2408 Gap junction does not participate in mechanisms of pulsatile release of gnrh in the rat hypothalamus

S254

2406

EFFECTSOFNORADRENALlNEDEPLETlONINTHEBEDNUCLEUSOFTHESTRIATERMINALlSON NEUROENDOCRINERESPONSESTOFEAR-RELATEDSTlMULIINTHERAT TATSUSHIONAKA.

CondItIoned

WANG-JIANG

ZOU,KINJl yAGl,De~t

ofPhvsiol.JlchiMed.

Sch ,Tochipi.329-04.Japan. in the rat. Non-

fear stIrnull mhtbit vasopressin and facilitate oxytocm release from the neurohypophysls

assoclatlvely applied fear stirnull (intermittently previously shown that noradrenalme

applied electric footshocks) also Induce slmllar neuroendocrine

depletion m the brain blocks neuroendocrine

responses to conditioned

responses. We have or non-associatively

applied fear stIrnull in the rat The bed nucleus of the strla termmalls (BNST) is considered to be Involved in neuroendocrine responses to stressful stimuli The BNST receives dense noradrenerglc mnervatlon Noradrenalme release m the BNST is facilitated during stressful stirnull. Here we examined whether noradrenalme depletion In the BNST blocks responses in vasopressin and oxytocin release to fear-related stIrnull m male rats 5-ADMP,

a neurotoxm selective to noradrenerglc

fibres was injected bilaterally into the BNST

under Avertm anaesthesla one week before experiments. The neurotoxm attenuated the oxytocm response but did not significantly affect vasopressm response to footshocks (0 8 mA, 50 Hz. I s) applied intermittently noradrenalme m the BNST

2407

IS

Involved selectively m the oxytocm response to fear-related stimuli in the rat.

LOCALIZATION

OF MIDBRAIN

IMMUNOHISTOCHEMISTRY YAMAMOTO’, Sch., Tokyo,

YOSHITAKA 113,2Misaki

every 30 s for 5 min. The results suggest that

AND

OKA’, Marine

CNRH

MASAMI

Biol. Station,

NEURONS:

TRACER

YOSHIMOTO’,

A DOUBLE

INJECTION

TO THE

LABELING SPINAL

CORD.

HIRONOBU

ITO’.

1Dept. of Anat.,

Sch. of Sci., Univ. of Tokyo,

Misaki,

238-02, Japan.

STUDY

BY

NAOYUKI Nippon

Med.

Inmost vertebratespecies, thereare three groupsof gonadotropin-releasinghormone (GnRH)neurons inthe brain. GnRH neuronsin the midbraintegmentumhavebeenreportedtoproduce chickenG&H-II. MidbrainGnRH neuronsin the dwarf gourami(Teleostei)are known to sendtheir neuritesto many brain regions and the spinalcord'. To study their unknown fuction(s), information on their morphologicalcharacteris indispensable.They are locatedquite near to the nucleusof the mediallongitudinalfasciculus(NMLF),which alsoprojectstotbe spinalcord. It is possiblethat GnFW neuronsand neurons of NMLF areintermingled.We performeda double labelingstudy by GnRH-immunohistochemistryand biocytininjection to thespinalcord.Althoughboth neuronalgroupsarelocatedatasimilarrostro-caudallevel,GnRHneuronsarelocatednearerto the mesencephalic ventricle. lYamamotoetal.J.Comp.Neurol. (1995)355: 354-368.

2408

GAP JUNCTION DOES NOT PARTICIPATE IN MECHANISMS OF PULSATILE RELEASE OF GNFW IN THE RAT HYPOTHALAMUS HIROMI HIRUMA, F'UKUKO KIMURA Dept. of Phvsiol., Yokohama Citv Univ. Sch. of Med., Yokohama, 236, Japan. Pulsatile release of gonadotropin releasing hormone (GnRH) results from the periodic and synchronous excitation of GnRH neurons. To determine whether gap junctional couplings participate in mechanisms of the pulsatile release of GnRH or not, we examined the effect of octanol, a gap junction blocker, on the pulsatile GnFW release from acutely isolated hypothalamic preparations of adult ovariectomized rats. Basal hypothalamus (8x8x2.5 mm) were superfused with artificial cerebrospinal fluid saturated with 95% O2 and 5% CO1 (34 "C). Concentrations of GnRH levels in the fluid collected in the vicinity of the median eminence were measured by enzyme immunoassay. Obvious pulses of GnRH (30-60 min intervals) were detected from 5 hours after dissection. Thereafter, the release kept pulsatile for more than 7 hours. This pulsatile release was not affected by continuous application (>2 hours) of 5 mM octanol. The result suggests that, in the rat hypothalamus, the gap junction does not participate in the periodicity or synchronization of activity of GnFU-lneurons.