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Article: Transneuronal degeneration in the midbrain central gray following chemical lesions in the ventromedial nucleus: A qualitative and quantitative analysis

TitleTransneuronal degeneration in the midbrain central gray following chemical lesions in the ventromedial nucleus: A qualitative and quantitative analysis
Authors
Issue Date1990
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscience
Citation
Neuroscience, 1990, v. 38 n. 2, p. 409-426 How to Cite?
AbstractIn the preceding experiments with electrolytic lesions of the ventromedial nucleus of the hypothalamus, showed pre- and postsynaptic degeneration in the midbrain central gray of the rat. The postsynaptic degeneration seen may indicate a transneuronal effect of the ventromedial nucleus on the midbrain central gray. Electrolytic lesions, however, destroy afferent endings and fibers in passage, so that the postsynaptic degeneration seen in the midbrain central gray may be due to retrograde degeneration of midbrain central gray afferents to the ventromedial nucleus or due to degeneration to fibers in passage. In order to distinguish among these possibilities, chemical, i.e. kainic acid and N-methyl aspartate, lesions were made in the ventromedial nucleus and the ultrastructure of the midbrain central gray and cerebral cortex was examined at various intervals following the lesions. Both of these excitotoxins have been shown to destroy neurons, sparing afferent terminals and fibers in passage. Animals receiving kainic acid lesions in the right ventromedial nucleus were permitted to survive for four, eight, and 20 days. Midbrain central gray tissue of unlesioned animals served as a control for both kainic acid and N-methyl aspartate lesions. In addition, other control animals received injections of the same amount of N-methyl aspartate in the right parietal cortex and were permitted to survive for four and eight days. For each of the above injection and survival conditions, the left cortex and subdivisions of the midbrain central gray were removed at processed for electron microscopy. Animals receiving ventromedial hypothalamic lesions with both kainic acid and N-methyl aspartate showed signs of pre- and postsynaptic degeneration. A quantitative analysis (General Linear Model Procedure) of degeneration was performed on the cortex and midbrain central gray of animals receiving N-methyl aspartate lesions in the ventromedial nucleus and cortex, and several parameters were measured. Animals receiving ventromedial hypothalamic lesions and surviving for eight and 20 days show significantly higher ratios of degenerating presynaptic elements to total presynaptic elements, degenerating postsynaptic elements to total postsynaptic elements, and degenerating total elements to total elements, in the midbrain central gray than in the cortex. Furthermore, the ratio of degenerating postsynaptic elements to total postsynaptic elements is larger than the other ratios. The effect of the selective destruction of ventromedial nucleus neurons, therefore, resulted in specific degeneration in the midbrain central gray but not in the cortex after eight and 20 days. The postsynaptic degeneration seen in the midbrain central gray after ventromedial hypothalamic lesions is due, therefore, to transneuronal degeneration, rather than retrograde degeneration of midbrain central gray afferents. These results suggest that ventromedial nucleus neurons which project to the midbrain central gray may be important in maintaining the integrity of some neurons in that region.
Persistent Identifierhttp://hdl.handle.net/10722/146615
ISSN
2015 Impact Factor: 3.231
2015 SCImago Journal Rankings: 1.768
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChung, SKen_HK
dc.contributor.authorCohen, RSen_HK
dc.contributor.authorPfaff, DWen_HK
dc.date.accessioned2012-05-08T03:21:17Z-
dc.date.available2012-05-08T03:21:17Z-
dc.date.issued1990en_HK
dc.identifier.citationNeuroscience, 1990, v. 38 n. 2, p. 409-426en_HK
dc.identifier.issn0306-4522en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146615-
dc.description.abstractIn the preceding experiments with electrolytic lesions of the ventromedial nucleus of the hypothalamus, showed pre- and postsynaptic degeneration in the midbrain central gray of the rat. The postsynaptic degeneration seen may indicate a transneuronal effect of the ventromedial nucleus on the midbrain central gray. Electrolytic lesions, however, destroy afferent endings and fibers in passage, so that the postsynaptic degeneration seen in the midbrain central gray may be due to retrograde degeneration of midbrain central gray afferents to the ventromedial nucleus or due to degeneration to fibers in passage. In order to distinguish among these possibilities, chemical, i.e. kainic acid and N-methyl aspartate, lesions were made in the ventromedial nucleus and the ultrastructure of the midbrain central gray and cerebral cortex was examined at various intervals following the lesions. Both of these excitotoxins have been shown to destroy neurons, sparing afferent terminals and fibers in passage. Animals receiving kainic acid lesions in the right ventromedial nucleus were permitted to survive for four, eight, and 20 days. Midbrain central gray tissue of unlesioned animals served as a control for both kainic acid and N-methyl aspartate lesions. In addition, other control animals received injections of the same amount of N-methyl aspartate in the right parietal cortex and were permitted to survive for four and eight days. For each of the above injection and survival conditions, the left cortex and subdivisions of the midbrain central gray were removed at processed for electron microscopy. Animals receiving ventromedial hypothalamic lesions with both kainic acid and N-methyl aspartate showed signs of pre- and postsynaptic degeneration. A quantitative analysis (General Linear Model Procedure) of degeneration was performed on the cortex and midbrain central gray of animals receiving N-methyl aspartate lesions in the ventromedial nucleus and cortex, and several parameters were measured. Animals receiving ventromedial hypothalamic lesions and surviving for eight and 20 days show significantly higher ratios of degenerating presynaptic elements to total presynaptic elements, degenerating postsynaptic elements to total postsynaptic elements, and degenerating total elements to total elements, in the midbrain central gray than in the cortex. Furthermore, the ratio of degenerating postsynaptic elements to total postsynaptic elements is larger than the other ratios. The effect of the selective destruction of ventromedial nucleus neurons, therefore, resulted in specific degeneration in the midbrain central gray but not in the cortex after eight and 20 days. The postsynaptic degeneration seen in the midbrain central gray after ventromedial hypothalamic lesions is due, therefore, to transneuronal degeneration, rather than retrograde degeneration of midbrain central gray afferents. These results suggest that ventromedial nucleus neurons which project to the midbrain central gray may be important in maintaining the integrity of some neurons in that region.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.meshCerebral Cortex - Ultrastructureen_US
dc.subject.meshFemaleen_US
dc.subject.meshKainic Acid - Pharmacologyen_US
dc.subject.meshMesencephalon - Physiology - Ultrastructureen_US
dc.subject.meshN-Methylaspartate - Pharmacologyen_US
dc.subject.meshNerve Degenerationen_US
dc.subject.meshNeurons - Physiologyen_US
dc.subject.meshParietal Lobe - Drug Effects - Physiologyen_US
dc.subject.meshPeriaqueductal Gray - Physiology - Ultrastructureen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Strainsen_US
dc.subject.meshSynapses - Ultrastructureen_US
dc.subject.meshVentromedial Hypothalamic Nucleus - Drug Effects - Physiology - Ultrastructureen_US
dc.titleTransneuronal degeneration in the midbrain central gray following chemical lesions in the ventromedial nucleus: A qualitative and quantitative analysisen_HK
dc.typeArticleen_HK
dc.identifier.emailChung, SK:skchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0306-4522(90)90038-6en_HK
dc.identifier.pmid2263321-
dc.identifier.scopuseid_2-s2.0-0025169570en_HK
dc.identifier.volume38en_HK
dc.identifier.issue2en_HK
dc.identifier.spage409en_HK
dc.identifier.epage426en_HK
dc.identifier.isiWOS:A1990EE09100011-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridCohen, RS=35560739900en_HK
dc.identifier.scopusauthoridPfaff, DW=36046651600en_HK

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