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Differential expression of opioid precursor-protein mRNAs in rat brain neurons: proenkephalin and prodynorphin
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DIFFERENTIAL PROENKEPHALIN
EXPRESSION
OF
OPIOID
PRECURSOR-PROTEIN
mRNAs
IN
RAT
BRAIN
NEURONS:
AND PRODYNORPHIN. YASUHIRO MORITA', HIROYUKI NAKAMURA't, m HASEGAWA*', SHIRO NAKAGAWA'., TAKASHI HIRONAKA'.zI --JIAN-HOUA w'3, AND ___._ MASAYA TOHYAMA', lDepartme& of Anatomy, Kagoshi.ma University Faculty of Medicine, 1208 -~ Usukicho. Kaaoshima 890; 'Research Division Iatron Laboratories Inc., 3-16-4 __--_-Yakuendai &D&bashi, Chiba 214; 3Department of .Qatomy, Osaka University Medical -_._1 School ,. 4-3-57. --_. Nakanoshima,. Kitaku, 530 Japan. -Osaka __I Differential expression of the mRNAs coding for preproenkephalin (PPE) and preprodynorphin (PPD) was examined in the rat brain by b situ hybridization histochemistry. The probes were cloned DNA complementary to rat PPE mRNA ISma Sac1 fragment from pYSEA1 by Yoshikaua et al., '84, JCB, 259:14301-14308) and synthetic DNA I50 bases: position 538-587 of the coding region1 for rat PPD mRNA. II) PPE mRNA-containing neurons were found in various regions throughout the rat PPD mRNA were mainly located in forebrain tissues, brain, while neurons expressing with positive neurons in the pnrabrachial region, solitary nucleus, and the caudal
part of the spinal nucleus of the trigeminal nerve. 12) The neuronal populations showing different opioid phenotypes appeared to be separated in various brain tissues (e.g. cerebral cortex, caudate-putamen nucleus, hypothalamic paraventricular nucleus, ventromedial hypothalamic nucleus, solitary nucleus, brain tissues contain either type of opioid neurons with etc.). (3) Several differential
gene
expression.
32. Neurotoxicology EFFECTS OF ACRYLAMIDE ON IA SENSORY NEURONS AND SPINAL MOTONEURONS IN RATS. YUHEI MIYATA, FUMIKO SAITOH*, and MASAYUKI KOMUKAI*, Department of Pharmacology, Nippon Medical School, Sendagi l-l-5, Bunkyo-ku, Tokyo 113, Japan. Acrylamide(ACR) is known to induce neurological disorders, called ACR LOSS of motor coordination is the main behavioral abnormality neuropathy. However, little is known about observed in animals intoxicated with ACR. In this study, we have examined underlying mechanisms for the impairment. components of the spinal reflex arc electrophysiologically in rats intoxicated Two weeks after daily treatment with ACR, excitatory postsynaptic with ACR. potentials recorded intracellularly were reduced remarkably, which can be explained, if not completely, by a loss of excitability of Ia sensory fibers at the distal site. Electrical properties of motoneurons were not affected by ACR. However, motor unit sizes were greatly decreased after 2 weeks of ACR treatment, while the number of motor units remained unchanged.
MAINfA~cApABILITyOF~TERMpoTENTIA~~INTHED~A~~~OF~ IMETHYLTIN-TRFATEDRATS. MATTHEWJ WAYNER*2,AND HIRQSHIYAMASHITA', 'Dept.of l'0SHIMAS.A~ DEBDRAHL ARMsIRGRIGX2, _I-_ -2Phvsiol.,-Univ.of &cup. and hvircn. Health,Kitakvu shu 807, Japa~Division of Life Sci., [.RSA,San Antonio,E 7828cUr The-&arkrnetal,trimethylG(IMT), produceshi-1 damageand diminisheslearningand potentiation (LTP)is an important model for memoryperformance.Sincehippocam@ long-term memoryprocesses,the learningin@rment inducedby TMI couldresultfran the disruption of LTP mechanism.Male Sprague-Cewley rats,weighing270-320g, were dosedvia gavagewith l%fl?. Animals receiveda dose of 7.5-9.0mg/kgTMI (n=9),IO-12ng/kg (High!lMT,n=5),or vehicle(control, n=9). Recordings ware carriedout underurethaneanesthesia(1.3g/kg, i.p.)with a platinumelectrode (50p, o.d.) 1 to 3 weeksafter the treatment. Baselineamplitudes of popllaticn EPSR in the dentategyrusfollowingstimulation of the perforantpath were largerin the controlgroup (4.120.9mV, mean?=) than thosein the TMI (1.4+0.7mV) and High TMl'(1.3+1.0 mV) group. Onset of EPSPswas shorterin the m-treated groups than-inthe controlgroup. tiver, relativeincreases in Epsp amplitude of the TMT group after tetanic stimulation were not different fran that of the control group. The time course of potentiaticn was similar in the 'lW and omtrol groups. These observations suggest that the learning irnpsirnwrtinduced by TMT resulted frana decreaseinnwber of hippaampa lneurans, but not from the disruption of specific synaptic mechanisms underlying LTP withinthe dentategyrus.
