Document 5 of 943
AU FUNK-G-D*; PARKIS-M-A; SELVARATNAM-S-R; WALSH-C
TI DEVELOPMENTAL MODULATION OF GLUTAMATERGIC INSPIRATORY DRIVE TO
HYPOGLOSSAL MOTONEURONS
AD *UNIV AUCKLAND, DEPT PHYSIOL, FAC MED & HLTH SCI, PRIVATE BAG 92019,
AUCKLAND, NEW ZEALAND
CY NEW ZEALAND
SO RESPIRATION PHYSIOLOGY, vol. 110, issue 2-3, (NOV, 1997) : pp. 125-137.
SB LifeSci
WK 12/21/1997
AB Proper function of hypoglossal motoneurons (XII MNs) innervating tongue
muscles is critical for respiratory control of the airway.
Morphological and electrophysiological properties of XII MNs change
during postnatal development, as do modulatory systems. Despite these
changes, the system producing respiratory movements must remain fully
functional throughout life. Modulatory systems have therefore received
considerable attention since coordination of their development with a
developing neuromuscular system may be critical for maintenance of
continuous, efficient breathing. Developmental modulation of XII
inspiratory activity by three transmitter systems is examined.
Thyrotropin-releasing hormone (TRH) mediates an increase in MN input
resistance (R-N) in juvenile but not neonate MNs, and this likely
underlies the developmental increase in TRH potentiation of inspiratory
activity. Norepinephrine (NE) potentiation of inspiratory activity,
which in the neonate is produced in part by an alpha(1)-mediated
increase in R-N, also increases postnatally. Effects of purinergic
transmission on XII inspiratory activity remain constant during the
first 2 weeks of postnatal development. Adenosine-triphosphate (ATP)
produces tonic excitation and inspiratory potentiation that likely
result from activation of postsynaptic P2 receptors. A secondary
inhibitory effect likely results from hydrolysis of ATP to adenosine
and activation of presynaptic A1 adenosine receptors. The functional
relevance of these postnatal changes is discussed. (C) 1997 Elsevier
Science B.V.
AA N
EA Y
LG eng
PT ARTICLE
RF 42
IN 0034-5687
SC WE: RESPIRATORY SYSTEM. UM: PHYSIOLOGY.
GA YJ541 (For ordering reprints from ISI)
KW CONTROL OF BREATHING; HYPOGLOSSAL MOTONEURONS; DEVELOPMENT,
POSTNATAL; MEDIATORS, ATP, NOREPINEPHRINE, THYROTROPIN-RELEASING
HORMONE; NERVE, HYPOGLOSSUS
KP THYROTROPIN-RELEASING-HORMONE; RAT BRAIN-STEM; IN-VITRO; SYNAPTIC
TRANSMISSION; RESPIRATORY RHYTHM; POSTNATAL CHANGES;
RECEPTOR-BINDING; NEONATAL RAT; NOREPINEPHRINE; MECHANISMS
Document 8 of 943
AU JEFTINIJA-S-D*; JEFTINIJA-K-V
TI ATP STIMULATES RELEASE OF EXCITATORY AMINO-ACIDS FROM CULTURED
SCHWANN-CELLS
AD *IOWA STATE UNIV, DEPT VET ANAT, NEUROSCI PROGRAM, AMES, IA 50011
ZP 50011
CY USA
SO NEUROSCIENCE, vol. 82, issue 3, (FEB, 1998) : pp. 927-934.
SB LifeSci
WK 12/14/1997
AB The release of excitatory amino acids from Schwann cell cultures in the
rat was monitored using high-performance liquid chromatography. The
basal concentration of glutamate and aspartate was 33 +/- 4 nM (mean
+/- S.E.M., n = 12) and 8 +/- 1 nM (mean +/- S.E.M., n = 12),
respectively. ATP (100 mu M) caused a receptor-mediated increase in
release of glutamate and aspartate from Schwann cell cultures. Bath
application of adenosine (100 mu M) was without effect on release of
excitatory amino acids suggesting involvement of P-2 receptors.
Suramin, a competitive antagonist al P-2 receptors, prevented the
response to ATP. The release of excitatory amino acids evoked by ATP
was not abolished in calcium-depleted saline. Pretreatment of the
Schwann cultures with 50 mu M
1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetracetic acid-acetoxymethyl
ester (BAPTA-AM) abolished the effect of ATP. ATP-evoked release of
glutamate from cultured Schwann cells was significantly reduced by
thapsigargin (1 mu M), an inhibitor of Ca2+-ATPase of the Ca2+ pump of
internal stores. U73122, a selective inhibitor of receptor-coupled
phospholipase C-dependent processes, abolished stimulatory effect of
ATP suggesting that ATP's action is mediated through an inositol
1,4,5,-triphosphate-sensitive calcium store. The action of ATP was not
blocked by L-trans-pyrrolidine-2,4-dicarboxylate, an inhibitor of the
electrogenic glutamate transporter, nor was it blocked in Na+-free
medium, and glutamate release was not stimulated by a depolarizing
stimulus, suggesting that ATP-evoked release of glutamate from Schwann
cells is not due to the reversal of the glutamate uptake. An anion
transport blocker, furosemide, reduced ATP-induced glutamate release.
These results suggest that ATP-stimulated glutamate and aspartate
release from Schwann cells may be through a calcium-dependent
furosemide-sensitive mechanism. (C) 1997 IBRO.
AA N
EA Y
LG eng
PT ARTICLE
RF 50
IN 0306-4522
SC RU: NEUROSCIENCES.
GA YG392 (For ordering reprints from ISI)
KW ATP; CALCIUM; FUROSEMIDE; GLUTAMATE; SCHWANN CELLS; SECRETION
KP CALCIUM-DEPENDENT RELEASE; P2Y PURINERGIC RECEPTOR; SMOOTH-MUSCLE
CELLS; SPINAL DORSAL HORN; EXTRACELLULAR ATP; PHOSPHOLIPASE-C;
POLYMORPHONUCLEAR NEUTROPHILS; ADENOSINE 5'-TRIPHOSPHATE;
INTRACELLULAR CALCIUM; SYNAPTIC TRANSMISSION
Document 21 of 943
AU DUAN-D-Y*; YE-L-Y; YAMAZAKI-J; HUME-J-R
TI PURINERGIC ACTIVATION OF A CFTR-LIKE CL- CHANNEL THROUGH
PROTEIN-KINASE-C IN MOUSE VENTRICULAR MYOCYTES
AD UNIV NEVADA, SCH MED, RENO, NV 89557
ZP 89557
CY USA
SO CIRCULATION, vol. 96, issue 8, suppl S (OCT 21, 1997) : pp. 4092-4092.
