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Electrophysiological and neurochemical characterization of neurons of the medial preoptic area in Japanese quail ( Coturnix japonica)
Intracellular recordings of medial preoptic neurons demonstrated that most neurons show a spontaneous firing, a linear I– V relationship and low-threshold-like events suppressed by the application of Ni 2+. Some neurons had a depolarizing sag of the membrane potential in response to hyperpolarizing...
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Published in: | Brain research 2004-12, Vol.1029 (2), p.224-240 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Intracellular recordings of medial preoptic neurons demonstrated that most neurons show a spontaneous firing, a linear
I–
V relationship and low-threshold-like events suppressed by the application of Ni
2+. Some neurons had a depolarizing sag of the membrane potential in response to hyperpolarizing current pulses. The majority of the cells exhibited a robust spontaneous synaptic activity suppressed by SR95531 (100 μM), a GABA
A receptor antagonist, and/or by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 μM), an (
RS)-α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate (KA) glutamate receptor antagonist. Most neurons were affected by the application of AMPA (10 μM), kainate (30 μM),
N-methyl-
d-aspartic acid (NMDA, 10 μM), isoguvacine (a GABA
A receptor agonist, 100 μM), dopamine (100 μM), and norepinephrine (100 μM). Biocytin injections coupled to aromatase immunocytochemistry identified 19 recorded neurons including 3 displaying a dense aromatase immunoreactivity. All of them responded to kainate, dopamine, and norepinephrine, while only one responded to isoguvacine and NMDA. Taken together, these results demonstrate a relative electrical and neurochemical homogeneity of the medial preoptic neurons, including a few aromatase-immunoreactive neurons that could be identified by immunocytochemistry after biocytin labeling of the recorded neurons. |
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ISSN: | 0006-8993 1872-6240 |
DOI: | 10.1016/j.brainres.2004.09.047 |