S Birnstiel

Loyola University Medical Center, Maywood, Illinois, United States

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Publications (6)18.03 Total impact

  • Susanne Birnstiel, Ernst Wülfert, S G Beck
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    ABSTRACT: Previous behavioural and electrophysiological studies have indicated that levetiracetam (ucb LO59) acts as an anticonvulsant drug in vivo. The purpose of the present study was to investigate the effects of levetiracetam on normal synaptic transmission and epileptiform activity in vitro. Intracellular recordings were obtained from the CA3 subfield of the rat hippocampal slice preparation. Levetiracetam in a concentration of 10 microM did not influence basic cell properties or normal synaptic transmission evoked by subthreshold and suprathreshold stimuli to the commissural pathway. However, it strongly inhibited the development of epileptiform bursting by the gamma-aminobutyric acid (GABA)A-receptor antagonist bicuculline (1-30 microM). Levetiracetam also decreased the size of bursts previously established by bicuculline. In experiments in which the glutamate-receptor agonist N-Methyl-D-Aspartate (NMDA) was used to generate spontaneous bursting, levetiracetam had no effect on the size of the bursts but decreased bursting frequency. The difference in effects of levetiracetam on bicuculline- and NMDA-induced bursting appeared to be dependent on the convulsant used, since in the presence of 10 microM bicuculline, levetiracetam decreased the size of NMDA-bursts to the same extent as the size of synaptically evoked bicuculline-bursts but had little effect on bursting frequency. The results show that under our experimental conditions, levetiracetam did not alter the components of normal synaptic transmission. However, levetiracetam at the concentrations studied inhibited epileptiform bursting induced by bicuculline and NMDA in vitro in a manner consistent with the profile of an antiepileptogenic drug.
    Archiv für Experimentelle Pathologie und Pharmakologie 12/1997; 356(5):611-8. · 2.36 Impact Factor
  • S G Beck, S Birnstiel, K C Choi, W A Pouliot
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    ABSTRACT: Fluoxetine is a 5-hydroxytryptamine (5-HT, serotonin)-selective reuptake inhibitor (SSRI) and is one of the main drugs used for the treatment of depression. Because it takes 2 to 3 weeks of treatment before clinical efficacy is manifest, the acute actions of fluoxetine cannot account for the clinical actions of the drug. The chronic effects of fluoxetine have not been completely delineated. The experiments detailed here investigate the chronic effects of fluoxetine on 5-HT and gamma-aminobutyric acid (GABA) receptor-mediated actions using intracellular recording techniques in hippocampal brain slices. Rats were treated with fluoxetine for 3 weeks via osmotic minipumps implanted s.c. Fluoxetine and norfluoxetine plasma levels were determined. The hippocampal pyramidal cell characteristics and the 5-HT1A and GABA(B) receptor-mediated hyperpolarization were measured in the CA1 and the CA3 subfields. The 5-HT4 receptor-mediated decrease in the slow afterhyperpolarization amplitude was also recorded in area CA1. The time constant, magnitude of the change in resistance during 300-ms hyperpolarizing current pulses and half-decay time of the sAHP were altered by chronic fluoxetine treatment in area CA1 pyramidal cells. No changes were seen in any of the active or passive membrane properties of the CA3 hippocampal pyramidal cells. Fluoxetine treatment increased the potency of 5-HT for the 5-HT1A receptor-mediated hyperpolarization in area CA1, but not area CA3, and decreased the potency of baclofen for the GABA(B) receptor-mediated hyperpolarization in area CA1, but not area CA3. The characteristics of the concentration-response curve for the 5-HT-mediated decrease in sAHP amplitude in area CA1 were not altered by fluoxetine treatment. Chronic fluoxetine selectively and differentially altered the cell characteristics and the 5-HT1A and GABA(B) receptor-mediated responses in area CA1 of the hippocampus, which forms the final common output of the hippocampus.
    Journal of Pharmacology and Experimental Therapeutics 05/1997; 281(1):115-22. · 3.86 Impact Factor
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    ABSTRACT: Fluoxetine is a 5-hydroxytryptamine (5-HT, serotonin)-selective reuptake inhibitor (SSRI) and is one of the main drugs used for the treatment of depression. Because it takes 2 to 3 weeks of treatment before clinical efficacy is manifest, the acute actions of fluoxetine cannot account for the clinical actions of the drug. The chronic effects of fluoxetine have not been completely delineated. The experiments detailed here investigate the chronic effects of fluoxetine on 5-HT and gamma-aminobutyric acid (GABA) receptor-mediated actions using intracellular recording techniques in hippocampal brain slices. Rats were treated with fluoxetine for 3 weeks via osmotic minipumps implanted s.c. Fluoxetine and norfluoxetine plasma levels were determined. The hippocampal pyramidal cell characteristics and the 5- HT1A and GABA(B) receptor-mediated hyperpolarization were measured in the CA1 and the CA3 subfields. The 5-HT4 receptor-mediated decrease in the slow afterhyperpolarization amplitude was also recorded in area CA1. The time constant, magnitude of the change in resistance during 300-ms hyperpolarizing current pulses and half-decay time of the sAHP were altered by chronic fluoxetine treatment in area CA1 pyramidal cells. No changes were seen in any of the active or passive membrane properties of the CA3 hippocampal pyramidal cells. Fluoxetine treatment increased the potency of 5-HT for the 5-HT1A receptor-mediated hyperpolarization in area CA1, but not area CA3, and decreased the potency of baclofen for the GABA(B) receptor-mediated hyperpolarization in area CA1, but not area CA3. The characteristics of the concentration- response curve for the 5-HT-mediated decrease in sAHP amplitude in area CA1 were not altered by fluoxetine treatment. Chronic fluoxetine selectively and differentially altered the cell characteristics and the 5-HT1A and GABA(B) receptor-mediated responses in area CA1 of the hippocampus, which forms the final common output of the hippocampus