SB LifeSci; ClinMed
WK 11/23/1997
AB No abstract available.
AA N
EA N
LG eng
PT MEETING ABSTRACT
IN 0009-7322
SC ZD: PERIPHERAL VASCULAR DISEASE. MA: HEMATOLOGY.
GA YC880 (For ordering reprints from ISI)
Document 24 of 943
AU JONES-S-J*; GRAY-C; BOYDE-A; BURNSTOCK-G
TI PURINERGIC TRANSMITTERS INHIBIT BONE-FORMATION BY CULTURED OSTEOBLASTS
AD *UNIV COLL LONDON, DEPT ANAT & DEV BIOL, GOWER ST, LONDON WC1E 6BT,
ENGLAND
CY ENGLAND
SO BONE, vol. 21, issue 5, (NOV, 1997) : pp. 393-399.
SB LifeSci; ClinMed
WK 11/16/1997
AB Adenosine triphosphate (ATP) and other purinoceptor agonists cause a
transient rise in [Ca2+](i) in cultured osteoblast-like cells and have
a mitogenic effect, as does parathyroid hormone (PTH), and there is
evidence that ATP and PTH can act synergistically on osteoblasts. The
likelihood that nucleotides, acting through purinoceptors, are
important local factors in bone remodeling is therefore considerable.
However, their effect on bone formation is unknown. We recently
developed a culture system in which appositional bone formation occurs
only in narrow grooves cut in a substratum. We have used this as an
assay to measure the effects of ATP (50 and 500 mu mol/L), ATP gamma S
(20 mu mol/L), 2-MeSATP (2 and 20 mu mol/L), uridine triphosphate (UTP)
(0.2, 2, and 20 mu mol/L), adenosine (20 mu mol/L), bovine PTH (0.25
and 0.5 IU/mL), rat PTH1-34 (10(-8) and 10(-7) mol/L), and rat
PTHrP1-40 (10(-9) and 10(-8) mol/L) on bone formation by rat calvarial
osteoblasts. The culture medium was renewed 3 times/week (every 2 or 3
days), and the number of bone loci and length and area of Alizarin
red-stained mineralized bone formed in the grooves of each specimen in
16-29 days were measured. Compared with controls, ATP gamma S,
2-MeSATP, and ATP reduced the amount of bone formed in a 2-3 week
culture period. Adenosine had no effect, and UTP either had no effect
or at 2 mu mol/L stimulated bone formation. PTH and PTHrP completely
abolished bone formation in 4 week cultures. Our findings are
consistent with evidence for more than one P2 purinoceptor subtype in
bone, and show for the first time that the effect of ATP on
appositional bone formation by osteoblasts in vitro is, like PTH and
PTHrP, inhibitory. (C) 1997 by Elsevier Science Inc. All rights
reserved.
AA N
EA Y
LG eng
PT ARTICLE
RF 40
IN 8756-3282
SC IA: ENDOCRINOLOGY AND METABOLISM.
GA YD853 (For ordering reprints from ISI)
KW OSTEOBLASTS; BONE FORMATION; ADENOSINE TRIPHOSPHATE; PURINOCEPTORS;
PARATHYROID HORMONE; PARATHYROID HORMONE RELATED PROTEIN
KP PARATHYROID-HORMONE; IN-VITRO; INTRACELLULAR CALCIUM; SIGNALING
PATHWAYS; CELLS; ATP; MINERALIZATION; PURINOCEPTORS; CHONDROCYTES;
OSTEOCLASTS
Document 26 of 943
AU COOK-S-P*; MCCLESKEY-E-W
TI DESENSITIZATION, RECOVERY AND CA2+-DEPENDENT MODULATION OF ATP-GATED
P2X RECEPTORS IN NOCICEPTORS
AD *OREGON HLTH SCI UNIV, VOLLUM INST, L474, PORTLAND, OR 97201
ZP 97201
CY USA
SO NEUROPHARMACOLOGY, vol. 36, issue 9, (SEP, 1997) : pp. 1303-1308.
SB LifeSci
WK 11/16/1997
AB We have shown the presence and activity of ATP-gated ion channels (P2X
receptors) in nociceptive nerve endings, supporting the theory that
these channels mediate some forms of nociception [Cook S. P.,
Vulchanova L., Hargreaves K. M., Elde R. and McCleskey E. W. (1997)
Distinct ATP receptors on pain-sensing and stretch-sensing neurons.
Nature 387, 505-508]. The kinetics and pharmacology of ATP-gated
currents in nociceptors suggest that the channels are comprised of
either homomeric or heteromeric combinations of P2X3 receptors.
Consistent with the diverse nature of P2X structure,
electrophysiological responses of rat tooth-pulp nociceptors fall into
two distinct classes based on desensitization and recovery kinetics.
Here, we quantified the dramatic differences in desensitization
kinetics of transient and persistent currents. The major component of
transient P2X current desensitized with a tau(decay) = 32 +/- 2 msec,
while persistent current desensitized >100-fold more slowly, tau(decay)
= 4000 +/- 320 msec, Both currents recovered from desensitization in
minutes: tau(recovery) = 4 min for transient current, and tau(decay) =
0.7 +/- 0.2 min for persistent current. Persistent current recovery
was often accompanied by a current ''overrecovery'' that averaged ca
threefold magnitude prior to desensitization. Comparison of ATP
current in elevated Ca-ext(2+) also revealed differences in transient
and persistent currents. In 2 mM Ca-ext(2+) medium, decrease of
Na-ext(+) resulted in an almost complete reduction of persistent, but
not transient, current. Subsequent elevation of Ca-ext(2+) greatly
increased the transient, but not persistent, current. Mechanistic
explanations for either the increase in transient current magnitude by
elevated Ca-ext(2+), or persistent current overrecovery may reflect
endogenous pathways for P2X receptor modulation. (C) 1997 Elsevier
Science Ltd.
