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Presynaptic action of neuropeptide Y in area CA1 of the rat hippocampal slice.
Author(s) -
Colmers W F,
Lukowiak K,
Pittman Q J
Publication year - 1987
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1987.sp016409
Subject(s) - excitatory postsynaptic potential , population spike , neuroscience , hippocampal formation , neuropeptide y receptor , slice preparation , stimulation , pyramidal cell , population , chemistry , hippocampus , glutamate receptor , electrophysiology , biology , long term potentiation , endocrinology , medicine , neuropeptide , inhibitory postsynaptic potential , biochemistry , receptor , environmental health
1. Neuropeptide tyrosine (neuropeptide Y, NPY), a recently isolated endogenous brain peptide, reduces the extracellular population spike evoked by stimulation of stratum radiatum in area CA1 of the in vitro rat hippocampal slice, without reducing the antidromically evoked population spike. To test the hypothesis that NPY acts presynaptically, intracellular recordings were made of pyramidal neurones of area CA1 in vitro. 2. Bath application of 10(‐6) M‐NPY causes a long‐lasting (1‐1.5 h), reversible reduction of the orthodromically evoked excitatory post‐synaptic potential (e.p.s.p.) recorded intracellularly from CA1 pyramidal neurones. This effect on the e.p.s.p. was dependent upon the concentration of NPY. 3. The resting membrane potential, slope input resistance, and action potential threshold, amplitude and duration of the CA1 pyramidal neurones were not affected by NPY. 4. The responses of CA1 pyramidal neurones to ionophoretic pulses of glutamate, applied to the dendrites during synaptic blockade, was also unaffected by NPY. 5. The evidence supports the hypothesis that NPY acts presynaptically in the CA1 region of hippocampus to reduce excitatory input to the pyramidal neurones.

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