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Somatostain and other neuropeptide mRNAS induced by kainic acid in the hippocampal granule and pyramidal cells
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CENTRAL CARDIOVASCULAR REGULATION OF TACHYKININ PEPTIDES: ROLE OF TACHYKININ NK-3 RECEPTORS IN THE PARAVENTRICULAR NUCLEUS (PVN) YUKIO TAKANO, YASUHISA NAKAYAMA, RYO SAITO, AND HIRO-0 KAMIYA, Department of Pharmacolonv. Faculty of Pharmaceutical Sciences, Fukuoka University. Fukuoka 814-01, Japan. Recent studies have shown the existence of three major tachykinin receptors, NK-1, NK-2 and NK-3. We previously found that central substance P, considered to be an endogenous ligand of NK-1 receptor, increased the blood pressure (BP) and heart rate via stimulation of sympathetic nerve activity. The present study was aimed to examine the possible mechanisms injections (i.c.v.) of central cardiovascular regulation by NK-3 agonists. Intracerebroventricular of tachykinin peptides caused dose-dependent increases in BP and heart rate in anesthetized rats. The pressor responses to NK-1 agonist were blocked by peripheral administration of pentolinium and phentolamine. The pressor response to the selective NK-3 agonist, senktide (lOpg, i.c.v.), was inhibited by peripheral pretreatment with vasopressin Vl receptor antagonist, and senktide caused an increase in plasma vasopressin level. In addition, the microinjection of senktide into the PVN increased the BP in the bilateral sinoaortic denervated rats. These results suggest that the central cardiovascular effects of senktide are mediated mainly by a release of vasopressin via stimulation of NK-3 receptor in the PVN.
EFFECTS OF PSYCHOGENICAGENTS ON CHOLECYSTOKININ GENE EXPRESSION UYA AND MICHIQ TORT1 Univet&y. I-5-45 Yv Tokyo 113. u Methamphetamine (MAP) and phencyclidine (PCP) are known to be the psychogenic agents which induce psychotic states similar to paranoid type of schizophrenia. On the other hand, cholecystokinin (CCK) is one of the peptide neurotransmitter whose dysregulations are assumed in the etiology of schizophrenia. In this study, we measured (3 mg/kg,
the level of CCKmRNA i.p.) or
cortex 20 min after the injections, Reduction
by the Northern
PCP (7.5 mg/kg, i.p.).
in CCKmRNA
blot analysis in the rat brain after single administration
Both MAP and
but had not significant
was also observed
effects
in the occipital
48 hoursafter thePCP injection.
compared with our previous findings that CCK turnover
of MAP
PCP decreased CCKmRNA level in the prefrontal
seemed
cortex
and the hippocampus.
These results are interesting when
to be reduced in the postmortem
brains
of
schizophrenics.
SOMATOSTAIN AND OTHER NEUROPEPTIDE mRNAS INDUCED BY KAINIC ACID IN THE HIPPOCAMPAL GRANULE AND PYRAMIDAL CELLS TAKANORI HASHIMOTO @_Q KUNIHIKO OBAT~o~a~qratoruBza~iNqequqro~~~~nstry. National Institute for phvsioloaical Sciences. Y 1.11. Ok c Continual electrical activation will lead to various long-lasting plastic changes in neurons through modification of their gene expression. Seizures were evoked in the rats by systemic administration of kainic acid and the expression of c-fos and several neuropeptide mRNAs were investigated in the hippocampal neurons with non-radioactive in situ hybridization using digoxigenin-labeled cRNA probes. Whereas c-fos mRNAs was induced rapidly in almost all hippocampal neurons. neuropeptide mRNAs were expressed in different subpopulations with different time- iourses. Three-twelve- hours after kainic acid administration, preprosomatostatin mRNA was induced in 8-50X of granule and pyramidal cells these which never had expressed it normally. Immunohistochemistry showed that and Preproenkephalin somatostatin peptide. cells also contained preprocholecystokinin mRNAs were always expressed in some granule and pyramidal cells. Kainic acid remarkably increased preproenkephalin-positive granule cells. There was no obvious change in preprocholecystokinin-expressing cell population These results suggest that the expression of these in the hippocampus. neuropeptides are under the different control and play different roles in neuronal function.
