ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 11
    facet.materialart.
    Unknown
    Comparison of two forms of long-term potentiation in single hippocampal neurons (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-29
    Description: In invertebrate nervous systems, some long-lasting increases in synaptic efficacy result from changes in the presynaptic cell. In the vertebrate nervous system, the best understood long-lasting change in synaptic strength is long-term potentiation (LTP) in the CA1 region of the hippocampus. Here the process is initiated postsynaptically, but the site of the persistent change is unresolved. Single CA3 hippocampal pyramidal cells receive excitatory inputs from associational-commissural fibers and from the mossy fibers of dentate granule cells and both pathways exhibit LTP. Although the induction of associational-commissural LTP requires in the postsynaptic cell N-methyl-D-aspartate (NMDA) receptor activation, membrane depolarization, and a rise in calcium, mossy fiber LTP does not. Paired-pulse facilitation, which is an index of increased transmitter release, is unaltered during associational-commissural LTP but is reduced during mossy fiber LTP. Thus, both the induction and the persistent change may be presynaptic in mossy fiber LTP but not in associational-commissural LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zalutsky, R A -- Nicoll, R A -- MH0437/MH/NIMH NIH HHS/ -- MH38256/MH/NIMH NIH HHS/ -- NS24205/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1619-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Physiology, University of California, San Francisco, CA 94114-0450.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2114039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Egtazic Acid/pharmacology ; Electric Stimulation ; Evoked Potentials ; Fluorides/pharmacology ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Membrane Potentials/drug effects ; Microelectrodes ; Neurons/drug effects/*physiology ; Synapses/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 12
    facet.materialart.
    Unknown
    Vesicular glutamate transporters 1 and 2 target to functionally distinct synaptic release sites (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-01
    Description: Vesicular glutamate transporters (VGLUTs) 1 and 2 show a mutually exclusive distribution in the adult brain that suggests specialization for synapses with different properties of release. Consistent with this distribution, inactivation of the VGLUT1 gene silenced a subset of excitatory neurons in the adult. However, the same cell populations exhibited VGLUT1-independent transmission early in life. Developing hippocampal neurons transiently coexpressed VGLUT2 and VGLUT1 at distinct synaptic sites with different short-term plasticity. The loss of VGLUT1 also reduced the reserve pool of synaptic vesicles. Thus, VGLUT1 plays an unanticipated role in membrane trafficking at the nerve terminal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fremeau, Robert T Jr -- Kam, Kaiwen -- Qureshi, Tayyaba -- Johnson, Juliette -- Copenhagen, David R -- Storm-Mathisen, Jon -- Chaudhry, Farrukh A -- Nicoll, Roger A -- Edwards, Robert H -- R01 EY001869/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2004 Jun 18;304(5678):1815-9. Epub 2004 Apr 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Graduate Programs in Neuroscience and Cell Biology, University of California San Francisco School of Medicine, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15118123" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/cytology/*metabolism ; Carrier Proteins/genetics/*metabolism ; Cell Membrane/physiology ; Cells, Cultured ; Cerebellum/metabolism/ultrastructure ; Excitatory Postsynaptic Potentials ; Glutamic Acid/metabolism ; Hippocampus/cytology/metabolism/ultrastructure ; In Situ Hybridization ; *Membrane Transport Proteins ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/metabolism ; Neurons/*metabolism/physiology ; Patch-Clamp Techniques ; Purkinje Cells/physiology ; Pyramidal Cells/metabolism ; Synapses/*metabolism/ultrastructure ; *Synaptic Transmission ; Synaptic Vesicles/*metabolism/physiology ; Vesicular Glutamate Transport Protein 1 ; Vesicular Glutamate Transport Protein 2 ; *Vesicular Transport Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 13
    facet.materialart.
    Unknown
    Dynamic interaction of stargazin-like TARPs with cycling AMPA receptors at synapses (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-06
    Description: Activity-dependent plasticity in the brain arises in part from changes in the number of synaptic AMPA receptors. Synaptic trafficking of AMPA receptors is controlled by stargazin and homologous transmembrane AMPA receptor regulatory proteins (TARPs). We found that TARPs were stable at the plasma membrane, whereas AMPA receptors were internalized in a glutamate-regulated manner. Interaction with AMPA receptors involved both extra- and intracellular determinants of TARPs. Upon binding to glutamate, AMPA receptors detached from TARPs. This did not require ion flux or intracellular second messengers. This allosteric mechanism for AMPA receptor dissociation from TARPs may participate in glutamate-mediated internalization of receptors in synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tomita, Susumu -- Fukata, Masaki -- Nicoll, Roger A -- Bredt, David S -- New York, N.Y. -- Science. 2004 Mar 5;303(5663):1508-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco, San Francisco, CA 94143-2140, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15001777" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology ; Animals ; Calcium Channels/analysis/*metabolism ; Cell Line ; Cells, Cultured ; Cerebral Cortex/chemistry/cytology ; Endocytosis ; Glutamic Acid/metabolism/pharmacology ; Humans ; Neuronal Plasticity ; Protein Binding ; Protein Structure, Tertiary ; Rats ; Receptors, AMPA/agonists/antagonists & inhibitors/*metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/*metabolism ; Xenopus laevis ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 14
    facet.materialart.
