Behavioural deficits and serotonin depletion in adult rats after transient infant nasal viral infection
Identifieur interne : 001467 ( Main/Exploration ); précédent : 001466; suivant : 001468Behavioural deficits and serotonin depletion in adult rats after transient infant nasal viral infection
Auteurs : A. K. Mohammed [Suède] ; O. Magnusson [Suède] ; J. Maehlen [Suède] ; F. Fonnum [Norvège] ; E. Norrby [Norvège] ; M. Schultzberg [Suède] ; K. Kristensson [Suède]Source :
- Neuroscience [ 0306-4522 ] ; 1990.
English descriptors
- KwdEn :
- Teeft :
- Activity test, Basal ganglia, Behaviour, Behavioural, Behavioural deficits, Behavioural tests, Body weight, Cerebral cortex, Choline acetyltransferase, Control animals, Cortical function, Diagonal band, Diagonal bands, Encephalitis lethargica, Experimental virus infections, Exploratory behaviour, First time period, Glutamate decarboxylase, Hippocampus, Homovanillic acid, Infection, Interaction effect, Karolinska institute, Last time period, Latency, Lesion, Locomotion, Locomotor, Locomotor activity, Locus coeruleus, Morris water maze task, Motor activity, Neuron, Noradrenergic neurons, Nucleus basalis, Occipital cortex, Olfactory, Olfactory bulbs, Olfactory epithelium, Olfactory system, Open field, Pairwise comparisons, Peripheral locomotion counts, Place navigation, Plenum press, Raphe, Raphe nuclei, Rat, Raven press, Retrograde transport, Selective infections, Serotonin, Serotonin depletion, Serotoninergic, Serotoninergic neurons, Significant group, Spontaneous motor activity, Stomatitis, Substantia nigra, Time interaction, Time interaction effect, Vesicular stomatitis virus, Viral, Viral infection, Virus infection.
Abstract
Abstract: Dysfunction of subcortical serotoninergic neurons has been implicated in some behaviour disturbances. The serotoninergic neurons in the dorsal and median raphe project widely in the brain. They innervate the olfactory bulbs and can be targets for exogenous agents attacking the olfactory epithelium and bulbs. We report here an injury to the serotoninergic neurons after intranasal infection in 12-day-old rats with a temperature-sensitive mutant of vesicular stomatitis virus. The brain infection was focal and transient. Viral antigens could no longer be detected 13–15 days after infection. In spite of this the animals, as adults, had a severe serotonin depletion in the cerebral cortex and hippocampus, and showed abnormal locomotor and explorative behaviour as well as learning deficits. The neocortex was histologically intact and parameters related to other neurotransmitters such as dopamine, noradrenaline, GABA and acetylcholine showed no marked changes.A relatively selective damage to serotoninergic nuclei as a result of virus neuroinvasion through a natural portal of entry, may constitute a new pathogenetic mechanism for cortical dysfunction and behavioural deficits.
Url:
DOI: 10.1016/0306-4522(90)90089-M
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Abstract: Dysfunction of subcortical serotoninergic neurons has been implicated in some behaviour disturbances. The serotoninergic neurons in the dorsal and median raphe project widely in the brain. They innervate the olfactory bulbs and can be targets for exogenous agents attacking the olfactory epithelium and bulbs. We report here an injury to the serotoninergic neurons after intranasal infection in 12-day-old rats with a temperature-sensitive mutant of vesicular stomatitis virus. The brain infection was focal and transient. Viral antigens could no longer be detected 13–15 days after infection. In spite of this the animals, as adults, had a severe serotonin depletion in the cerebral cortex and hippocampus, and showed abnormal locomotor and explorative behaviour as well as learning deficits. The neocortex was histologically intact and parameters related to other neurotransmitters such as dopamine, noradrenaline, GABA and acetylcholine showed no marked changes.A relatively selective damage to serotoninergic nuclei as a result of virus neuroinvasion through a natural portal of entry, may constitute a new pathogenetic mechanism for cortical dysfunction and behavioural deficits.</div>
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