Effect of carbamazepine, oxcarbazepine and lamotrigine on the increase in extracellular glutamate elicited by veratridine in rat cortex and striatum.

Lamotrigine, carbamazepine and oxcarbazepine inhibit veratrine-induced neurotransmitter release from rat brain slices in concentrations corresponding to those reached in plasma or brain in experimental animals or humans after anticonvulsant doses, presumably due to their sodium channel blocking properties. Microdialysis measurements of extracellular glutamate and aspartate were carried out in conscious rats in order to investigate whether corresponding effects occur in vivo Veratridine (10 microM) was applied via the perfusion medium to the cortex and the corpus striatum in the presence of the glutamate uptake inhibitor L-trans-pyrrolidine-2,4-dicarboxylic acid (1 mM in perfusion medium). Maximally effective anticonvulsant doses of carbamazepine (30 mg/kg), oxcarbazepine (60 mg/kg) and lamotrigine (15 mg/kg) were given orally.

Determination of rat brain and plasma levels of the orally active GABAB antagonist 3-amino-propyl-n-butyl-phosphinic acid (CGP 36742) by a new GC/MS method.

An involvement of GABAergic neurons has been suggested in the process of memory consolidation based on anatomical evidence and increasing physiological and biochemical data. With the advent of orally active GABAB antagonists, such as CGP 36742, the question of their therapeutic value, for example in Alzheimer's disease, becomes relevant. Therefore, a new GC/MS method was developed to determine the concentration of CGP 36742 (3-amino-propyl-n-butyl phosphinic acid) in various intra- and extracerebral tissues after different routes of application.

Effects of CGP 28014 on the in vivo release and metabolism of dopamine in the rat striatum assessed by brain microdialysis.

The effects on rat striatal dopamine (DA) metabolism of systemic and local administration of CGP 28014, an inhibitor of catechol-O-methyl-transferase (COMT), were studied by in vivo microdialysis. CGP 28014 (30 mg/kg i.p.

Displacement of in vivo binding of [3H]brofaromine to rat intestinal monoamine oxidase A by orally administered tyramine.

The reversibility of the interaction of inhibitors with monoamine oxidase (MAO) is thought to provide a safety valve with respect to tyramine potentiation. We sought experimental evidence for this concept by studying the binding of orally administered [3H]brofaromine to the A-form of MAO in the rat ileum. Specific binding, defined by pretreatment with 10 mg/kg clorgyline p.

Weak effects of local and systemic administration of the GABA uptake inhibitor, SK&F 89976, on extracellular GABA in the rat striatum.

The effects of local and systemic administration of the potent GABA uptake inhibitor, SK&F 89976, on GABA overflow from the striatum of conscious rats were investigated in brain dialysis experiments. Administration of the compound via the dialysis probe at concentrations of 25 or 100 mumol/l significantly increased basal GABA overflow about 2-fold. Overflow evoked by 104 mmol/l K+ remained unaltered at the lower and was almost doubled at the higher concentrations; this increase did, however, not reach statistical significance.