AA N
EA Y
LG eng
PT ARTICLE
RF 25
IN 0028-3908
SC TU: PHARMACOLOGY AND PHARMACY. RU: NEUROSCIENCES.
GA YD892 (For ordering reprints from ISI)
KW SENSORY NEURONS; P2X RECEPTOR; DESENSITIZATION; PURINERGIC;
NOCICEPTOR
KP RAT SENSORY NEURONS; ION CHANNELS; EXTRACELLULAR ATP; ZN2+;
RESPONSES; CURRENTS; CELLS
Document 28 of 943
AU COLLO-G; NEIDHART-S; KAWASHIMA-E; KOSCOVILBOIS-M; NORTH-R-A;
BUELL-G*
TI TISSUE DISTRIBUTION OF THE P2X(7) RECEPTOR
AD *GLAXO WELLCOME RES & DEV LTD, GENEVA BIOMED RES INST, PLAN LES OUATES,
CH-1228 GENEVA, SWITZERLAND
GLAXO WELLCOME RES & DEV LTD, GENEVA BIOMED RES INST, CH-1228 GENEVA,
SWITZERLAND
CY SWITZERLAND
SO NEUROPHARMACOLOGY, vol. 36, issue 9, (SEP, 1997) : pp. 1277-1283.
SB LifeSci
WK 11/16/1997
AB The P2X(7) receptor is a bifunctional molecule. The binding of ATP
induces within milliseconds the opening of a channel selective for
small cations, and within seconds a larger pore opens which allows
permeation by molecules as large as propidium dyes (629 Da). In situ
hybridization using a digoxigenin-labelled riboprobe, and
immunohistochemistry using an antibody raised against a C-terminal
peptide sequence, were used to determine the distribution of the P2X(7)
receptor mRNA and protein in rat and mouse tissues and cell lines. The
brain of newborn rats showed a 6 kb RNA by Northern blotting, but this
was not detectable in adult brain. By in situ hybridization and
immunohistochemistry, there was heavy labelling of ependymal cells in
both newborn and adult brain, but the brain parenchyma showed no
labelling. However, P2X(7) receptor-immunoreactive cells appeared in
the penumbral region around an area of necrosis evoked by prior
occlusion of the middle cerebral artery, suggesting expression of the
receptor by activated microglia. NTW8 cells, a mouse microglial cell
Line, strongly expressed the P2X(7) receptor mRNA and protein. The
P2X(7) receptor mRNA and protein were also observed in the majority of
bone marrow cells, including those separately identified by their
expression of other antigens as granulocytes, monocyte/macrophages and
B lymphocytes. The expression of P2X(7) receptor by brain macrophages
rather than neurons would be consistent with a role in brain repair
following inflammation, infarction or immune insult. (C) 1997 Elsevier
Science Ltd.
AA N
EA Y
LG eng
PT ARTICLE
RF 33
IN 0028-3908
SC TU: PHARMACOLOGY AND PHARMACY. RU: NEUROSCIENCES.
GA YD892 (For ordering reprints from ISI)
KW IN SITU HYBRIDIZATION; IMMUNOHISTOCHEMISTRY; P2X(7) RECEPTOR;
MACROPHAGE; MONOCYTE; MICROGLIA; PURINERGIC RECEPTORS; ATP
KP GATED ION CHANNELS; EXTRACELLULAR ATP; P-2X RECEPTOR; MICROGLIAL
CELLS; PLASMA-MEMBRANE; MOUSE-BRAIN; PURINOCEPTORS; RAT; RELEASE
Document 47 of 943
AU NIEBER-K; POELCHEN-W; ILLES-P*
TI ROLE OF ATP IN FAST EXCITATORY SYNAPTIC POTENTIALS IN LOCUS-COERULEUS
NEURONS OF THE RAT
AD *UNIV LEIPZIG, INST PHARMAKOL & TOXIKOL, D-04107 LEIPZIG, GERMANY
UNIV LEIPZIG, INST PHARMAKOL & TOXIKOL, D-04107 LEIPZIG, GERMANY
UNIV LEIPZIG, INST PHARM, ABT PHARMAKOL NAT WISSENSCH, D-04103 LEIPZIG,
GERMANY
CY GERMANY
SO BRITISH JOURNAL OF PHARMACOLOGY, vol. 122, issue 3, (OCT, 1997) : pp.
423-430.
SB LifeSci
WK 10/19/1997
AB 1. Intracellular recordings were made in a pontine slice preparation
of the rat brain containing the nucleus locus coeruleus (LC). The
pressure application of alpha,beta-methylene ATP (alpha,beta-meATP)
caused reproducible depolarizations which were depressed by suramin (30
mu M) and abolished by suramin (100 mu M).
Pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS; 10, 30
mu M) also concentration-dependently inhibited the
alpha,beta-meATP-induced depolarization, although with a much slower
timecourse than suramin. Almost complete inhibition developed with 30
mu M PPADS. Reactive blue 2 (30 mu M) did not alter the effect of
alpha,beta-meATP, while reactive blue 2 (100 mu M) slightly depressed
it.
2. Pressure-applied
(S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)
also depolarized LC neurones. Kynurenic acid (500 mu M) depressed and
6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 50 mu M) abolished the
response to AMPA. Suramin (100 mu M) potentiated the AMPA effect.
3. Pressure-applied noradrenaline hyperpolarized LC neurones. Suramin
(100 mu M) did not after the effect of noradrenaline.
4. Focal electrical stimulation evoked biphasic synaptic potentials
consisting of a fast depolarization (p.s.p.) followed by a slow
hyperpolarization (i.p.s.p.). A mixture of
D(-)-2-amino-5-phosphonopentanoic acid (AP-5; 50 mu M), CNQX (50 mu M)
and picrotoxin (100 mu M) depressed both the p.s.p. and the i.p.s.p.