DIFFERENTIAL PROENKEPHALIN
EXPRESSION
OF
OPIOID
PRECURSOR-PROTEIN
mRNAs
IN
RAT
BRAIN
NEURONS:
AND PRODYNORPHIN. YASUHIRO MORITA', HIROYUKI NAKAMURA't, m HASEGAWA*', SHIRO NAKAGAWA'., TAKASHI HIRONAKA'.zI --JIAN-HOUA w'3, AND ___._ MASAYA TOHYAMA', lDepartme& of Anatomy, Kagoshi.ma University Faculty of Medicine, 1208 -~ Usukicho. Kaaoshima 890; 'Research Division Iatron Laboratories Inc., 3-16-4 __--_-Yakuendai &D&bashi, Chiba 214; 3Department of .Qatomy, Osaka University Medical -_._1 School ,. 4-3-57. --_. Nakanoshima,. Kitaku, 530 Japan. -Osaka __I Differential expression of the mRNAs coding for preproenkephalin (PPE) and preprodynorphin (PPD) was examined in the rat brain by b situ hybridization histochemistry. The probes were cloned DNA complementary to rat PPE mRNA ISma Sac1 fragment from pYSEA1 by Yoshikaua et al., '84, JCB, 259:14301-14308) and synthetic DNA I50 bases: position 538-587 of the coding region1 for rat PPD mRNA. II) PPE mRNA-containing neurons were found in various regions throughout the rat PPD mRNA were mainly located in forebrain tissues, brain, while neurons expressing with positive neurons in the pnrabrachial region, solitary nucleus, and the caudal
part of the spinal nucleus of the trigeminal nerve. 12) The neuronal populations showing different opioid phenotypes appeared to be separated in various brain tissues (e.g. cerebral cortex, caudate-putamen nucleus, hypothalamic paraventricular nucleus, ventromedial hypothalamic nucleus, solitary nucleus, brain tissues contain either type of opioid neurons with etc.). (3) Several differential
gene
expression.
32. Neurotoxicology EFFECTS OF ACRYLAMIDE ON IA SENSORY NEURONS AND SPINAL MOTONEURONS IN RATS. YUHEI MIYATA, FUMIKO SAITOH*, and MASAYUKI KOMUKAI*, Department of Pharmacology, Nippon Medical School, Sendagi l-l-5, Bunkyo-ku, Tokyo 113, Japan. Acrylamide(ACR) is known to induce neurological disorders, called ACR LOSS of motor coordination is the main behavioral abnormality neuropathy. However, little is known about observed in animals intoxicated with ACR. In this study, we have examined underlying mechanisms for the impairment. components of the spinal reflex arc electrophysiologically in rats intoxicated Two weeks after daily treatment with ACR, excitatory postsynaptic with ACR. potentials recorded intracellularly were reduced remarkably, which can be explained, if not completely, by a loss of excitability of Ia sensory fibers at the distal site. Electrical properties of motoneurons were not affected by ACR. However, motor unit sizes were greatly decreased after 2 weeks of ACR treatment, while the number of motor units remained unchanged.
MAINfA~cApABILITyOF~TERMpoTENTIA~~INTHED~A~~~OF~ IMETHYLTIN-TRFATEDRATS. MATTHEWJ WAYNER*2,AND HIRQSHIYAMASHITA', 'Dept.of l'0SHIMAS.A~ DEBDRAHL ARMsIRGRIGX2, _I-_ -2Phvsiol.,-Univ.of &cup. and hvircn. Health,Kitakvu shu 807, Japa~Division of Life Sci., [.RSA,San Antonio,E 7828cUr The-&arkrnetal,trimethylG(IMT), produceshi-1 damageand diminisheslearningand potentiation (LTP)is an important model for memoryperformance.Sincehippocam@ long-term memoryprocesses,the learningin@rment inducedby TMI couldresultfran the disruption of LTP mechanism.Male Sprague-Cewley rats,weighing270-320g, were dosedvia gavagewith l%fl?. Animals receiveda dose of 7.5-9.0mg/kgTMI (n=9),IO-12ng/kg (High!lMT,n=5),or vehicle(control, n=9). Recordings ware carriedout underurethaneanesthesia(1.3g/kg, i.p.)with a platinumelectrode (50p, o.d.) 1 to 3 weeksafter the treatment. Baselineamplitudes of popllaticn EPSR in the dentategyrusfollowingstimulation of the perforantpath were largerin the controlgroup (4.120.9mV, mean?=) than thosein the TMI (1.4+0.7mV) and High TMl'(1.3+1.0 mV) group. Onset of EPSPswas shorterin the m-treated groups than-inthe controlgroup. tiver, relativeincreases in Epsp amplitude of the TMT group after tetanic stimulation were not different fran that of the control group. The time course of potentiaticn was similar in the 'lW and omtrol groups. These observations suggest that the learning irnpsirnwrtinduced by TMT resulted frana decreaseinnwber of hippaampa lneurans, but not from the disruption of specific synaptic mechanisms underlying LTP withinthe dentategyrus.