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Article: Alteration in the levels of thyrotropin releasing hormone, substance P and enkephalins in the spinal cord, brainstem, hypothalamus and midbrain of the Wobbler mouse at different stages of the motoneuron disease

TitleAlteration in the levels of thyrotropin releasing hormone, substance P and enkephalins in the spinal cord, brainstem, hypothalamus and midbrain of the Wobbler mouse at different stages of the motoneuron disease
Authors
Issue Date1992
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscience
Citation
Neuroscience, 1992, v. 50 n. 1, p. 209-222 How to Cite?
AbstractThe present study was undertaken to quantify selected neuropeptides (thyrotropin releasing hormone, substance P, methionine and leucine enkephalin) in the cervical spinal cord and other regions of the central nervous system of Wobbler mice by radioimmunoassays during several stages of the motoneuron disease compared with age- and sex-matched normal phenotype littermates. In Wobbler spinal cord, thyrotropin releasing hormone is higher early in the disease, whereas in the brainstem it is higher at a later stage. Substance P in spinal cord is also higher late in the disease. Leucine enkephalin levels are greater at all stages in diseased spinal cord and brainstem, but methionine enkephalin increases only late in the disease. Highly significant increases of the peptides (except thyrotropin releasing hormone) appear in hypothalamus and midbrain only late in the motoneuron disease. Regression analyses show that thyrotropin releasing hormone in spinal cord and brainstem decreases normally with age in the control mice and at a faster rate related to the extent of motor impairment in Wobbler mice. Thyrotropin releasing hormone and methionine enkephalin in the Wobbler brainstem correlate (P < 0.05) with the progress of the motoneuron disease. Methionine enkephalin increases faster in Wobbler brainstem and decreases faster in control spinal cord with age. The increase of leucine enkephalin in the Wobbler spinal cord correlates significantly with age and with the progress of the disease, but leucine enkephalin declines slightly with age in the controls. The changes of substance P in spinal cord and brainstem do not correlate significantly with the progress of the disease. In the hypothalamus, increasing values for substance P in control specimens and enkephalins in Wobbler specimens are significantly correlated with age. However, in the midbrain, higher methionine and leucine enkephalin levels are significantly associated with age only in the control mice. Alterations of neuropeptides in the Wobbler mouse spinal cord and brainstem may result from the degeneration of bulbospinal raphe neurons projecting to the ventral spinal cord, or from primary afferent or interneuronal nerve terminals. The data imply that the neuronal degeneration process in the Wobbler motoneuron disease is not limited to motoneurons. In the spinal cord, the data support our previous hypothesis that neuronal sprouting presynaptic to the motoneurons may account for increased neuropeptide concentrations. Alternatively, synthesis and/or degradation of these peptides may be altered. In addition, it is proposed that enkephalinergic neurons may develop abnormally in Wobbler mice. The early increase of leucine enkephalin in the Wobbler spinal cord possibly indicates its importance in the etiology of the motoneuron disease.
Persistent Identifierhttp://hdl.handle.net/10722/151502
ISSN
2015 Impact Factor: 3.231
2015 SCImago Journal Rankings: 1.768
ISI Accession Number ID
Errata

 