    Unknown
    Endocannabinoid signaling in the brain (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-27
    Description: The primary psychoactive ingredient in cannabis, Delta9-tetrahydrocannabinol (Delta9-THC), affects the brain mainly by activating a specific receptor (CB1). CB1 is expressed at high levels in many brain regions, and several endogenous brain lipids have been identified as CB1 ligands. In contrast to classical neurotransmitters, endogenous cannabinoids can function as retrograde synaptic messengers: They are released from postsynaptic neurons and travel backward across synapses, activating CB1 on presynaptic axons and suppressing neurotransmitter release. Cannabinoids may affect memory, cognition, and pain perception by means of this cellular mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Rachel I -- Nicoll, Roger A -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):678-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, 139-74, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11976437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/metabolism ; Brain/*metabolism ; Cannabinoid Receptor Modulators ; Cannabinoids/*metabolism ; Endocannabinoids ; Humans ; Mental Processes ; Mice ; Neurons/*metabolism ; Neurotransmitter Agents/metabolism ; Pain ; Receptors, Cannabinoid ; Receptors, Drug/*metabolism ; *Signal Transduction ; Synapses/*metabolism ; Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 15
    facet.materialart.
    Unknown
    LTP requires a reserve pool of glutamate receptors independent of subunit type (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-12-14
    Description: Long-term potentiation (LTP) of synaptic transmission is thought to be an important cellular mechanism underlying memory formation. A widely accepted model posits that LTP requires the cytoplasmic carboxyl tail (C-tail) of the AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor subunit GluA1. To find the minimum necessary requirement of the GluA1 C-tail for LTP in mouse CA1 hippocampal pyramidal neurons, we used a single-cell molecular replacement strategy to replace all endogenous AMPA receptors with transfected subunits. In contrast to the prevailing model, we found no requirement of the GluA1 C-tail for LTP. In fact, replacement with the GluA2 subunit showed normal LTP, as did an artificially expressed kainate receptor not normally found at these synapses. The only conditions under which LTP was impaired were those with markedly decreased AMPA receptor surface expression, indicating a requirement for a reserve pool of receptors. These results demonstrate the synapse's remarkable flexibility to potentiate with a variety of glutamate receptor subtypes, requiring a fundamental change in our thinking with regard to the core molecular events underlying synaptic plasticity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998843/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998843/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Granger, Adam J -- Shi, Yun -- Lu, Wei -- Cerpas, Manuel -- Nicoll, Roger A -- R01 MH070957/MH/NIMH NIH HHS/ -- England -- Nature. 2013 Jan 24;493(7433):495-500. doi: 10.1038/nature11775. Epub 2012 Dec 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Graduate Program, University of California San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235828" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Deletion ; Long-Term Potentiation/*physiology ; Mice ; Models, Neurological ; Protein Structure, Tertiary ; Protein Subunits/*metabolism ; Protein Transport ; Receptors, AMPA/chemistry/deficiency/genetics/metabolism ; Receptors, Ionotropic Glutamate/*chemistry/*metabolism ; Receptors, Kainic Acid/metabolism ; Synapses/metabolism ; Synaptic Transmission
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 16
    facet.materialart.
    Unknown
    Epilepsy-related ligand/receptor complex LGI1 and ADAM22 regulate synaptic transmission (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-23
    Description: Abnormally synchronized synaptic transmission in the brain causes epilepsy. Most inherited forms of epilepsy result from mutations in ion channels. However, one form of epilepsy, autosomal dominant partial epilepsy with auditory features (ADPEAF), is characterized by mutations in a secreted neuronal protein, LGI1. We show that ADAM22, a transmembrane protein that when mutated itself causes seizure, serves as a receptor for LGI1. LGI1 enhances AMPA receptor-mediated synaptic transmission in hippocampal slices. The mutated form of LGI1 fails to bind to ADAM22. ADAM22 is anchored to the postsynaptic density by cytoskeletal scaffolds containing stargazin. These studies in rat brain indicate possible avenues for understanding human epilepsy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukata, Yuko -- Adesnik, Hillel -- Iwanaga, Tsuyoshi -- Bredt, David S -- Nicoll, Roger A -- Fukata, Masaki -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1792-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genomics and Proteomics, National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8522, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990550" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/chemistry/genetics/*metabolism ; Animals ; Calcium Channels/metabolism ; Cell Line ; Cerebellar Cortex/metabolism ; Cerebral Cortex/metabolism ; Epilepsies, Partial/physiopathology ; Hippocampus/metabolism/*physiology ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Ligands ; Membrane Proteins/metabolism ; Mice ; N-Methylaspartate/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Proteins/*metabolism ; Rats ; Receptors, AMPA/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism ; *Synaptic Transmission ; Transfection ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 17
    facet.materialart.
