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Madden JA, Kalbfleisch JH, Harder DR. Distribution of excitatory junction potential amplitude in cat cerebral arteries: examination of its quantal nature and modulation by opiates. J Cell Physiol. 1987;131(2):262-6doi: 10.1002/jcp.1041310217.
Madden, J. A., Kalbfleisch, J. H., & Harder, D. R. (1987). Distribution of excitatory junction potential amplitude in cat cerebral arteries: examination of its quantal nature and modulation by opiates. Journal of cellular physiology, 131(2), 262-6. https://doi.org/10.1002/jcp.1041310217
Madden, J A, et al. "Distribution of excitatory junction potential amplitude in cat cerebral arteries: examination of its quantal nature and modulation by opiates." Journal of cellular physiology vol. 131,2 (1987): 262-6. doi: https://doi.org/10.1002/jcp.1041310217
Madden JA, Kalbfleisch JH, Harder DR. Distribution of excitatory junction potential amplitude in cat cerebral arteries: examination of its quantal nature and modulation by opiates. J Cell Physiol. 1987 May;131(2):262-6. doi: 10.1002/jcp.1041310217. PMID: 2438292.
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J Cell Physiol. 1987 May;131(2):262-6. doi: 10.1002/jcp.1041310217.

Distribution of excitatory junction potential amplitude in cat cerebral arteries: examination of its quantal nature and modulation by opiates.

Journal of cellular physiology

J A Madden, J H Kalbfleisch, D R Harder

PMID: 2438292 DOI: 10.1002/jcp.1041310217

Abstract

We used scorpion venom to release small amounts of an excitatory neurotransmitter from adventitial nerves in cat left anterior descending cerebral artery. We used glass microelectrodes to measure and record postsynaptic electrical events of minimal amplitude. These events were similar to postsynaptic spontaneous and electrically evoked excitatory junction potentials (ejp's) seen in skeletal muscle. We performed a frequency analysis of the ejp amplitudes to determine if they fit a unimodal or multimodal distribution. We also investigated the effects of phentolamine, norepinephrine, hydromorphone, and morphine on ejp amplitude and frequency in the artery. Statistical analysis of the ejp frequency and amplitude revealed a multipeaked distribution with decreasing peaks. These results were similar to the distribution reported for acetylcholine release in skeletal muscle. The ejps were inhibited by phentolamine, which suggested that these events were adrenergically mediated. Norepinephrine and the opiates, hydromorphone and morphine, reduced the frequency and amplitude of the ejp's. The vessels also constricted to increasing doses of norepinephrine both under control conditions and in the presence of opiate. These results suggest that norepinephrine blocks the ejp's by a feedback mechanism at the presynaptic membrane and that endorphins and/or enkephalins, also acting at this presynaptic site, may modulate neurotransmission in the cerebral circulation.

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