DC FieldValueLanguage
dc.contributor.authorYung, KKLen_HK
dc.contributor.authorTang, Fen_HK
dc.contributor.authorFielding, Ren_HK
dc.contributor.authorDu, YHen_HK
dc.contributor.authorVaccaGalloway, LLen_HK
dc.date.accessioned2012-06-26T06:24:03Z-
dc.date.available2012-06-26T06:24:03Z-
dc.date.issued1992en_HK
dc.identifier.citationNeuroscience, 1992, v. 50 n. 1, p. 209-222en_HK
dc.identifier.issn0306-4522en_HK
dc.identifier.urihttp://hdl.handle.net/10722/151502-
dc.description.abstractThe present study was undertaken to quantify selected neuropeptides (thyrotropin releasing hormone, substance P, methionine and leucine enkephalin) in the cervical spinal cord and other regions of the central nervous system of Wobbler mice by radioimmunoassays during several stages of the motoneuron disease compared with age- and sex-matched normal phenotype littermates. In Wobbler spinal cord, thyrotropin releasing hormone is higher early in the disease, whereas in the brainstem it is higher at a later stage. Substance P in spinal cord is also higher late in the disease. Leucine enkephalin levels are greater at all stages in diseased spinal cord and brainstem, but methionine enkephalin increases only late in the disease. Highly significant increases of the peptides (except thyrotropin releasing hormone) appear in hypothalamus and midbrain only late in the motoneuron disease. Regression analyses show that thyrotropin releasing hormone in spinal cord and brainstem decreases normally with age in the control mice and at a faster rate related to the extent of motor impairment in Wobbler mice. Thyrotropin releasing hormone and methionine enkephalin in the Wobbler brainstem correlate (P < 0.05) with the progress of the motoneuron disease. Methionine enkephalin increases faster in Wobbler brainstem and decreases faster in control spinal cord with age. The increase of leucine enkephalin in the Wobbler spinal cord correlates significantly with age and with the progress of the disease, but leucine enkephalin declines slightly with age in the controls. The changes of substance P in spinal cord and brainstem do not correlate significantly with the progress of the disease. In the hypothalamus, increasing values for substance P in control specimens and enkephalins in Wobbler specimens are significantly correlated with age. However, in the midbrain, higher methionine and leucine enkephalin levels are significantly associated with age only in the control mice. Alterations of neuropeptides in the Wobbler mouse spinal cord and brainstem may result from the degeneration of bulbospinal raphe neurons projecting to the ventral spinal cord, or from primary afferent or interneuronal nerve terminals. The data imply that the neuronal degeneration process in the Wobbler motoneuron disease is not limited to motoneurons. In the spinal cord, the data support our previous hypothesis that neuronal sprouting presynaptic to the motoneurons may account for increased neuropeptide concentrations. Alternatively, synthesis and/or degradation of these peptides may be altered. In addition, it is proposed that enkephalinergic neurons may develop abnormally in Wobbler mice. The early increase of leucine enkephalin in the Wobbler spinal cord possibly indicates its importance in the etiology of the motoneuron disease.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscienceen_HK
dc.relation.ispartofNeuroscienceen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshBrain Stem - Metabolismen_US
dc.subject.meshChromatography, Gelen_US
dc.subject.meshEnkephalin, Leucine - Metabolismen_US
dc.subject.meshEnkephalin, Methionine - Metabolismen_US
dc.subject.meshEnkephalins - Metabolismen_US
dc.subject.meshHypothalamus - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMesencephalon - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Neurologic Mutantsen_US
dc.subject.meshMotor Neuron Disease - Genetics - Metabolism - Physiopathologyen_US
dc.subject.meshOrgan Specificityen_US
dc.subject.meshSpinal Cord - Metabolismen_US
dc.subject.meshSubstance P - Metabolismen_US
dc.subject.meshThyrotropin-Releasing Hormone - Metabolismen_US
dc.titleAlteration in the levels of thyrotropin releasing hormone, substance P and enkephalins in the spinal cord, brainstem, hypothalamus and midbrain of the Wobbler mouse at different stages of the motoneuron diseaseen_HK
dc.typeArticleen_HK
dc.identifier.emailTang, F: ftang@hkucc.hku.hken_HK
dc.identifier.emailFielding, R: fielding@hku.hken_HK
dc.identifier.authorityTang, F=rp00327en_HK
dc.identifier.authorityFielding, R=rp00339en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0306-4522(92)90393-Gen_HK
dc.identifier.pmid1383870-
dc.identifier.scopuseid_2-s2.0-0026744114en_HK
dc.identifier.volume50en_HK
dc.identifier.issue1en_HK
dc.identifier.spage209en_HK
dc.identifier.epage222en_HK
dc.identifier.isiWOS:A1992JM22600018-
dc.publisher.placeNetherlandsen_HK
dc.relation.erratumdoi:10.1016/0306-4522(93)90448-O-
dc.relation.erratumeid:eid_2-s2.0-0027320558-
dc.identifier.scopusauthoridYung, KKL=36840201600en_HK
dc.identifier.scopusauthoridTang, F=7201979770en_HK
dc.identifier.scopusauthoridFielding, R=7102200484en_HK
dc.identifier.scopusauthoridDu, YH=10840454500en_HK
dc.identifier.scopusauthoridVaccaGalloway, LL=6602468305en_HK

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