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Modulation of low-frequency-induced synaptic depression in the developing CA3-CA1 hippocampal synapses by NMDA and metabotropic glutamate receptor activation.

Strandberg, Joakim, 1978 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology
Wasling, Pontus, 1970 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology
Gustafsson, Bengt, 1946 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology
 (creator_code:org_t)
American Physiological Society, 2009
2009
Engelska.
Ingår i: Journal of neurophysiology. - : American Physiological Society. - 0022-3077 .- 1522-1598. ; 101:5, s. 2252-62
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Brief test-pulse stimulation (0.2-0.05 Hz) of naïve (previously nonstimulated) developing hippocampal CA3-CA1 synapses leads to a substantial synaptic depression, explained by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) silencing. Using field recordings in hippocampal slices from P8 to P12 rats, we examined this depression of naïve synapses using more prolonged test-pulse stimulation as well as low-frequency (1 Hz) stimulation (LFS). We found that 900 stimuli produced depression during stimulation to approximately 40% of the naïve level independent of whether test-pulse stimulation or LFS was used. This result was also observed during combined blockade of N-methyl-d-aspartate/metabotropic glutamate receptors (NMDAR/mGluRs) although the depression was smaller (to approximately 55% of naïve level). Using separate blockade of either NMDARs or mGluRs, we found that this impairment of the depression resulted from the NMDAR, and not from the mGluR, blockade. In fact, during NMDAR blockade alone, depression was smaller even than that observed during combined blockade. We also found that mGluR blockade alone facilitated the LFS-induced depression. In conclusion, test-pulse stimulation produced as much depression as LFS when applied to naïve synapses even when allowing for NMDAR and mGluR activation. Our results seem in line with the notion that NMDARs and mGluRs may exert a bidirectional control on AMPA receptor recruitment to synapses.

Nyckelord

Animals
Animals
Newborn
Biophysics
Electric Stimulation
methods
Excitatory Amino Acid Antagonists
pharmacology
Excitatory Postsynaptic Potentials
drug effects
physiology
Hippocampus
cytology
Long-Term Synaptic Depression
drug effects
physiology
Neural Pathways
physiology
Rats
Rats
Wistar
Receptors
Metabotropic Glutamate
antagonists & inhibitors
physiology
Receptors
N-Methyl-D-Aspartate
antagonists & inhibitors
physiology
Synapses
drug effects
physiology

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