Under these conditions suramin (100 mu M) markedly inhibited the
p.s.p., but did not alter the i.p.s.p. In the combined presence of
AP-5 (50 mu M), CNQX (50 mu M), picrotoxin (100 mu M), strychnine (0.1
mu M), tropisetron (0.5 mu M) and hexamethonium (100 mu M), a high
concentration of suramin (300 mu M) almost abolished the p.s.p.
without changing the i.p.s.p.
5. In the presence of kynurenic acid (500 mu M) and picrotoxin (100 mu
M), PPADS (30 mu M) depressed the p.s.p. Moreover, the application of
suramin (100 mu M) to the PPADS (30 mu M)-containing medium failed to
cause any further inhibition. Neither PPADS (30 mu M) nor suramin (100
mu M) altered the i.p.s.p.
6. It was concluded that the cell somata of LC. neurones are endowed
with excitatory P2-purinoceptors. ATP may be released either as the
sole transmitter from purinergic neurones terminating at the LC or as a
co-transmitter of noradrenaline from recurrent axon collaterals or
dendrites of the LC neurones themselves.
AA N
EA Y
LG eng
PT ARTICLE
RF 47
IN 0007-1188
SC TU: PHARMACOLOGY AND PHARMACY. CQ: BIOCHEMISTRY AND MOLECULAR BIOLOGY.
GA XZ409 (For ordering reprints from ISI)
KW ATP; NORADRENALINE; LOCUS COERULEUS
KP GATED ION CHANNELS; NERVOUS-SYSTEM; CERULEUS NEURONS;
P-2-PURINOCEPTOR ANTAGONISTS; ADENOSINE 5'-TRIPHOSPHATE; P-2X
PURINOCEPTORS; GUINEA-PIG; IN-VITRO; RECEPTOR; INHIBITION
Document 61 of 943
AU BARDONI-R*; GOLDSTEIN-P-A; LEE-C-J; GU-J-G; MACDERMOTT-A-B
TI ATP P-2X RECEPTORS MEDIATE FAST SYNAPTIC TRANSMISSION IN THE DORSAL
HORN OF THE RAT SPINAL-CORD
AD *UNIV MODENA, SEZ FISIOL, DIPARTIMENTO SCI BIOMED, VIA CAMPI 287,
I-41100 MODENA, ITALY
COLUMBIA UNIV, DEPT PHYSIOL & CELLULAR BIOPHYS, NEW YORK, NY 10032
COLUMBIA UNIV, DEPT ANESTHESIOL, NEW YORK, NY 10032
COLUMBIA UNIV, CTR NEUROBIOL & BEHAV, NEW YORK, NY 10032
ZP 10032
CY ITALY
USA
SO JOURNAL OF NEUROSCIENCE, vol. 17, issue 14, (JUL 15, 1997) : pp.
5297-5304.
SB LifeSci
WK 09/21/1997
AB ATP has been proposed to mediate synaptic transmission in the spinal
card dorsal horn, particularly in the pathway carrying nociceptive
information. Using transverse spinal cord slices from postnatal rats,
we show that EPSCs mediated by P-2x receptors, and presumably activated
by synaptically released ATP, are evoked in a subpopulation of spinal
cord lamina II neurons, a region known to receive strong input from
nociceptive primary afferents. The P-2x receptors on acutely
dissociated dorsal horn neurons are nondesensitizing, insensitive to
alpha beta methylene ATP, and show strong but variable sensitivity to
the antagonists suramin and
pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS). These
characteristics are consistent with a heterogeneous population of P-2x
receptors, the composition of which includes P-2x2 P-2x4 and P-2x6
receptor subtypes. Our results suggest that ATP-activated P-2x
receptors in lamina II of the rat spinal cord may play a role in
transmitting or modulating nociceptive information.
AA N
EA Y
LG eng
PT ARTICLE
RF 36
IN 0270-6474
SC RU: NEUROSCIENCES.
GA XV075 (For ordering reprints from ISI)
KW ATP; PURINERGIC RECEPTORS; SYNAPTIC TRANSMISSION; SPINAL CORD; RAT;
PATCH-CLAMP TECHNIQUE; SLICE PREPARATION
KP GATED ION CHANNELS; INTRACELLULAR CALCIUM; EXTRACELLULAR ATP;
SENSORY NEURONS; FAST KINETICS; CURRENTS; BRAIN; NMDA; CELLS
Document 68 of 943
AU CHO-H; HARADA-N*; YAMASHITA-T
TI EXTRACELLULAR ATP-INDUCED CA2+ MOBILIZATION OF TYPE-I SPIRAL
GANGLION-CELLS FROM THE GUINEA-PIG COCHLEA
AD *KANSAI MED UNIV, DEPT OTOLARYNGOL, MORIGUCHI, OSAKA 570, JAPAN
KANSAI MED UNIV, DEPT OTOLARYNGOL, MORIGUCHI, OSAKA 570, JAPAN
CY JAPAN
SO ACTA OTO-LARYNGOLOGICA, vol. 117, issue 4, (JUL, 1997) : pp. 545-552.
SB LifeSci; ClinMed
WK 09/07/1997
AB Intracellular calcium concentrations ([Ca2+](i)) in type I cochlear
spiral ganglion cells (SGCs) of the guinea pig were measured by digital
imaging microscopy and the Ca2+-sensitive dye Fura-2. Extracellular
ATP induced elevation of [Ca2+](i) in type T SGCs in a
concentration-dependent manner. The ATP-induced elevation of [Ca2+](i)
in SGC was even evident in the Ca2+-free solution, thereby suggesting
that ATP induces a Ca2+-release from intracellular stores in SGCs.
Suramin and reactive blue 2, both antagonists for the P-2-purinergic
receptor, inhibited the [Ca2+](i) increase in SGCs induced by
extracellular ATP in a dose-dependent manner. Adenosine did not induce
any changes of [Ca2+](i) in SGC. These results suggest that type I SGCs
may possess P-2-purinergic receptor but not P-1-purinergic receptor.