    Journal of Pharmacology and Experimental Therapeutics 01/1997; 281(1):115-122. · 3.89 Impact Factor
  • S Birnstiel, S G Beck
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    ABSTRACT: Corticosterone (CT) treatment decreases the magnitude of the 5-hydroxytryptamine (5-HT)1A receptor-mediated hyperpolarization in rat CA1 hippocampal pyramidal neurons. In the present study, we examined the short- and long-term effects of CT on the functionally excitatory 5-HT4 receptor-mediated decrease in the amplitude of the slow afterhyperpolarization (sAHP) that follows a calcium spike and the concomitant decrease in sAHP half decay time. Rats were adrenalectomized (ADX) 2 weeks before the experiment. Data for concentration-response curves were obtained with sharp electrode current clamp recordings in the CA1 pyramidal cell layer of hippocampal slices. Significant changes were found in the 5-HT4 receptor-mediated decrease in sAHP amplitude. The Emax of the 5-HT4 response was significantly increased in cells from ADX rats when the superfusion medium contained 1 nM CT. Short-term administration of 100 nM CT did not alter the 5-HT4 response. Chronic treatment with low concentrations of CT decreased the Emax of the 5-HT4 response. Treatment with CT concentrations that mimic conditions of chronic stress decreased the Emax of the 5-HT4 response and shifted the EC50 to the right. Based on these results we conclude that the magnitude and the potency of the 5-HT4 receptor-mediated decrease in sAHP amplitude is altered by CT. Because the short- and long-term effects of CT treatment are not the same, the actions of CT are time and concentration dependent. CT modulation of the 5-HT4 response is different from its modulation of the 5-HT1A response.
    Journal of Pharmacology and Experimental Therapeutics 07/1995; 273(3):1132-8. · 3.86 Impact Factor
  • S Birnstiel, T J List, S G Beck
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    ABSTRACT: The hypothalamic-pituitary-adrenocortical (HPA) axis controls the levels of plasma corticosterone (CT) in the rat and the levels of cortisol in man. CT is important in maintaining homeostasis and regulating energy production. Homeostasis is maintained by basal activation of the hippocampal-HPA axis. In response to stress CT secretion is increased. CT activation of receptors in the hippocampus provides feedback inhibition of the HPA axis to return the system to basal activity. There are two types of CT receptors: the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR). CT has a 10-fold higher affinity for MR than GR. Normal basal levels of CT occupy the majority of the MR. During the diurnal surge of CT and following the presentation of a stressful stimulus, the MR and GR are both maximally occupied. To begin to understand how CT influences the hippocampal-HPA axis, intracellular recording techniques in the hippocampal brain slice preparation were used to determine how high concentrations of CT may alter cell characteristics and/or evoked synaptic activity. Two treatment groups were used, i.e., adrenalectomized (ADX) and ADX with CT pellet replacement (ADX+CT) that produced plasma blood levels equal to that seen in a normal rat in the morning. Acute administration of 100 nM CT decreased action potential threshold and the number of action potentials elicited by a depolarizing current pulse in cells from both the ADX and ADX+CT treated rats. The amplitude of the evoked excitatory postsynaptic potentials (EPSP) or inhibitory postsynaptic potentials (IPSP) declined in cells recorded from ADX animals and ADX rats acutely treated with high concentrations of CT (ADX/CT).(ABSTRACT TRUNCATED AT 250 WORDS)
    Synapse 07/1995; 20(2):117-24. · 2.43 Impact Factor
  • S G Beck, S Birnstiel, W A Pouliot, K C Choi
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    ABSTRACT: The hippocampus contains interneurons that release gamma-aminobutyric acid (GABA). GABA hyperpolarizes hippocampal CA1 and CA3 pyramidal cells through activation of GABAB postsynaptic receptors. GABAB and 5-hydroxytryptamine1A (5-HT1A) receptors share effector mechanism(s). Agonist potency and the maximal hyperpolarization produced by 5-HT1A receptor activation is different between the CA1 and CA3 subfields. We determined that baclofen, a selective GABAB agonist, was more potent and produced a greater maximal response in area CA3 than in CA1. The larger magnitude of the response can be attributed partly to the larger input resistance of CA3 neurons. GABAB receptor-effector coupling differences between area CA1 and CA3 are proposed as the mechanism underlying the baclofen response incongruities.
    Neuroreport 02/1995; 6(2):310-2. · 1.64 Impact Factor