The N-methyl-d-aspartate receptor antagonist CPP alters synapse and spine structure and impairs long-term potentiation and long-term depression induced morphological plasticity in dentate gyrus of the awake rat

Two opposing types of plasticity at excitatory synapses in the hippocampus, long-term potentiation and depression, require N-methyl-D-aspartate receptor activation and Ca2+ influx for their induction.The direction of the change in synaptic strength is determined by a balance between phosphorylation and dephosphorylation, as regulated by protein kinases and phosphatases that are activated selectively by different levels of intracellular Ca2+.

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Conditions for the Induction of Long-Term Potentiation and Long-Term Depression by Conjunctive Pairing in the Dentate Gyrus In Vitro

Journal of Neurophysiology ◽

10.1152/jn.1997.78.5.2569 ◽

1997 ◽

Vol 78 (5) ◽

pp. 2569-2573 ◽

Cited By ~ 14

Author(s):

Yue Wang ◽

Jianqun Wu ◽

Michael J. Rowan ◽

Roger Anwyl

Keyword(s):

Membrane Potential ◽

Dentate Gyrus ◽

Kinase Inhibitor ◽

Long Term Potentiation ◽

Ruthenium Red ◽

Long Term Depression ◽

Afferent Stimulation ◽

Term Potentiation

Wang, Yue, Jianqun Wu, Michael J. Rowan, and Roger Anwyl. Conditions for the induction of long-term potentiation and long-term depression by conjunctive pairing in the dentate gyrus in vitro. J. Neurophysiol. 78: 2569–2573, 1997. The conditions under which long-term potentiation (LTP) and long-term depression (LTD) of excitatory postsynaptic currents were induced by the conjunctive pairing-type protocol of afferent stimulation and postsynaptic depolarization were studied in the medial perforant pathway-granule cell synapse of the dentate gyrus in vitro. The conjunctive pairing of 1-Hz afferent stimulation and steady state postsynaptic depolarization to 0 mV did not induce LTP or LTD. Inhibition of LTD induction with a phosphatase inhibitor or ruthenium red resulted in induction of LTP after the conjunctive pairing. Such LTP induction was N-methyl-d-aspartate dependent. Conversely, inhibition of LTP induction with a kinase inhibitor resulted in LTD induction after the conjunctive pairing. Thus the failure to induce LTP or LTD with the pairing protocol involving depolarization to 0 mV membrane potential was due to simultaneous activation of intracellular processes that generate the induction of LTP and LTD. Increasing the frequency of afferent stimulation to 200 Hz, even for just eight stimuli, resulted in LTP induction. The studies show that two factors govern the induction of LTP/LTD, membrane potential and frequency of afferent stimulation, with either increased depolarization or increased afferent stimulation favoring LTP induction.

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Refining the temporal definition of an association at the neuronal level using long-term potentiation and long-term depression in the dentate gyrus

Neuroscience Letters ◽

10.1016/0304-3940(91)90365-z ◽

1991 ◽

Vol 126 (1) ◽

pp. 37-40 ◽

Cited By ~ 8

Author(s):

Hossein Hashemzadeh-Gargari ◽

Costa M. Colbert ◽

William B Levy

Keyword(s):

Dentate Gyrus ◽

Long Term Potentiation ◽

Long Term Depression ◽

Term Potentiation ◽

Definition Of

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Persistent memories of long-term potentiation and the N-methyl-d-aspartate receptor

Brain and Neuroscience Advances ◽

10.1177/2398212819848213 ◽

2019 ◽

Vol 3 ◽

pp. 239821281984821 ◽

Cited By ~ 7

Author(s):

TVP Bliss ◽

GL Collingridge

Keyword(s):

Synaptic Plasticity ◽

Long Term Potentiation ◽

Brain Disorders ◽

Molecular Pharmacology ◽

Cellular Mechanisms ◽

Long Term Depression ◽

Aspartate Receptor ◽

Term Potentiation ◽

Core Feature

In this article, we describe our involvement in the early days of research into long-term potentiation. We start with a description of the early experiments conducted in Oslo and London where long-term potentiation was first characterised. We discuss the ways in which the molecular pharmacology of glutamate receptors control the induction and expression of long-term potentiation and its counterpart, long-term depression. We then go on to summarise the extraordinary advances in understanding the cellular mechanisms of synaptic plasticity that have taken place in the subsequent half century. Finally, the increasing evidence that impaired long-term potentiation is a core feature of many brain disorders (LToPathies) is addressed by way of a few selected examples.

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