Extracellular ATP induced a [Ca2+](i) increase in type I SGCs, with and
without neuritic processes, while L-glutamate increased [Ca2+](i) in
type I SGCs with neuritic processes, but not SGCs without neuritic
processes. The ATP-induced [Ca2+](i) increase was almost equal in both
soma and processes. Therefore, the distribution of P-2-purinergic
receptor in type I SGCs may be homogeneous in soma and processes.
Based on these observations, we suggest that extracellular ATP may act
as a neurotransmitter or neuromodulator of the hair cell-afferent nerve
synapse in the guinea pig cochlea.
AA N
EA Y
LG eng
PT ARTICLE
RF 25
IN 0001-6489
SC TD: OTORHINOLARYNGOLOGY.
GA XR784 (For ordering reprints from ISI)
KW AFFERENT NEUROTRANSMITTER; ATP; COCHLEA; FURA-2; P-2-PURINERGIC
RECEPTOR; SPIRAL GANGLION CELLS
KP HAIR-CELLS; NEUROTRANSMITTERS; RESPONSES; CURRENTS; CALCIUM
Document 175 of 943
AU HARTLEY-S-A; KOZLOWSKI-R-Z*
TI ELECTROPHYSIOLOGICAL CONSEQUENCES OF PURINERGIC RECEPTOR STIMULATION IN
ISOLATED RAT PULMONARY ARTERIAL MYOCYTES
AD *UNIV OXFORD, DEPT PHARMACOL, MANSFIELD RD, OXFORD OX1 3QT, ENGLAND
UNIV OXFORD, DEPT PHARMACOL, OXFORD OX1 3QT, ENGLAND
CY ENGLAND
SO CIRCULATION RESEARCH, vol. 80, issue 2, (FEB, 1997) : pp. 170-178.
SB LifeSci
WK 02/16/1997
AB Neither the electrophysiological effects of purinergic receptor
stimulation nor the role of ATP in regulating the tone of pulmonary
arterial smooth muscle has been determined. Therefore, we investigated
the effects of purine nucleotides on acutely dissociated smooth muscle
cells from rat small pulmonary arteries using the patch-clamp recording
technique. Extracellular application of ATP activated a fast transient
inward current (which decayed in the continued presence of the
nucleotide) and produced sustained periodic oscillations of
predominantly inward current. Pharmacological and anion substitution
experiments revealed that the transient inward current was carried by
the movement of cations. In contrast, the peri odic oscillations of
current were due primarily to a Ca2+-activated Cl- current (I-Cl,I-Ca)
dependent on the release of Ca2+ from intracellular stores.
Experiments using ATP analogues revealed the following order of potency
for activation of the fast transient inward current: 2-methylthio ATP
(2-meSATP)>ATP>alpha,beta-methylene ATP (alpha,beta-meATP)much greater
than ADP>UTP=adenosine. Cross desensitization was seen between
applications of ATP, alpha,beta-meATP, and 2-meSATP, suggesting that
these agonists act via a common site. The order of potency for
activation of I-Ca,I-Cl was UTP=ATP much greater than ADP greater than
or equal to 2-meSATP>alpha,beta-meATP=adenosine. Both the fast
transient inward current and I-Cl,I-Ca evoked by ATP and its analogues
were abolished by the nonselective P-2 purinoceptor antagonist suramin.
These results show the existence of P-2X and P-2U purinoceptor subtypes
in pulmonary arterial smooth muscle cells. Stimulation of these
receptors results in activation of a fast transient inward cation
current and I-Cl,I-Ca, respectively. It is likely that ATP acts via
these receptor subtypes to regulate pulmonary arterial tone under
physiological or pathological conditions.
AA N
EA Y
LG eng
PT ARTICLE
RF 54
IN 0009-7330
SC MA: HEMATOLOGY. ZD: PERIPHERAL VASCULAR DISEASE.
GA WE959 (For ordering reprints from ISI)
KW PULMONARY ARTERY; P-2 PURINOCEPTOR; PURINE NUCLEOTIDE; CL- CHANNEL
KP SMOOTH-MUSCLE CELLS; RABBIT PORTAL-VEIN; ADENOSINE-TRIPHOSPHATE; EAR
ARTERY; P2-PURINOCEPTOR SUBTYPES; P2-PURINERGIC RECEPTORS;
EXTRACELLULAR ATP; ENDOTHELIAL-CELLS; SENSORY NEURONS; ION CHANNELS
Document 183 of 943
AU HALLIDAY-F-C*; GIBB-A-J
TI NEUROPHARMACOLOGY - A PART FOR PURINES IN PATTERN GENERATION
AD *UNIV COLL LONDON, DEPT PHARMACOL, GOWER ST, LONDON WC1E 6BT, ENGLAND
CY ENGLAND
SO CURRENT BIOLOGY, vol. 7, issue 1, (JAN 1, 1997) : pp. R47-R49.
SB LifeSci
WK 02/09/1997
AB Purinergic transmission has been found to play a key role in the neural
control of rhythmic swimming behaviour in Xenopus embryos; it may have
similar importance in other vertebrate motor behaviours.
AA N
EA Y
LG eng
PT ARTICLE
RF 12
IN 0960-9822
SC CQ: BIOCHEMISTRY AND MOLECULAR BIOLOGY. CU: BIOLOGY.
GA WE221 (For ordering reprints from ISI)
KP EXPRESSION; RECEPTOR
Document 24 of 943
AU JONES-S-J*; GRAY-C; BOYDE-A; BURNSTOCK-G
TI PURINERGIC TRANSMITTERS INHIBIT BONE-FORMATION BY CULTURED OSTEOBLASTS
AD *UNIV COLL LONDON, DEPT ANAT & DEV BIOL, GOWER ST, LONDON WC1E 6BT,
ENGLAND
CY ENGLAND
SO BONE, vol. 21, issue 5, (NOV, 1997) : pp. 393-399.
SB LifeSci; ClinMed
WK 11/16/1997
AB Adenosine triphosphate (ATP) and other purinoceptor agonists cause a
transient rise in [Ca2+](i) in cultured osteoblast-like cells and have
a mitogenic effect, as does parathyroid hormone (PTH), and there is
evidence that ATP and PTH can act synergistically on osteoblasts. The
likelihood that nucleotides, acting through purinoceptors, are
important local factors in bone remodeling is therefore considerable.
