol 12,13-dibutyrate, are convulsant in the pico-nanomolar range in mice.
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Administration of phorbol 12-myristate,13-acetate (PMA, 10 fmol-10 nmol) or phorbol 12,13-dibutyrate (PDB, 0.2-495 nmol) (i.c.v.) to mice induced: hindlimb scratching, tremor, myoclonic jerks, hyperlocomotion, clonic seizure, followed by death or recovery. CD50 values for clonic seizures for PMA and
Microglial ROS production in an electrical rat post-status epilepticus model of epileptogenesis.
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Reactive oxygen species and inflammatory signaling have been identified as pivotal pathophysiological factors contributing to epileptogenesis. Considering the development of combined anti-inflammatory and antioxidant treatment strategies with antiepileptogenic potential, a characterization of the
Differential regulation of the nerve growth factor and brain-derived neurotrophic factor genes in L929 mouse fibroblasts.
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Nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are structurally related survival and differentiation factors for distinct sets of peripheral and central neurons. The regulation of NGF gene expression has been extensively studied in L929 mouse fibroblasts. L929 cells also
Effects of phenobarbital on leukocyte activation: membrane potential, actin polymerization, chemotaxis, respiratory burst, cytokine production, and lymphocyte proliferation.
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Leukocyte activation is known to involve cell membrane potential changes. Phenobarbital, an anesthetic and anticonvulsant that can inhibit neuronal membrane depolarization, may also affect leukocyte activation. Measuring membrane potential, actin polymerization, chemotaxis, superoxide production,
Synaptotagmin IV is an immediate early gene induced by depolarization in PC12 cells and in brain.
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Subtractive library construction and differential screening were used to identify a cDNA for a cell type-specific immediate early gene induced in rat PC12 pheochromocytoma cells. Sequencing identified the protein product of this gene as rat synaptotagmin IV (SytIV). Synaptotagmins are synaptic
Desensitization of somatostatin-induced inhibition of low extracellular magnesium concentration-induced calcium spikes in cultured rat hippocampal neurons.
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Neuronal excitability is inhibited by somatostatin, which might play important roles in seizure and neuroprotection. The possibility of whether the effect of somatostatin on neurotransmission is susceptible to desensitization was investigated. We tested the effects of prolonged exposure to
H(2)O(2) induces upregulation of Fas and Fas ligand expression in NGF-differentiated PC12 cells: modulation by cAMP.
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Fas, (APO-1/CD95), a transmembrane glycoprotein belonging to the tumor necrosis (TNF) receptor superfamily, transduces apoptotic death upon crosslinking by its cognate ligand (FasL). As upregulation of Fas/FasL expression occurs in neuropathological conditions (e.g., stroke, central nervous system
Mechanisms of hyperthermia-induced depression of GABAergic synaptic transmission in the immature rat hippocampus.
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Clinical observations and experimental studies have shown that hyperthermia can provoke febrile seizures, which are the most common type of pathological brain activity in children. We previously demonstrated that hyperthermia produced a depression of GABAergic neurotransmission in the hippocampus of
Mediation by membrane protein kinase C of zinc-induced oxidative neuronal injury in mouse cortical cultures.
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Transsynaptic movement of endogenous zinc may play a key role in selective neuronal death after brain ischemia and prolonged seizures. As to the mechanism, we have reported recently that zinc-induced neuronal death occurs mainly by oxidative stress in cortical cultures. Here we present evidence
Lithium enhances neuronal muscarinic excitation by presynaptic facilitation.
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The mechanisms underlying the psychotropic actions of lithium are not established, but modulation of endogenous brain neurotransmitter systems is likely to be important. Several interactions of lithium with muscarinic responses have been reported, including a marked potentiation of seizures produced
The differential roles of PEA15 phosphorylations in reactive astrogliosis and astroglial apoptosis following status epilepticus.
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Up to this day, the roles of PEA15 expression and its phosphorylation in seizure-related events have not been still unclear. In the present study, we found that PEA15 was distinctly phosphorylated in reactive astrocytes and apoptotic astrocytes in the rat hippocampus following
A phase I clinical trial of 12- O-tetradecanoylphorbol-13-acetate for patients with relapsed/refractory malignancies.
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Phorbol esters activate protein kinase C and modulate a variety of downstream cell signaling pathways. 12-O-tetradecanoylphorbol-13-acetate (TPA) is a phorbol ester that induces differentiation or apoptosis in a variety of cell lines at low concentrations. A phase I dose escalation trial of TPA was
Caffeine-induced inhibition of the activity of glutamate transporter type 3 expressed in Xenopus oocytes.
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Caffeine has been known to trigger seizures, however, the precise mechanism about the proconvulsive effect of caffeine remains unclear. Glutamate transporters play an important role to maintain the homeostasis of glutamate concentration in the brain tissue. Especially, dysfunction of excitatory
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