scholarly journals Nerve growth factor favours long-term depression over long-term potentiation in layer II-III neurones of rat visual cortex

2004 ◽  
Vol 559 (2) ◽  
pp. 497-506 ◽  
Author(s):  
Alfredo Brancucci ◽  
Nicola Kuczewski ◽  
Sonia Covaceuszach ◽  
Antonino Cattaneo ◽  
Luciano Domenici
Keyword(s):  
Visual Cortex ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Long Term Potentiation ◽  
Long Term Depression ◽  
Nerve Growth ◽  
Term Potentiation

Nerve growth factor inhibits the expression of long-term potentiation in hippocampal slices

Neuroreport ◽  
1993 ◽  
Vol 4 (2) ◽  
pp. 147-150 ◽  
Author(s):  
V. Tancredi ◽  
G. DʼArcangelo ◽  
D. Mercanti ◽  
P. Calissano
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Nerve Growth ◽  
Term Potentiation

Lentiviral-mediated overexpression of nerve growth factor (NGF) prevents beta-amyloid [25–35]-induced long term potentiation (LTP) decline in the rat hippocampus

2015 ◽  
Vol 1624 ◽  
pp. 398-404 ◽  
Author(s):  
Shukhrat S. Uzakov ◽  
Andrey D. Ivanov ◽  
Sergey V. Salozhin ◽  
Vladimir A. Markevich ◽  
Natalia V. Gulyaeva
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Beta Amyloid ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Nerve Growth ◽  
Term Potentiation

Metabotropic glutamate receptors and visual cortical synaptic plasticity

1995 ◽  
Vol 73 (9) ◽  
pp. 1312-1322 ◽  
Author(s):  
T. Kamishita ◽  
H. Haruta ◽  
N. Torii ◽  
T. Tsumoto ◽  
T. P. Hicks
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Metabotropic Glutamate Receptors ◽  
Excitatory Amino Acid ◽  
Long Term Potentiation ◽  
Receptor Subtype ◽  
Long Term Depression ◽  
Metabotropic Receptor ◽  
Term Potentiation

Two forms of use-dependent synaptic plasticity, called long-term potentiation (LTP) and long-term depression (LTD), can be elicited in the visual cortex following different paradigms of electrophysiological stimulation. These neurobiological phenomena often are considered as necessary components of models for the alteration in function of the nervous system that must occur at some level for the establishment and (or) maintenance of memory engrams, for learning processes, or for the consolidation of active neural connections and regression of inactive contacts in the developing brain. It has been postulated that for LTP and LTD to be produced in the hippocampus, activation of a particular subtype of excitatory amino acid receptor, the metabotropic receptor, is a critical requirement. Only recently has it become possible to test this hypothesis directly, as a new compound, (±)-α-methyl-4-carboxyphenylglycine (MCPG), has been introduced and the suggestion made that it selectively antagonizes the metabotropic receptor. This substance has been tested in the present study on responses recorded from slices of rat visual cortex and has been found both to block the activation of the metabotropic receptor and to interfere selectively with the form of synaptic plasticity called LTD. It thus appears from the experiments reported in this paper as though the metabotropic receptor subtype that is blocked by MCPG is required for the expression of LTD but not for the expression of LTP, in the visual cortex of adult rats.Key words: excitatory amino acids, long-term potentiation, long-term depression, visual cortex, (±)-α-methyl-4-carboxyphenylglycine (MCPG).

scholarly journals Layer 2/3 Synapses in Monocular and Binocular Regions of Tree Shrew Visual Cortex Express mAChR-Dependent Long-Term Depression and Long-Term Potentiation

2008 ◽  
Vol 100 (1) ◽  
pp. 336-345 ◽  
Author(s):  
Portia McCoy ◽  
Thomas T. Norton ◽  
Lori L. McMahon
Keyword(s):  
Visual Cortex ◽  
Learning And Memory ◽  
Tree Shrew ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Muscarinic Acetylcholine Receptors ◽  
Long Term Depression ◽  
Term Potentiation ◽  
Layer 2

Acetylcholine is an important modulator of synaptic efficacy and is required for learning and memory tasks involving the visual cortex. In rodent visual cortex, activation of muscarinic acetylcholine receptors (mAChRs) induces a persistent long-term depression (LTD) of transmission at synapses recorded in layer 2/3 of acute slices. Although the rodent studies expand our knowledge of how the cholinergic system modulates synaptic function underlying learning and memory, they are not easily extrapolated to more complex visual systems. Here we used tree shrews for their similarities to primates, including a visual cortex with separate, defined regions of monocular and binocular innervation, to determine whether mAChR activation induces long-term plasticity. We find that the cholinergic agonist carbachol (CCh) not only induces long-term plasticity, but the direction of the plasticity depends on the subregion. In the monocular region, CCh application induces LTD of the postsynaptic potential recorded in layer 2/3 that requires activation of m3 mAChRs and a signaling cascade that includes activation of extracellular signal-regulated kinase (ERK) 1/2. In contrast, layer 2/3 postsynaptic potentials recorded in the binocular region express long-term potentiation (LTP) following CCh application that requires activation of m1 mAChRs and phospholipase C. Our results show that activation of mAChRs induces long-term plasticity at excitatory synapses in tree shrew visual cortex. However, depending on the ocular inputs to that region, variation exists as to the direction of plasticity, as well as to the specific mAChR and signaling mechanisms that are required.

Voltage-Sensitive Calcium Currents Are Acutely Increased by Nerve Growth Factor in PC12 Cells

1999 ◽  
Vol 82 (6) ◽  
pp. 2847-2852 ◽  
Author(s):  
Min Jia ◽  
Minxu Li ◽  
Xu-Wen Liu ◽  
Hao Jiang ◽  
Phillip G. Nelson ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Calcium Current ◽  
Calcium Uptake ◽  
Growth Factor Receptor ◽  
Long Term Potentiation ◽  
Calcium Currents ◽  
Nerve Growth

Whole cell calcium currents were recorded from PC12 cells with the perforated patch technique. Currents were evoked by step depolarization from a holding potential of −90 mV. Nerve growth factor (NGF) increased calcium currents through L-type calcium channels by >75% within 3–5 min. This increase was inhibited by K-252a, by nifedipine, and by inhibition or down-regulation of kinase C. Brain-derived neurotrophic factor (BDNF) also increased calcium current, but to a smaller extent. Thus increases in calcium current can be linked to activation of either the high- or the low-affinity nerve growth factor receptor. Increases in presynaptic calcium uptake appear to be a crucial element in the short-term actions of the neurotrophins on neurotransmitter release leading to long-term potentiation. Also, the control of calcium uptake is likely to be an important factor in the long-term actions of the neurotrophins on neuronal survival and neuronal protection. The present data indicate that the PC12 cell may be a useful model for studying the effect of the neurotrophins on calcium uptake.

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