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36. Uric acid effects on evoked potentials in rat hippocampal slices
A16
Abstracts/Journal of Neuroscience Methods (1994) A1-A28
release of GABA is a sign of this interaction. Characterization of this phenomenon is essential for understanding of physiological plasticity of hippocampal functions. In our studies on coronal hippocampal slices in a superfusion system the glutamate agonists (NMDA, kainate, quisqalate and AMPA) evoked a transient Ca2+-dependent release of [3H]GABA via ionotropic NMDA- and non-NMDA receptors. This evoked release may be the basis of physiological feedback inhibition of principal excitatory neurons in the hippocampus. Glutamate and quisqalate also activated metabotropic receptors and evoked a long-lasting Ca2+-inde pendent release of GABA. Such an excessive release may diminish the inhibition via GABA autoreceptors and may increase excitation of principal cells. This may contribute to generation of long-term potentiation. A reduction of the functional disulfide bridges in the NMDA-type glutamate receptors causes a huge, longlasting GABA release both in the presence and absence of external Ca 2+. This release is probably pathological and contributes to the overexcitation and death of excitatory neurons. The neuroprotection of the endogenous thiol redox agent glutathione is partly explicable by its efficacy to prevent such a release of GABA.
36. URIC ACID EFFECTS ON EVOKED POTENTIALS IN RAT HIPPOCAMPAL SLICES V.I. Khihcenco, O.G. Safronova, U.I. Rovda
Institute of Medical and Biological Cybernetics, SB RAMS, Novosibrisk, State Medical Institute, Kemerovo, Russia The hippocampal slice preparation is a useful model for the investigation of cellular and molecular mechanisms of biologically active substances. It is well known that patients with increased uric acid levels (associated with gout) exhibit unique features of central nervous system function. Uric acid (2,6,8-trioxypurine), the end product of purinergic metabolism, not only has biologically active precursors, but on its own can also influence neuronal function. Electrophysiological experiments were carried out on rat hippocampal slices 300-400 /zm in thickness. We have studied the effects of uric acid on population spikes which were evoked and recorded in the CA1 region via an electrical stimulation of the Schaffer collateral fibers, using standard techniques and analytical means. The application of uric acid to rat hippocampal slices elicited a decrease in population spike latency
accompanied by an increase in population spike amplitude. Uric acid could produce these effects either by modifying the electrical characteristics of the neuronal membrane or by modulating the synaptic efficiency.
37. EFFECTS OF ANISOSMOTIC MEDIA AND HYPOXIA ON EXCITABILITY AND INTRINSIC OPTICAL PROPERTIES OF HIPPOCAMPAL SLICES
N.R. Kreisman, J.C. LaManna, S.-C. Liao, J.R. Alcala
Departments of Neurology, Anatomy, and Biomedical Engineering, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA; Department of Physiology, Tulane Univ. School of Medicine, New Orleans, LA 70112, USA Intrinsic optical properties of in vitro brain slices change as cells swell. The objective of the present study was to correlate neuronal excitability ana cell swelling during osmotic changes and hypoxia. Orthodromic population spike amplitudes were measured with glass micropipettes in CA1 stratum pyramidale of 400-~zm-thick rat hippocampal slices. Slices were incubated in physiological saline at 32 +_ I°C in an interface chamber. Transmitted light from a quartz-halogen source was detected with a silicon photodiode coupled to a dissecting microscope. The optical field was approximately 0.5 × 1.5 mm. Decreasing osmolarity of the medium by 30-45 m O s m / l from a basal level of 295300 mOsm/1 caused a 7.5_+ 2.4% decrease in light transmittance (n = 10) and a 46.6 +_ 16.0% increase in population spike amplitude (n =5). Conversely, an equivalent increase in bath osmolarity caused a 6.9 +_ 1.6% increase in light transmittance (n = 7) and a 32.8_+ 8.7% decrease in population spike amplitude (n = 4). Hypoxia often produced a triphasic change in light transmittance consisting of a slow increase ( A T / T = + 5.4 +_ 0.7%; n = 16), followed by a slow decrease ( A T / T = - 17.6 _+ 3.2%; n = 14), and finally a rapid decrease ( A T / T = -31.1 +_ 2.4%; n = 11), which was coincident with anoxic depolarization. These results suggest marked cell swelling during maintained hypoxia. In separate experiments, light transmittance through submerged slices was imaged with an 8-bit CCD video camera. The largest optical changes were in the stratum radiatum, followed by stratum pyramidale and stratum oriens. In contrast to the results on slices in the interface chamber, optical changes in submerged slices were consistently reversed but comparable in amplitude. This might be explained by the optical properties of the slice-medium interface.