However, their effect on bone formation is unknown. We recently
developed a culture system in which appositional bone formation occurs
only in narrow grooves cut in a substratum. We have used this as an
assay to measure the effects of ATP (50 and 500 mu mol/L), ATP gamma S
(20 mu mol/L), 2-MeSATP (2 and 20 mu mol/L), uridine triphosphate (UTP)
(0.2, 2, and 20 mu mol/L), adenosine (20 mu mol/L), bovine PTH (0.25
and 0.5 IU/mL), rat PTH1-34 (10(-8) and 10(-7) mol/L), and rat
PTHrP1-40 (10(-9) and 10(-8) mol/L) on bone formation by rat calvarial
osteoblasts. The culture medium was renewed 3 times/week (every 2 or 3
days), and the number of bone loci and length and area of Alizarin
red-stained mineralized bone formed in the grooves of each specimen in
16-29 days were measured. Compared with controls, ATP gamma S,
2-MeSATP, and ATP reduced the amount of bone formed in a 2-3 week
culture period. Adenosine had no effect, and UTP either had no effect
or at 2 mu mol/L stimulated bone formation. PTH and PTHrP completely
abolished bone formation in 4 week cultures. Our findings are
consistent with evidence for more than one P2 purinoceptor subtype in
bone, and show for the first time that the effect of ATP on
appositional bone formation by osteoblasts in vitro is, like PTH and
PTHrP, inhibitory. (C) 1997 by Elsevier Science Inc. All rights
reserved.
AA N
EA Y
LG eng
PT ARTICLE
RF 40
IN 8756-3282
SC IA: ENDOCRINOLOGY AND METABOLISM.
GA YD853 (For ordering reprints from ISI)
KW OSTEOBLASTS; BONE FORMATION; ADENOSINE TRIPHOSPHATE; PURINOCEPTORS;
PARATHYROID HORMONE; PARATHYROID HORMONE RELATED PROTEIN
KP PARATHYROID-HORMONE; IN-VITRO; INTRACELLULAR CALCIUM; SIGNALING
PATHWAYS; CELLS; ATP; MINERALIZATION; PURINOCEPTORS; CHONDROCYTES;
OSTEOCLASTS
Document 20 of 85
AU THORNE-P-R*; HOUSLEY-G-D
TI PURINERGIC SIGNALING IN SENSORY SYSTEMS
AD *UNIV AUCKLAND, DEPT PHYSIOL, PRIVATE BAG 92019, AUCKLAND, NEW ZEALAND
CY NEW ZEALAND
SO SEMINARS IN THE NEUROSCIENCES, vol. 8, issue 4, (AUG, 1996) : pp.
233-246.
SB LifeSci
WK 08/18/1996
AB Extracellular purines play multiple roles in a variety of sensory
systems acting as neural signalling and humoral factors via
purinoceptors. For example, ATP and adenosine have a neurosignalling
role in autonomic sensory-motor reflexes, mechanoreception and
chemoreception mediated via vagus nerve afferents, and in, nociception.
Purinergic neuromodulation of vision via adenosine in the retina is
well established and there is mounting evidence for a neuromodulatory
role for ATP in the inner ear. Humoral purinergic actions are found in
the eye where adenosine clearly has an important vascular and humoral
influence and in the inner ear where ATP probably regulates fluid
homeostasis, hearing sensitivity and development. Clearly purinergic
signalling underpins the physiology of many of the body's sensory
systems. (C) 1996 Academic Press Ltd
AA N
EA Y
LG eng
PT REVIEW
RF 143
IN 1044-5765
SC RU: NEUROSCIENCES.
GA VA666 (For ordering reprints from ISI)
KW EYE; HEARING; INNER EAR; NOCICEPTION; OLFACTION
KP GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; CHICK-EMBRYO RETINA;
NONADRENERGIC NONCHOLINERGIC NEUROTRANSMISSION; ADENOSINE
5'-TRIPHOSPHATE ATP; OLFACTORY RECEPTOR NEURONS; H-3 NORADRENALINE
RELEASE; CILIARY EPITHELIAL-CELLS; ISOLATED VAGUS NERVE; DORSAL HORN
NEURONS
Document 29 of 85
AU BURNSTOCK-G*
TI NORADRENALINE AND ATP - COTRANSMITTERS AND NEUROMODULATORS
AD *UNIV LONDON UNIV COLL, DEPT ANAT & DEV BIOL, GOWER ST, LONDON WC1E
6BT, ENGLAND
UNIV COLL LONDON, CTR NEUROSCI, LONDON, ENGLAND
CY ENGLAND
SO JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, vol. 46, issue 4, (DEC, 1995)
: pp. 365-384.
SB LifeSci
WK 01/14/1996
AB Adenosine 5'-triphosphate (ATP) is a cotransmitter with noradrenaline
(NA) in sympathetic nerves supplying the vas deferens and a number of
blood vessels. ATP is responsible for the excitatory junctional
potentials (EJPs) in response to single nerve impulses and the initial
twitch responses of the smooth muscle, while NA produces the
longer-lasting tonic contractions. The proportions of ATP to NA vary
between different sympathetic nerves; they also change during
development and in some pathological conditions, including
hypertension. Prejunctional neuromodulation of release of the two
cotransmitters appears to involve independent mechanisms and is
frequency dependent; this raises the question of whether ATP and NA are
stored in separate vesicles or whether there are subpopulations of
sympathetic nerves with a predominance of ATP or NA. ATP and NA have
synergistic postjunctional actions, whether excitatory (as in the vas
deferens and most blood vessels) or inhibitory (as in rabbit coronary
vessels). It is suggested that use of the term 'adrenergic nerves' as a
synonym for sympathetic nerves is no longer appropriate, although
'adrenergic transmission' or 'purinergic transmission' are still useful
terms.
AA N
EA Y
LG eng
PT ARTICLE
RF 195
IN 0867-5910
SC UM: PHYSIOLOGY.
