The Journal of Neuroscience, October 15, 2002, 22(20):8932-8941
In Situ GABAergic Modulation of Synchronous
Gonadotropin Releasing Hormone-1 Neuronal Activity
Joseph Patrick
Moore Jr,
Eric
Shang, and
Susan
Wray
Cellular and Developmental Neurobiology Section, National Institute
of Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, Maryland 20892
Evidence indicates that gonadotropin releasing hormone-1 [GnRH-1,
also known as luteinizing hormone releasing hormone (LHRH)] neurons
can exhibit synchronized neuroendocrine secretory activity before
entrance into the CNS. In this study, we used calcium imaging to
evaluate patterns of activity in individual, embryonic, GnRH-1 neurons
as well as population dynamics of GnRH-1 neurons in mouse nasal
explants maintained for 1 versus 3 weeks. Independent of age, GnRH-1
neurons displayed significant calcium peaks that synchronized at an
interval of ~20 min across multiple GnRH-1 cells within an explant.
Acute tetrodotoxin treatment decreased the amplitude of calcium peaks
in individual GnRH-1 neurons and the duration but not the frequency of
synchronized activity in the population of GnRH-1 neurons. Acute
GABAB receptor antagonism increased the frequency of
synchronized neuronal activity at both ages, whereas acute
GABAA receptor antagonism decreased calcium oscillations in
individual GNRH-1 cells as well as synchronization of the calcium pulses within the GnRH-1 population at the 1 week time point to background non-GNRH-1 cell levels. These results indicate that developing GnRH-1 neurons rely heavily on GABAergic signaling to
initiate synchronized bouts of activity but thereafter, possess an
innate capacity for synchronized activity patterns that are modulated
by, but not completely dependent on GABAergic signaling.
Key words:
LHRH; GnRH; GABA; explant culture; development; synchronous pulses; calcium oscillations
Copyright © 2002 Society for Neuroscience 0270-6474/02/22208932-10$05.00/0