$97 EFFECTS OF ATRIAL NATRIURETIC POLYPEPTIDE ON RAT HYPOTHALAMIC NEURONS IN VITRO
.# HIROSHI YAMASHITA, of 0ccup.
SHIGERU 0KUYA
Environ.
Health,
Sch.
.
, HIROSHI KANNAN and MASANORI KASAI , Med.,
Dept.
of Physiol., Univ.
Kitakyushu 807 and #Dept. of Int. Med., Yamaguchi Univ.,
Seh. Med., Ube 755, Japan Extracellular hypothalamic nucleus
recordings
slice
(PVN),
were
preparation;
and
made
from
175
spontaneously
active
15 in the supraoptic nucleus (SON),
73 in the anteroventral third ventricle (AV3V).
the
and 30 (41%) of 73 AV3V cells showed inhibitory responses. PVN
and
AV3V
decreased
dose-dependently to ANP.
The
The
of
ANP
Thirty-six
applied at 10-7 M.
PVN.
experiments,
cells
concentration
ANP,
ANP or excited by AII,
AV3V and PVN,
PVN
to
evoke effect
and
high
II
(AII)
Twelve showed inhibitory responses to ANP and 9 excitatory responses to AII. In AII and arginine-vasopressin (AVP) were each applied to neurones in
by AII and 20 were excited by AVP.
conclude that ANP
atrial
The inhibitory
in the AV3V were tested with both ANP and angiotensin
Of the 40 cells tested with all three
excited
coronal
rates of 7 cells in
still persisted after synaptic transmission had been suppressed with a low Ca 2+
medium.
other
rat
paraventrioular
but 19 (22~) of 87
firing
threshold
inhibitory responses in the PVN was i0-I0 M and in the AV3V was i0-II M.
Mg 2+
in
the
Bath application of
natriuretic polypeptide (ANP) 10 -7 M had no effect on 15 SON cells tested; cells
cells
87 in
peptides at 10 -7 M, No neurones
7 were inhibited by ANP,
the
14 were
in either PVN or AV3V were inhibited
by
but four neurones in the PVN were inhibited by ANP and excited by AVP.
We
has central actions which include a direct inhibitory effect on neurones in
the
but no direct effect on magnocellular neurones in the SON; and that ANP may have the
opposite action to AII and AVP in both the PVN and AVSV.
T H E MECH/LNISM OF T H E E F F E C T OF E S T R A D I O L V E N T R O M E D I A L HYPOTHALILMIC N E U R O N S JUNICHI OOMURA. Fukuoka
NABEKURA*, Department 812, J a p a n
ON T H E
EXCITABILITY
OF M E D I A L
AMYGDALA
AND
TAKETSUGU MINAMI*, ATSUO FUKUDA*, CHITOSE ITO* and YUTAKA of P h y s i o l o g y , Faculty of M e d i c i n e , Kyushu University 60,
E s t r a d i o l can be c o n c e n t r a t e d in the m e d i a l a m y g d a l a ( M e d - A M G ) , a n d v e n t r o m e d i a l hypothalamus (VMH). R e c e n t l y , the r a p i d e f f e c t s of e s t r o g e n on n e u r a l e x c i t a b i l i t y h a v e b e e n r e p o r t e d for t h e s e t a r g e t sites. Intracellular recordings were obtained f r o m M e d - A M G a n d V M H n e u r o n s to d e f i n e the m e c h a n i s m of t h e r a p i d e f f e c t on the n e u r a l m e m b r a n e in v i t r o . All f e m a l e r a t s w e r e o v a r i e c t o m i z e d b i l a t e r a l l y a n d t w o weeks after the operation, a s i n g l e p r i m i n g of e s t r a d i o l benzoate was injected subcutaneously. T w o d a y s later, c o r o n a l b r a i n s l i c e s w e r e made. i) 1 7 B - e s t r a d i o l , not 17s-estradiol, hyperpolarized the M e d - A M G neurons associated with increased men~brane c ~ n d u c t a n c e . T h e r e v e r s a l p o t e n t i a l for 1 7 8 - e s t r a d i o l s i f t e d by c h a n g e of e x t.e r n a.l K. c.o n c . entrations • T h e e s t r a d i o l + ~h y p e r p o l a r i z a t i o n p e r s i s t e d u n d e r the e l l m l n a t l o n of s y n a p t l c i n p u t s by use of Ca free s o l u t l o n and the s u p p r e s s l o n of p r o t e i n s y n t h e s i s by a c t i n o m y c i n D and c y c l o h e x i m i d e . T h e d e g r e e of t h i s e f f e c t w a s c h a n g e d a c c o r d i n g to the 1 7 8 - e s t r a d i o l c o n c e n t r a t i o n . The Hill's coefficiency was a~proximately i. These results indicated that 178-estradiol directly changed the K conductances of p o s t s y n a p t i c men%brane. Significant differences of the e s t r a d i o l r e s p o n d i n g r a t e s b e t w e e n m a l e s (8%) and f e m a l e s (27%) w e r e d e m o n s t r a t e d . 2) In V M H neurons, one type of n e u r o n was depolarized by 17B-estradiol with d e c r e a s e d men~brane p o t a s s i u m c o n d u c t a n c e . T h i s d e p o l a r i z a t i o n w a s a u g m e n t e d b y the application of i s o b u t y l m e t h y l x a n t h i n (IBMX) or f o r s k o l i n . From this evidence, 1 7 8 - e s t r a d i o l d e p o l a r i z a t i o n m i g h t be m e d i a t e d t h r o u g h an i n c r e a s e in i n t r a c e l l u l a r cyclic AMP. Anothe~ type of neuron was hyperpolarized, in association with i n c r e a s e d menkbrane K-- c o n d u c a t a n c e . This hyperpolarization w a s a u g m e n t e d by I B M X but not forskolin. Med-/LMG a n d VM_H n e u r o n s s h o w e d the r a p i d r e s p o n s e s against e s t r o g e n t h a t m i g h t be i n v o l v e d in the i n t e g r a t i o n of c h e m o s e n s o r y i n f o r m a t i o n . .
.