GA TM027 (For ordering reprints from ISI)
KW PURINERGIC; SYMPATHETIC; HYPERTENSION; PLASTICITY; NEUROPEPTIDES;
NEUROTRANSMISSION
KP PIG VAS-DEFERENS; SYMPATHETIC-NERVE STIMULATION; RABBIT EAR ARTERY;
DOG MESENTERIC-ARTERY; SMOOTH-MUSCLE CELLS; VASCULAR
ADRENERGIC-NERVES; BETA-METHYLENE ATP; RAT CAUDAL ARTERY;
GUINEA-PIG; ADENOSINE-TRIPHOSPHATE
Document 66 of 85
AU BURNSTOCK-G*
TI PHYSIOLOGICAL AND PATHOLOGICAL ROLES OF PURINES - AN UPDATE
AD *UNIV LONDON UNIV COLL, DEPT ANAT & DEV BIOL, GOWER ST, LONDON WC1E
6BT, ENGLAND
UNIV LONDON UNIV COLL, CTR NEUROSCI, LONDON WC1E 6BT, ENGLAND
CY ENGLAND
SO DRUG DEVELOPMENT RESEARCH, vol. 28, issue 3, (MAR, 1993) : pp. 195-206.
SB LifeSci
WK 04/11/1993
AB In this review article, the early history of studies of purinergic
neurotransmission and of purinoceptor subclassification is described.
This is followed by a survey of current knowledge of the distribution
of purinoceptors and of the physiological roles of purines in the
nervous system, muscle, secretory, endocrine and immune cells, as well
as in spermatocytes, osteoblasts, fibroblasts, and tumour cells.
Recent studies of transduction mechanisms for different purinoceptor
subtypes, as well as reports of the molecular properties of encoding
genes for purinoceptors, are reviewed. The evolution of purinergic
mechanisms and the long-term 'trophic' actions of purines are
discussed. Finally, the clinical potential of purines and related
compounds for various cardiovascular and behavioural disorders, as well
as for inflammation and cancer are considered.
AA N
EA Y
LG eng
PT ARTICLE
RF 216
IN 0272-4391
SC TU: PHARMACOLOGY AND PHARMACY.
GA KV613 (For ordering reprints from ISI)
KP A1 ADENOSINE RECEPTOR; PIG VAS-DEFERENS; VASCULAR ENDOTHELIAL-CELLS;
CEREBRAL CORTICAL-NEURONS; BRAIN MESSENGER-RNA; OUTER HAIR-CELLS;
PROTEIN KINASE-C; EXTRACELLULAR ATP; GUINEA-PIG; SENSORY NEURONS
Document 81 of 85
AU CRAIG-C-G*; WHITE-T-D
TI LOW-LEVEL N-METHYL-D-ASPARTATE RECEPTOR ACTIVATION PROVIDES A
PURINERGIC INHIBITORY THRESHOLD AGAINST FURTHER
N-METHYL-D-ASPARTATE-MEDIATED NEUROTRANSMISSION IN THE CORTEX
AD *DALHOUSIE UNIV, DEPT PHARMACOL, HALIFAX B3H 4H7, NS, CANADA
CY CANADA
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, vol. 260, issue
3, (MAR, 1992) : pp. 1278-1284.
SB LifeSci
WK 01/01/1992
AB N-methyl-D-aspartate (NMDA) is 33 times more potent at releasing
adenosine than it is at releasing [H-3]norepinephrine from slices of
rat parietal cortex. Consequently, maximal adenosine release occurs at
levels of NMDA receptor activation which release little norepinephrine.
The potential modulatory role of the adenosine released during NMDA
receptor activation on NMDA-evoked [H-3]norepinephrine release was
investigated. The A1-selective agonist
R-(-)N6-(2-phenylisopropyl)adenosine (10-mu-M) decreased 100-mu-M
NMDA-evoked [H-3]norepinephrine release by 27%; this was reversed by
the P1 antagonist 8-phenyltheophylline (8-PT, 10-mu-M), indicating that
NMDA-evoked norepinephrine release from cortical slices is susceptible
to purinergic modulation. On the other hand, 8-PT had no effect on
[H-3]norepinephrine release evoked by 100-mu-M NMDA, suggesting that
endogenous adenosine, released during NMDA receptor activation, does
not modulate [H-3]norepinephrine release. However, [H-3]norepinephrine
release precedes adenosine release, so that the released adenosine may
not be temporally available to modulate [H-3]norepinephrine release.
Pretreatment with a concentration of NMDA (10-mu-M) which releases
substantial endogenous adenosine, but very little [H-3]norepinephrine
decreased subsequent 100-mu-M NMDA-evoked [H-3]norepinephrine release
by 52%. 8-PT partially reversed this inhibition, indicating that
prereleased adenosine, acting at P1 purinoceptors, modulated subsequent
NMDA-evoked [H-3]norepinephrine release. These results suggest that
adenosine, released during submaximal NMDA receptor activation, may
provide an inhibitory threshold which must be overcome in order for
other NMDA-mediated processes to proceed maximally.
AA N
EA Y
LG eng
PT ARTICLE
RF 60
IN 0022-3565
SC TU: PHARMACOLOGY AND PHARMACY.
GA HJ019 (For ordering reprints from ISI)
KP LONG-TERM POTENTIATION; CENTRAL NERVOUS-SYSTEM; RAT HIPPOCAMPAL
SLICES; EXCITATORY AMINO-ACIDS; EVOKED RELEASE; EPILEPTIFORM
ACTIVITY; ENDOGENOUS ADENOSINE; NMDA RECEPTORS; GLUTAMATE RELEASE;
AMINOBUTYRIC-ACID
CP Copyright US/Pacific, Current Contents(tm) from ISI, all rights reserved.
Document 199 of 943
AU BRAKE-A-J*; JULIUS-D
TI SIGNALING BY EXTRACELLULAR NUCLEOTIDES
AD *UNIV CALIF SAN FRANCISCO, DEPT MOL & CELLULAR PHARMACOL, CELL BIOL
PROGRAM, SAN FRANCISCO, CA 94143
UNIV CALIF SAN FRANCISCO, DEPT MOL & CELLULAR PHARMACOL, PROGRAM
NEUROSCI, SAN FRANCISCO, CA 94143
ZP 94143
CY USA
SO ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, vol. 12, (1996) : pp.
519-541.