Abstracts/Journal of Neuroscience Methods (1994) A1-A28
release of GABA is a sign of this interaction. Characterization of this phenomenon is essential for understanding of physiological plasticity of hippocampal functions. In our studies on coronal hippocampal slices in a superfusion system the glutamate agonists (NMDA, kainate, quisqalate and AMPA) evoked a transient Ca2+-dependent release of [3H]GABA via ionotropic NMDA- and non-NMDA receptors. This evoked release may be the basis of physiological feedback inhibition of principal excitatory neurons in the hippocampus. Glutamate and quisqalate also activated metabotropic receptors and evoked a long-lasting Ca2+-inde pendent release of GABA. Such an excessive release may diminish the inhibition via GABA autoreceptors and may increase excitation of principal cells. This may contribute to generation of long-term potentiation. A reduction of the functional disulfide bridges in the NMDA-type glutamate receptors causes a huge, longlasting GABA release both in the presence and absence of external Ca 2+. This release is probably pathological and contributes to the overexcitation and death of excitatory neurons. The neuroprotection of the endogenous thiol redox agent glutathione is partly explicable by its efficacy to prevent such a release of GABA.
36. URIC ACID EFFECTS ON EVOKED POTENTIALS IN RAT HIPPOCAMPAL SLICES V.I. Khihcenco, O.G. Safronova, U.I. Rovda
Institute of Medical and Biological Cybernetics, SB RAMS, Novosibrisk, State Medical Institute, Kemerovo, Russia The hippocampal slice preparation is a useful model for the investigation of cellular and molecular mechanisms of biologically active substances. It is well known that patients with increased uric acid levels (associated with gout) exhibit unique features of central nervous system function. Uric acid (2,6,8-trioxypurine), the end product of purinergic metabolism, not only has biologically active precursors, but on its own can also influence neuronal function. Electrophysiological experiments were carried out on rat hippocampal slices 300-400 /zm in thickness. We have studied the effects of uric acid on population spikes which were evoked and recorded in the CA1 region via an electrical stimulation of the Schaffer collateral fibers, using standard techniques and analytical means. The application of uric acid to rat hippocampal slices elicited a decrease in population spike latency
accompanied by an increase in population spike amplitude. Uric acid could produce these effects either by modifying the electrical characteristics of the neuronal membrane or by modulating the synaptic efficiency.
37. EFFECTS OF ANISOSMOTIC MEDIA AND HYPOXIA ON EXCITABILITY AND INTRINSIC OPTICAL PROPERTIES OF HIPPOCAMPAL SLICES
N.R. Kreisman, J.C. LaManna, S.-C. Liao, J.R. Alcala
Departments of Neurology, Anatomy, and Biomedical Engineering, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA; Department of Physiology, Tulane Univ. School of Medicine, New Orleans, LA 70112, USA Intrinsic optical properties of in vitro brain slices change as cells swell. The objective of the present study was to correlate neuronal excitability ana cell swelling during osmotic changes and hypoxia. Orthodromic population spike amplitudes were measured with glass micropipettes in CA1 stratum pyramidale of 400-~zm-thick rat hippocampal slices. Slices were incubated in physiological saline at 32 +_ I°C in an interface chamber. Transmitted light from a quartz-halogen source was detected with a silicon photodiode coupled to a dissecting microscope. The optical field was approximately 0.5 × 1.5 mm. Decreasing osmolarity of the medium by 30-45 m O s m / l from a basal level of 295300 mOsm/1 caused a 7.5_+ 2.4% decrease in light transmittance (n = 10) and a 46.6 +_ 16.0% increase in population spike amplitude (n =5). Conversely, an equivalent increase in bath osmolarity caused a 6.9 +_ 1.6% increase in light transmittance (n = 7) and a 32.8_+ 8.7% decrease in population spike amplitude (n = 4). Hypoxia often produced a triphasic change in light transmittance consisting of a slow increase ( A T / T = + 5.4 +_ 0.7%; n = 16), followed by a slow decrease ( A T / T = - 17.6 _+ 3.2%; n = 14), and finally a rapid decrease ( A T / T = -31.1 +_ 2.4%; n = 11), which was coincident with anoxic depolarization. These results suggest marked cell swelling during maintained hypoxia. In separate experiments, light transmittance through submerged slices was imaged with an 8-bit CCD video camera. The largest optical changes were in the stratum radiatum, followed by stratum pyramidale and stratum oriens. In contrast to the results on slices in the interface chamber, optical changes in submerged slices were consistently reversed but comparable in amplitude. This might be explained by the optical properties of the slice-medium interface.