    Unknown
    Bidirectional control of quantal size by synaptic activity in the hippocampus (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: Analysis of strontium-induced asynchronous release of quanta from stimulated synapses revealed that long-term potentiation and long-term depression in the CA1 region of the mammalian hippocampus are associated with an increase and a decrease, respectively, in quantal size. At a single set of synapses, the increase in quantal size seen with long-term potentiation was completely reversed by depotentiating stimuli. Long-term potentiation and depression are also associated with an increase and decrease, respectively, in the frequency of quantal events, consistent with an all-or-none regulation (up or down) of clusters of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, a change in the release of transmitter, or both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oliet, S H -- Malenka, R C -- Nicoll, R A -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1294-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco 94143-0450, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638114" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Electric Stimulation ; Evoked Potentials ; Guinea Pigs ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Long-Term Potentiation/*physiology ; Neuronal Plasticity/*physiology ; Neurons/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/physiology ; Strontium/pharmacology ; Synapses/*physiology ; *Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 18
    facet.materialart.
    Unknown
    Learning mechanisms: the case for CaM-KII (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lisman, J -- Malenka, R C -- Nicoll, R A -- Malinow, R -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2001-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Brandeis University, Waltham, MA 02254, USA. lisman@binah.cc.brandeis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221509" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Hippocampus/metabolism ; *Long-Term Potentiation ; Memory ; Mice ; Mice, Transgenic ; Phosphorylation ; Receptors, AMPA/*metabolism ; Signal Transduction ; Synapses/*metabolism ; *Synaptic Transmission ; Vision, Ocular
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 19
    facet.materialart.
    Unknown
    Mediation of hippocampal mossy fiber long-term potentiation by cyclic AMP (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: Repetitive activation of hippocampal mossy fibers evokes a long-term potentiation (LTP) of synaptic responses in pyramidal cells in the CA3 region that is independent of N-methyl-D-aspartate receptor activation. Previous results suggest that the site for both the induction and expression of this form of LTP is presynaptic. Experimental elevation of cyclic adenosine 3',5'-monophosphate (cAMP) both mimics and interferes with tetanus-induced mossy fiber LTP, and blockers of the cAMP cascade block mossy fiber LTP. It is proposed that calcium entry into the presynaptic terminal may activate Ca(2+)-calmodulin-sensitive adenylyl cyclase I which, through protein kinase A, causes a persistent enhancement of evoked glutamate release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisskopf, M G -- Castillo, P E -- Zalutsky, R A -- Nicoll, R A -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1878-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Graduate Program, University of California, San Francisco 94143-0450.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916482" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; *Carbazoles ; Colforsin/pharmacology ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Glutamates/metabolism/pharmacology ; Glutamic Acid ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Indoles/pharmacology ; Isoquinolines/pharmacology ; *Long-Term Potentiation/drug effects ; Models, Biological ; Nerve Fibers/*physiology ; Presynaptic Terminals/metabolism ; Pyramidal Cells/physiology ; Pyrroles/pharmacology ; *Sulfonamides ; Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 20
    facet.materialart.
    Unknown
    Long-term potentiation: evidence against an increase in transmitter release probability in the CA1 region of the hippocampus (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: It is widely accepted that N-methyl-D-aspartate (NMDA)-receptor-dependent long-term potentiation (LTP) in the CA1 region of the hippocampus is triggered postsynaptically, but there is considerable debate as to the site at which the increase in synaptic strength is expressed. The irreversible open-channel blocking action of the NMDA receptor antagonist MK-801 has been used to test whether the probability of transmitter release (Pr) is increased during LTP. Although the rate of decline of the amplitude of the NMDA receptor-mediated excitatory postsynaptic current (EPSC) in the presence of MK-801 strongly depends on Pr, the rate of decline of the EPSC evoked at synapses expressing LTP is identical to that observed at synapses not expressing LTP. These findings are difficult to reconcile with models in which the expression of LTP is due to an increase in Pr.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manabe, T -- Nicoll, R A -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1888-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dizocilpine Maleate/pharmacology ; Guinea Pigs ; Hippocampus/*metabolism ; In Vitro Techniques ; *Long-Term Potentiation ; Male ; Neurotransmitter Agents/*metabolism ; Receptors, AMPA/antagonists & inhibitors/physiology ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*physiology ; Synapses/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...