In vivo effects of phenytoin and phenobarbital on GABA receptors in rat cerebral cortex and cerebellum

The in vivo effects of anticonvulsants on specific binding of [3H]GABA in the rat brain were examined in male Wistar rats. Acute treatment with phenobarbital increased specific [3H]GABA binding in the cerebral cortex, whereas repeated treatment with phenobarbital failed to change [3H]GABA binding. [3H]GABA binding in the cerebellum was not influenced by phenobarbital administration. Acute treatment with phenytoin produced no change in [3H]GABA binding, whereas repeated treatment with phenytoin caused a significant increase in [3H]GABA binding in the cerebellum, but not in the cerebral cortex. The effects of these anticonvulsants may be due, at least in part, to GABA receptor-mediated mechanisms.     

Non-linear regression analysis for estimating the intraoperative motor evoked potential recovery time after bolus neuromuscular blockade

Journal of Clinical Monitoring and Computing - The recovery time of the motor evoked potential (MEP) amplitude following a neuromuscular blockade (NMB) during surgery is useful for interpreting...     

Effect of DN-1417, a synthetic thyrotropin-releasing hormone analogue, on [3H]GABA binding in the cerebellum of ataxic rats

The neonatal administration of cytocine arabinoside (40 mg/kg, s.c.) induced marked ataxia and hypoplastic cerebellum in male Sprague-Dawley rats. Specific [3H]GABA binding in the cerebellum was significantly reduced by cytosine arabinoside, whereas [3H]GABA binding in the cerebral cortex was not changed. The administration of DN-1417 (1 mg/100 g body wt., i.p.), a synthetic derivative of thyrotropin-releasing hormone (TRH), significantly increased [3H]GABA binding in the cerebellum of cytosine arabinoside-induced ataxic rats. These results suggest that TRH may play a role in regulating GABA receptors involved in the function of the rat cerebellum.     

Inhibition by DN-1417 (a TRH derivative) of [3H]GABA binding in the rat brain

The administration of DN-1417, a synthetic derivative of TRH with more potent central action, significantly reduced specific [3H]GABA binding in the cerebellum, whereas [3H]GABA binding in the cerebral cortex was not changed. Scatchard analysis showed that the decreased [3H]GABA binding in the cerebellum was due to decreased binding sites of both high and low affinities. [3H]GABA binding to brain synaptic membranes was not affected by the addition of either TRH or DN-1417 in vitro. These findings suggest that TRH may play a role in regulating GABA receptors in the rat cerebellum.     

Effects of 4-weeks of treatment with lithium and olanzapine on long-term potentiation in hippocampal area CA1

Neuroplastic theories propose that lithium has robust neuroprotective and neurotrophic actions leading to the up-regulation of synaptic plasticity, and this action may be associated with the efficacy of lithium in the treatment of bipolar disorder. Olanzapine, an atypical antipsychotic drug, is efficacious in the treatment of bipolar disorder. It has been suggested that olanzapine may also up-regulate synaptic plasticity by its neuroprotective and neurotrophic actions, and this action may be related to antipsychotic and anti-manic effects of the drug. However, few studies have directly examined whether these drugs alter synaptic plasticity.