- Email: [email protected]
616 Modulation by prostaglandin E2 of bradykinin-induced increase in intracellular free calcium concentration in cultured trigeminal ganglion cells
Sll ACTIONS OF ACIDIC FIBROBLAST GROWTH FACTOR ON PLASMA CORTICOSTERONE AND NEURONAL ACTIVITY OF PARAVENTRICULAR NUCLEUS IN RATS. KAZUO SASAKI, YUTAKA OOMURA, ITSURO MATSUMOTO. Fat of Eng.. Toyama Univ.. Toyama 930, Inst. of Bio-Active
615
Sci.,
Nippon Zoki.,
Hyogo
673-14.
Intracerebroventricular significantly was In
experiments
neurons
in
standard about
the
50%
activity
of by
of or
PVPc aFGF.
which
of rats,
a high The
part low
tested.
results
activates
suggest the
acidic
corticosterone
Cazt,
neurons
of
Nagasaki
increased of
the
Mgzt Of
that
Nagasaki growth
in anesthetized
rats,
releasing
factor
the
activity
in
paraventricular
medium. these,
Univ.,
fibroblast
anti-corticotropin aFGF
parvocellular
medium
mechanism
plasma
by preinfusion
slice
of Med.,
infusion
increased
blocked
Fat
nucleus
CRF also about
aFGF
hypothalamo-pituitary-adrenal
is
about
the
increased half
implicated
852.
in
(aFGF)
factor and
the
(CRF) 45%
of
recorded under.
activity
increased a CRF
increase antibody.
(PVPc) the
also
Japan.
a in
their
regulating
axis.
616
Modulation by prostaglandin Et of bradykinin-induced increase in intracellular free calcium concentration in cultured trigeminal ganglion cells. TAKASHI YAMADA*, SADAAKI MAEDA, SOU TAKIUCHI ,YASUHIRO 001, MAKIO SAEKI, TAKASIII NOKUBI* and KIHICHI SAITO. Department of Pharmacology, *2nd Department of Prosthetic Dentistry, Fatuity of Dentistry, Osaka University, Osaka 565, Japan. Our previous study demonstrated that bradykinin increased intracellular free calcium concentration ( [Ca”ji) via bradykinin 82 receptors in primary cultured trigeminal ganglion cells of guinea pig. In this study, to investigate the correlation between bradykinin B2 receptors and prostaglandin E(PGE) receptor subtypes, we examined the effect of PGE2, 17-phenyl-trinor PGE2(EPt receptor agonist) and butaprost(EP2 receptor agonist) on the increase of [Ca2*ji induced by bradykinrn in cultured TG cells. PGE2(5fi M), 17phenyl-trinor PGE2(0.1-10~ M) and butaprost (O.l-10~ M) did not give any change in [Ca2+]i,but markedly enhanced the bradykinin-Induced increase of [Ca’*ji. Among of those three, 17-phenyl-trinor PGE2was most potent. These results suggest that both EPt and EP2 receptors are involved in modulating the nociceptive information induced by bradykinrn in primary sensory neurons.
CHOLECYSTOKININERGIC MODULATION OF VENTRAL TEGMENTAL DOPAMINERGICINPUTS TO THE POSTERIORNUCLEUSACCUMBENSIN RATS. IKUE MUGURUMA’ , KATSUHIDE KARIYAz. MINORUODA2. SATORUSHIMAMUNE’. MASAHIKO NOMUR43. IUNICHI TANAKAs. iDent. of Human Dev., Naruto Univ. of Educ., Tokushima 772, zRes.Lab.. Tot-ii Co.. Chiba 267, 3Dent. of Phvsiol.. Saitama Med. Sch., Saitama 350-04. Tanan.
617
To clarify the role of cholecystokinin (CCK) in the regulation of central dopaminergic systems, we examined whether CCK activates the dopaminergic pathways from the ventral tegmental area (VTA) to the posterior nucleus accumbens (PNAc). 1) Twenty-two neurons in the VTA were antidromically activated by electrical stimulation of the PNAc in urethane-anesthetized rats. Iontophoretic application of sulfated-CCK octapeptide (CCK-8s) excited the activity of 7 of the identified units, but did not affect the remaining units. 2) A total of 54 PNAc neurons was tested for a response to CCK-8S (0.1 pg) injections into the VTA. Of the units tested, 14 displayed an increase and one exhibited a reduction in ongoing activity following the injections. 3) To verify whether microinjection of CCK-8S (0.1 pg) into the VTA affects dopamine (DA) metabolism in the PNAc, extracellular levels of DA, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were monitored using microdialysis techniques in awake rats. CCK-8S injected into the VTA elicited an increase in DOPAC and HVA contents in the PNAc, but did not affect the DA level. Similar injections of vehicle (1% NaHCOs) did not have an effect. These results imply that CCK may serve to activate the VTA dopaminergic pathways to the PNAc, thereby causing enhanced activity of PNAc neurons. (Supported
in part by Grants 05780602
and 06780675
from the Ministry of Education, Science and Culture, Japan, to J.T.)
