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Neuropeptide Y does not alter NMDA conductances in CA3 pyramidal neurons: a slice-patch study
1Department of Pharmacology, University of Alberta, Edmonton, Canada.
Neuroscience Letters
|April 27, 1992
Summary
Neuropeptide Y (NPY) does not directly enhance N-methyl-D-aspartate (NMDA) responses in hippocampal CA3 cells. While NPY inhibits excitatory neurotransmission, it does not appear to alter postsynaptic NMDA receptor function.
Area of Science:
- Neuroscience
- Neuropharmacology
- Cellular Electrophysiology
Background:
- Neuropeptide Y (NPY) is known to presynaptically inhibit hippocampal excitatory neurotransmission.
- Emerging evidence suggests NPY might potentiate N-methyl-D-aspartate (NMDA)-mediated responses via sigma/phencyclidine (PCP) binding sites.
Purpose of the Study:
- To investigate the hypothesis that NPY potentiates NMDA-mediated excitatory responses in hippocampal CA3 pyramidal cells.
- To determine if NPY directly affects postsynaptic NMDA receptor function.
Main Methods:
- Slice-patch voltage clamp recordings were performed on CA3 pyramidal cells in the hippocampus.
- The effects of NPY on NMDA-induced inward currents and mossy fiber-elicited excitatory postsynaptic currents were examined.
Main Results:
- NPY did not alter inward currents elicited by direct iontophoresis of NMDA onto CA3 cell dendrites.
- NPY significantly reduced excitatory postsynaptic currents evoked by mossy fiber stimulation.
Conclusions:
- NPY does not appear to directly modulate postsynaptic NMDA receptor activity in hippocampal CA3 cells.
- The observed reduction in excitatory postsynaptic currents suggests NPY's action may be presynaptic or involve other neurotransmitter systems.