Role of Egr1 in Hippocampal Synaptic Enhancement Induced by Tetanic Stimulation and Amputation

Autor: Jeffrey Milbrandt, Zhican Qu, Feng Wei, Min Zhuo, Zao C. Xu
Rok vydání: 2000
Předmět:
Male
Time Factors
hippocampus
Long-Term Potentiation
Glutamic Acid
Pain
Nonsynaptic plasticity
Biology
Receptors
N-Methyl-D-Aspartate
Synaptic Transmission
Amputation
Surgical
Immediate-Early Proteins
Rats
Sprague-Dawley
Mice
03 medical and health sciences
0302 clinical medicine
Memory
Synaptic augmentation
Metaplasticity
Animals
Early Growth Response Protein 1
030304 developmental biology
Mice
Knockout
0303 health sciences
Neuronal Plasticity
Post-tetanic potentiation
Brief Report
Pyramidal Cells
Excitatory Postsynaptic Potentials
Nociceptors
Long-term potentiation
Cell Biology
Anatomy
Immunohistochemistry
Electric Stimulation
Rats
DNA-Binding Proteins
Synaptic fatigue
NMDA
nervous system
Synapses
Synaptic plasticity
Egr1
LTP
Tetanic stimulation
Neuroscience
030217 neurology & neurosurgery
Transcription Factors
Zdroj: The Journal of Cell Biology
ISSN: 1540-8140
0021-9525
DOI: 10.1083/jcb.149.7.1325
Popis: Hippocampal neurons fire spikes when an animal is at a particular location or performs certain behaviors in a particular place, providing a cellular basis for hippocampal involvement in spatial learning and memory. In a natural environment, spatial memory is often associated with potentially dangerous sensory experiences such as noxious or painful stimuli. The central sites for such pain-associated memory or plasticity have not been identified. Here we present evidence that excitatory glutamatergic synapses within the CA1 region of the hippocampus may play a role in storing pain-related information. Peripheral noxious stimulation induced excitatory postsynaptic potentials (EPSPs) in CA1 pyramidal cells in anesthetized animals. Tissue/nerve injury caused a rapid increase in the level of the immediate-early gene product Egr1 (also called NGFI-A, Krox24, or zif/268) in hippocampal CA1 neurons. In parallel, synaptic potentiation induced by a single tetanic stimulation (100 Hz for 1 s) was enhanced after the injury. This enhancement of synaptic potentiation was absent in mice lacking Egr1. Our data suggest that Egr1 may act as an important regulator of pain-related synaptic plasticity within the hippocampus.
Databáze: OpenAIRE
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