JN Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Neurophysiol 70: 1469-1475, 1993;
0022-3077/93 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sakamoto, Y.
Right arrow Articles by Sakuma, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sakamoto, Y.
Right arrow Articles by Sakuma, Y.

Journal of Neurophysiology, Vol 70, Issue 4 1469-1475, Copyright © 1993 by APS

ARTICLES

Estrogen-sensitive neurons in the female rat ventral tegmental area: a dual route for the hormone action

Y. Sakamoto, S. Suga and Y. Sakuma
Department of Physiology I, Hirosaki University School of Medicine, Japan.

1. Electrical stimulation of the ventral part of the midbrain central gray (CG) elicited antidromic action potentials in 136 neurons in the ventral tegmental area (VTA) of 23 urethan-anesthetized ovariectomized female rats. 2. Antidromic action potentials were positive-negative biphasic and completed mostly within 2.4 ms. Many had a notch in their initial positive deflection, at which antidromic potentials often failed to propagate into the neuronal soma. 3. The latency for antidromic activation ranged 1.0-10.5 ms, and the threshold was 100-1,700 microA. The relative refractory period was 0.8-2.8 ms. In 23 neurons (17%) gradual changes in stimulus intensity caused latency jumps, suggesting that their axons terminate or spread into branches in stimulation sites. 4. The parameters for antidromic activation were compared among 12 animals with a subcutaneous Silastic capsule of estrogen and 11 others with a blank capsule. Estrogen raised the mean threshold from 675 +/- 40 (SE) microA (n = 69) to 908 +/- 40 microA (n = 67). At the same time, estrogen significantly decreased the probability of the antidromic propagation from 63 to 41%. No changes were detected in the latency or the refractory period. 5. The probability distribution of the threshold was different in ovariectomized animals from that in estrogen-treated animals. Estrogen increased the number of cells with thresholds in the 1,300- to 1,500-microA range. 6. The probability of antidromic propagation was stable in each neuron to stimuli repeated at 1.0 Hz. Electrical stimulation of the preoptic area (POA) with a 30-s train of 50-microA pulses at 100 Hz increased the probability of antidromic propagation into the soma.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
 J. Neurosci.Home page
M. Febo, C. F. Ferris, and A. C. Segarra
Estrogen Influences Cocaine-Induced Blood Oxygen Level-Dependent Signal Changes in Female Rats
J. Neurosci., February 2, 2005; 25(5): 1132 - 1136.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online