SB LifeSci
WK 01/12/1997
AB ATP and other nucleotides can be released from cells through regulated
pathways, or following the loss of plasma membrane integrity. Once
outside the cell, these compounds take on new roles as intercellular
signaling molecules that elicit a broad spectrum of physiological
responses through the activation of numerous cell surface receptor
subtypes. This review summarizes recent advances in the molecular
characterization of ATP receptors and discusses roles for cloned
receptors in established and novel physiological processes.
AA N
EA Y
LG eng
PT REVIEW
RF 112
IN 1081-0706
SC CQ: BIOCHEMISTRY AND MOLECULAR BIOLOGY. DR: CELL BIOLOGY. HY:
DEVELOPMENTAL BIOLOGY.
GA VY428 (For ordering reprints from ISI)
KW PURINERGIC RECEPTORS; LIGAND-GATED ION CHANNELS; SYNAPTIC
TRANSMISSION; APOPTOSIS
KP SMOOTH-MUSCLE CELLS; GATED ION CHANNELS; VASCULAR ENDOTHELIAL-CELLS;
EPITHELIAL NA+ CHANNEL; RAT VAS-DEFERENS; CYSTIC-FIBROSIS; ATP
RECEPTOR; SYNAPTIC TRANSMISSION; FUNCTIONAL EXPRESSION;
GLUTAMATE-RECEPTOR
CP Copyright US/Pacific, Current Contents(tm) from ISI, all rights reserved.
Document 9 of 14
AU CONIGRAVE-A-D*; JIANG-L
TI REVIEW - CA2+-MOBILIZING RECEPTORS FOR ATP AND UTP
AD *UNIV SYDNEY, DEPT BIOCHEM G08, SYDNEY, NSW 2006, AUSTRALIA
CY AUSTRALIA
SO CELL CALCIUM, vol. 17, issue 2, (FEB, 1995) : pp. 111-119.
SB LifeSci
WK 03/12/1995
AB Extracellular nucleotides are potent Ca2+ mobilizing agents, A variety
of receptors for extracellular ATP are recognised. Some are involved
in fast neuronal transmission and operate as ligand-gated ion channels.
Others are involved in the paracrine or autocrine modulation of cell
function. Many receptors of this type are coupled to
phosphoinositide-specific phospholipase C and, in some cases, other
phospholipases. One of these receptors (P-2z), however, also appears
to operate, at least in part, as a ligand-gated ion channel.
Pharmacological data suggest that one nucleotide receptor subtype
(currently designated P-2U) responds selectively to either a purine
nucleotide, ATP, or a pyrimidine nucleotide, UTP. According to an
alternative view, ATP and UTP recognise distinct receptors. Because of
the diversity of receptors for extracellular nucleotides this may be
the case in some cells. Nevertheless, a G-protein coupled receptor
that confers both ATP and UTP sensitivity has been cloned, expressed in
cultured cell lines and sequenced. This receptor appears to have two
ligand binding domains that may partially overlap. The nature of this
overlap is discussed and a simple model presented. Activation of the
receptor protein via one or other ligand binding domain may underlie
some of the more subtle differences between the effects of ATP and UTP.
AA N
EA Y
LG eng
PT REVIEW
RF 73
IN 0143-4160
SC DR: CELL BIOLOGY.
GA QH397 (For ordering reprints from ISI)
KP INOSITOL PHOSPHOLIPID BREAKDOWN; RENAL MESANGIAL CELLS; PAROTID
ACINAR-CELLS; SMOOTH-MUSCLE CELLS; EXTRACELLULAR ATP; HL60 CELLS;
G-PROTEINS; P2-PURINERGIC RECEPTORS; PYRIMIDINE NUCLEOTIDES;
HUMAN-NEUTROPHILS
Document 13 of 14
AU MOSQUEDAGARCIA-R*
TI ADENOSINE AS A THERAPEUTIC AGENT
AD VANDERBILT UNIV, MED CTR, SCH MED, DEPT MED, DIV CLIN PHARMACOL,
NASHVILLE, TN 37232
VANDERBILT UNIV, MED CTR, SCH MED, DEPT OBSTET & GYNECOL, NASHVILLE, TN
37232
ZP 37232
CY USA
SO CLINICAL AND INVESTIGATIVE MEDICINE-MEDECINE CLINIQUE ET EXPERIMENTALE,
vol. 15, issue 5, (OCT, 1992) : pp. 445-455.
SB LifeSci; ClinMed
WK 01/01/1992
AB Adenosine, an endogenous nucleoside has been recently approved for use
in the treatment of paroxysmal supraventricular tachycardia. Adenosine
is nearly 100% effective in terminating tachycardia in which the
atrioventricular node forms part of the reentrant circuit. Although
most ventricular tachycardias are insensitive to adenosine, this
substance is effective in ventricular tachycardia induced by
catecholamines or exercise. An intravenous bolus dose of 6 mg is the
initial dose. If no effect is noted a further bolus of 12 mg can be
given. The most common side effects are dyspnea, chest pressure and
facial flushing. This article reviews, in addition, some of the
comparative trials with verapamil and adenosine triphosphate, some of
the additional therapeutic indications, the possible mechanisms of
action in cardiac tissue, and the type of purinergic receptors involved
in the antiarrhythmic effects of adenosine.
AA N
EA Y
LG eng
PT REVIEW
RF 71
IN 0147-958X
SC QA: MEDICINE, RESEARCH AND EXPERIMENTAL.
GA KB547 (For ordering reprints from ISI)
KP PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA; SUPRA-VENTRICULAR
TACHYCARDIA; CORONARY-ARTERY DISEASE; GUINEA-PIG;
ATRIOVENTRICULAR-CONDUCTION; INTRAVENOUS ADENOSINE; NORMOTENSIVE
RATS; ACUTE MANAGEMENT; CONSCIOUS MAN; SINUS NODE
--
Terrence Brannon * brannon at lnc.usc.edu * http://lnc.usc.edu/~brannon
USC, HNB, 3614 Watt Way, Los Angeles, CA 90089-2520 * (213) 740-3397
Got Milk? Should you? http://www.milk.com vs. http://www.notmilk.com
