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  • 1
    Publication Date: 1980-12-05
    Description: Synaptic excitation of hippocampal cells during blockade of synaptic inhibition results in an epileptiform "burst" potential followed by a prolonged afterhyperpolarization. This afterhyperpolarization resembles the one that is seen after the epileptic interictal spike and that is considered of critical importance in preventing seizure development. The afterhyperpolarization produced in the presence of y-aminobutyric acid antagonists is associated with a conductance increase and is inhibitory. It can occur in an all-or-none fashion after a burst, is independent of chloride, and is depressed by barium. The afterhyperpolarization has a reversal potential of (-86) millivolts, and the reversal potential is strongly dependent on the extracellular concentration of potassium. The afterhyperpolarization appears to be an intrinsic, inhibitory potassium potential mediated by calcium. This finding has implications for understanding the cellular mechanisms of epilepsy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alger, B E -- Nicoll, R A -- 9 F32 NS05744-02/NS/NINDS NIH HHS/ -- GM-23478/GM/NIGMS NIH HHS/ -- NS-00287/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1980 Dec 5;210(4474):1122-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7444438" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology ; Epilepsy/*physiopathology ; Hippocampus/*physiopathology ; In Vitro Techniques ; Male ; Membrane Potentials ; Neural Inhibition ; Potassium/*physiology ; Pyramidal Tracts/physiopathology ; gamma-Aminobutyric Acid/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1981-05-22
    Description: In hippocampal CAl pyramidal cells, orthodromic synaptic excitation is followed by an early hyperpolarization mediated by gamma-aminobutyric acid (GABA) and a late non-GABA-mediated hyperpolarization that has properties consistent with an increase in potassium conductance. Depolarizations produced by iontophoretically applied glutamate are followed by hyperpolarizations that have features in accordance with an increase in potassium conductance. The hyperpolarizations are independent of chloride and resistant to tetradotoxin but are blocked by a low-calcium, high-cobalt medium. Voltage clamping the glutamate depolarization does not reduce the subsequent hyperpolarization, indicating that the hyperpolarization results from a direct increase in calcium conductance produced by glutamate, rather than from activation of voltage-sensitive calcium channels. A single transmitter, possibly acting on one type of receptor and channel, may initiate both excitation and inhibition in the same postsynaptic cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nicoll, R A -- Alger, B E -- NS 15764/NS/NINDS NIH HHS/ -- NS-00287/NS/NINDS NIH HHS/ -- NS07067/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1981 May 22;212(4497):957-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6262912" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicuculline/pharmacology ; Calcium/*pharmacology ; Electric Conductivity ; Electric Stimulation ; Glutamates/pharmacology ; Hippocampus/*physiology ; In Vitro Techniques ; Membrane Potentials/drug effects ; Neural Inhibition/drug effects ; Potassium/*physiology ; Pyramidal Tracts/*physiology ; Rats ; *Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-09-23
    Description: The hippocampal slice preparation was used to study the role of acetylcholine as a synaptic transmitter. Bath-applied acetylcholine had three actions on pyramidal cells: (i) depolarization associated with increased input resistance, (ii) blockade of calcium-activated potassium responses, and (iii) blockade of accommodation of cell discharge. All these actions were reversed by the muscarinic antagonist atropine. Stimulation of sites in the slice known to contain cholinergic fibers mimicked all the actions. Furthermore, these evoked synaptic responses were enhanced by the cholinesterase inhibitor eserine and were blocked by atropine. These findings provide electrophysiological support for the role of acetylcholine as a synaptic transmitter in the brain and demonstrate that nonclassical synaptic responses involving the blockade of membrane conductances exist in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cole, A E -- Nicoll, R A -- MH00437/MH/NIMH NIH HHS/ -- NS-16485/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1299-301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612345" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*physiology ; Animals ; Atropine/pharmacology ; Electric Stimulation ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Membrane Potentials/drug effects ; Physostigmine/pharmacology ; Rats ; Receptors, Muscarinic/physiology ; Synapses/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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