CENTRAL CARDIOVASCULAR REGULATION OF TACHYKININ PEPTIDES: ROLE OF TACHYKININ NK-3 RECEPTORS IN THE PARAVENTRICULAR NUCLEUS (PVN) YUKIO TAKANO, YASUHISA NAKAYAMA, RYO SAITO, AND HIRO-0 KAMIYA, Department of Pharmacolonv. Faculty of Pharmaceutical Sciences, Fukuoka University. Fukuoka 814-01, Japan. Recent studies have shown the existence of three major tachykinin receptors, NK-1, NK-2 and NK-3. We previously found that central substance P, considered to be an endogenous ligand of NK-1 receptor, increased the blood pressure (BP) and heart rate via stimulation of sympathetic nerve activity. The present study was aimed to examine the possible mechanisms injections (i.c.v.) of central cardiovascular regulation by NK-3 agonists. Intracerebroventricular of tachykinin peptides caused dose-dependent increases in BP and heart rate in anesthetized rats. The pressor responses to NK-1 agonist were blocked by peripheral administration of pentolinium and phentolamine. The pressor response to the selective NK-3 agonist, senktide (lOpg, i.c.v.), was inhibited by peripheral pretreatment with vasopressin Vl receptor antagonist, and senktide caused an increase in plasma vasopressin level. In addition, the microinjection of senktide into the PVN increased the BP in the bilateral sinoaortic denervated rats. These results suggest that the central cardiovascular effects of senktide are mediated mainly by a release of vasopressin via stimulation of NK-3 receptor in the PVN.
EFFECTS OF PSYCHOGENICAGENTS ON CHOLECYSTOKININ GENE EXPRESSION UYA AND MICHIQ TORT1 Univet&y. I-5-45 Yv Tokyo 113. u Methamphetamine (MAP) and phencyclidine (PCP) are known to be the psychogenic agents which induce psychotic states similar to paranoid type of schizophrenia. On the other hand, cholecystokinin (CCK) is one of the peptide neurotransmitter whose dysregulations are assumed in the etiology of schizophrenia. In this study, we measured (3 mg/kg,
the level of CCKmRNA i.p.) or
cortex 20 min after the injections, Reduction
by the Northern
PCP (7.5 mg/kg, i.p.).
in CCKmRNA
blot analysis in the rat brain after single administration
Both MAP and
but had not significant
was also observed
effects
in the occipital
48 hoursafter thePCP injection.
compared with our previous findings that CCK turnover
of MAP
PCP decreased CCKmRNA level in the prefrontal
seemed
cortex
and the hippocampus.
These results are interesting when
to be reduced in the postmortem
brains
of
schizophrenics.
SOMATOSTAIN AND OTHER NEUROPEPTIDE mRNAS INDUCED BY KAINIC ACID IN THE HIPPOCAMPAL GRANULE AND PYRAMIDAL CELLS TAKANORI HASHIMOTO @_Q KUNIHIKO OBAT~o~a~qratoruBza~iNqequqro~~~~nstry. National Institute for phvsioloaical Sciences. Y 1.11. Ok c Continual electrical activation will lead to various long-lasting plastic changes in neurons through modification of their gene expression. Seizures were evoked in the rats by systemic administration of kainic acid and the expression of c-fos and several neuropeptide mRNAs were investigated in the hippocampal neurons with non-radioactive in situ hybridization using digoxigenin-labeled cRNA probes. Whereas c-fos mRNAs was induced rapidly in almost all hippocampal neurons. neuropeptide mRNAs were expressed in different subpopulations with different time- iourses. Three-twelve- hours after kainic acid administration, preprosomatostatin mRNA was induced in 8-50X of granule and pyramidal cells these which never had expressed it normally. Immunohistochemistry showed that and Preproenkephalin somatostatin peptide. cells also contained preprocholecystokinin mRNAs were always expressed in some granule and pyramidal cells. Kainic acid remarkably increased preproenkephalin-positive granule cells. There was no obvious change in preprocholecystokinin-expressing cell population These results suggest that the expression of these in the hippocampus. neuropeptides are under the different control and play different roles in neuronal function.