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Electrophysiological identification of a pathway from the septal area to the medial amygdala: Sensitivity to estrogen and luteinzing hormone‐releasing hormone
Author(s) -
Dudley Carol A.,
Lee Yong,
Moss Robert L.
Publication year - 1990
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890060207
Subject(s) - orthodromic , excitatory postsynaptic potential , amygdala , inhibitory postsynaptic potential , neuroscience , endocrinology , electrophysiology , medicine , chemistry , stimulation , biology
Medial amygdala neurons responsive to electrical stimulationof the medial septal area were electrophysiologically identified in ovariectomized, urethane‐anesthetized female rats. Peristimulus time histograms were collected and used to define the orthodromic response. The action of iontophoretically applied luteinzing hormone‐releasing hormone (LHRH) and an LHRH fragment, Ac‐LHRH 5–10 , on the activity of were identified as orthodromically responsive. Three types of orthodromic responses were observed: excitatory, inhibitory, and complex. Priming the animals with 5 μg estradiol benzoate (EB) 48 hr prior to recording had no effect on the overall number of neurons responding to septal area stimulation, but EB priming did significantly reduce the percentage of orthodromically excited neurons. The firing rate of the majority of amygdala neurons responsive to septal area stimularion was not affected by iontophoretically applied LHRH (59 of 76) or LHRH fragment (41 of 65). In some cases, application of LHRH (10 of 76) or Ac‐LHRH 5‐10 (12 of 55) produced a change in neuronal firing that was similar in direction to the orthodromically evoked response. When applied during the collection of peristimulus time histograms, both peptides were also able to modulate the orthodromically evoked response (five of 18 cells tested with LHRH and three of 14 cells tesed with Ac‐LHRH 5‐10 ). The results demonstrate a large projection from the septal area to the amygdala, one component of which is altered by estrogen priming. The findings suggest that LHRH released from septal neurons may act as a neurotransmitter and a neuromodulator in the medial amygdala; however, the large number of neurons unaffected by the decapeptide indicates that the role of LHRH at this synapse is subservient to that of another tranmitter (s).