Publications by authors named "Kim Quasthoff"

Primary dissociated brain tissue from rodents is widely used in a variety of different scientific methods to investigate cellular processes in vitro. Often, for this purpose cell cultures need to be generated just on time, requiring extensive animal lab infrastructure. We show here that cryopreservation and thawing of dissociated tissue from rat cerebral cortex at embryonic day 18 is feasible without affecting its ability to form functional neuronal networks in vitro.

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Background: Anti-NMDA-encephalitis is caused by antibodies against the N-methyl-D-aspartate receptor (NMDAR) and characterized by a severe encephalopathy with psychosis, epileptic seizures and autonomic disturbances. It predominantly occurs in young women and is associated in 59% with an ovarian teratoma.

Results: We describe effects of cerebrospinal fluid (CSF) from an anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis patient on in vitro neuronal network activity (ivNNA).

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Background: Neuronal degeneration in multiple sclerosis has been linked to oxidative stress. Dimethyl fumarate is a promising novel oral therapeutic option shown to reduce disease activity and progression in patients with relapsing-remitting multiple sclerosis. These effects are presumed to originate from a combination of immunomodulatory and neuroprotective mechanisms.

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Unlabelled: The objective of the present work is to image functional alterations in hepatic encephalopathy (HE) by ammonia-induced changes of in vitro-neuronal network activity and to identify counteracting strategies. Synchronous bursting behavior of rat cortical cells which is the result of synaptic interaction of excitatory and inhibitory neurons was recorded in vitro on microelectrode arrays (MEAs) after ammonium chloride exposure. In order to test the involvement of astrocytic glutamine metabolism and N-methyl-d-aspartic acid- (NMDA-) receptor function in the observed ammonia-induced network dysregulation and to identify potentially protective strategies, we investigated effects of the glutamine synthetase (GS) inhibitor methionine-sulfoximine (MSO) and the NMDA-receptor antagonist DL-2-Amino-5-phosphono-pentanoic acid (AP-5), respectively.

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Background: Because of their lipophilicity, persistent organic pollutants (POPs) cross the human placenta, possibly affecting central nervous system development. Most POPs are known aryl hydrocarbon receptor (AhR) ligands and activators of AhR signaling. Therefore, AhR activation has been suggested to cause developmental neurotoxicity (DNT).

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