615
Sci.,
Nippon Zoki.,
Hyogo
673-14.
Intracerebroventricular significantly was In
experiments
neurons
in
standard about
the
50%
activity
of by
of or
PVPc aFGF.
which
of rats,
a high The
part low
tested.
results
activates
suggest the
acidic
corticosterone
Cazt,
neurons
of
Nagasaki
increased of
the
Mgzt Of
that
Nagasaki growth
in anesthetized
rats,
releasing
factor
the
activity
in
paraventricular
medium. these,
Univ.,
fibroblast
anti-corticotropin aFGF
parvocellular
medium
mechanism
plasma
by preinfusion
slice
of Med.,
infusion
increased
blocked
Fat
nucleus
CRF also about
aFGF
hypothalamo-pituitary-adrenal
is
about
the
increased half
implicated
852.
in
(aFGF)
factor and
the
(CRF) 45%
of
recorded under.
activity
increased a CRF
increase antibody.
(PVPc) the
also
Japan.
a in
their
regulating
axis.
616
Modulation by prostaglandin Et of bradykinin-induced increase in intracellular free calcium concentration in cultured trigeminal ganglion cells. TAKASHI YAMADA*, SADAAKI MAEDA, SOU TAKIUCHI ,YASUHIRO 001, MAKIO SAEKI, TAKASIII NOKUBI* and KIHICHI SAITO. Department of Pharmacology, *2nd Department of Prosthetic Dentistry, Fatuity of Dentistry, Osaka University, Osaka 565, Japan. Our previous study demonstrated that bradykinin increased intracellular free calcium concentration ( [Ca”ji) via bradykinin 82 receptors in primary cultured trigeminal ganglion cells of guinea pig. In this study, to investigate the correlation between bradykinin B2 receptors and prostaglandin E(PGE) receptor subtypes, we examined the effect of PGE2, 17-phenyl-trinor PGE2(EPt receptor agonist) and butaprost(EP2 receptor agonist) on the increase of [Ca2*ji induced by bradykinrn in cultured TG cells. PGE2(5fi M), 17phenyl-trinor PGE2(0.1-10~ M) and butaprost (O.l-10~ M) did not give any change in [Ca2+]i,but markedly enhanced the bradykinin-Induced increase of [Ca’*ji. Among of those three, 17-phenyl-trinor PGE2was most potent. These results suggest that both EPt and EP2 receptors are involved in modulating the nociceptive information induced by bradykinrn in primary sensory neurons.
CHOLECYSTOKININERGIC MODULATION OF VENTRAL TEGMENTAL DOPAMINERGICINPUTS TO THE POSTERIORNUCLEUSACCUMBENSIN RATS. IKUE MUGURUMA’ , KATSUHIDE KARIYAz. MINORUODA2. SATORUSHIMAMUNE’. MASAHIKO NOMUR43. IUNICHI TANAKAs. iDent. of Human Dev., Naruto Univ. of Educ., Tokushima 772, zRes.Lab.. Tot-ii Co.. Chiba 267, 3Dent. of Phvsiol.. Saitama Med. Sch., Saitama 350-04. Tanan.
617
To clarify the role of cholecystokinin (CCK) in the regulation of central dopaminergic systems, we examined whether CCK activates the dopaminergic pathways from the ventral tegmental area (VTA) to the posterior nucleus accumbens (PNAc). 1) Twenty-two neurons in the VTA were antidromically activated by electrical stimulation of the PNAc in urethane-anesthetized rats. Iontophoretic application of sulfated-CCK octapeptide (CCK-8s) excited the activity of 7 of the identified units, but did not affect the remaining units. 2) A total of 54 PNAc neurons was tested for a response to CCK-8S (0.1 pg) injections into the VTA. Of the units tested, 14 displayed an increase and one exhibited a reduction in ongoing activity following the injections. 3) To verify whether microinjection of CCK-8S (0.1 pg) into the VTA affects dopamine (DA) metabolism in the PNAc, extracellular levels of DA, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were monitored using microdialysis techniques in awake rats. CCK-8S injected into the VTA elicited an increase in DOPAC and HVA contents in the PNAc, but did not affect the DA level. Similar injections of vehicle (1% NaHCOs) did not have an effect. These results imply that CCK may serve to activate the VTA dopaminergic pathways to the PNAc, thereby causing enhanced activity of PNAc neurons. (Supported
in part by Grants 05780602
and 06780675
from the Ministry of Education, Science and Culture, Japan, to J.T.)