Behavioural deficits and serotonin depletion in adult rats after transient infant nasal viral infection
| Autor: | J. Maehlen, Marianne Schultzberg, F Fonnum, Krister Kristensson, A.K. Mohammed, E. Norrby, O. Magnusson |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2003 |
| Předmět: |
Serotonin
VSV vesicular stomatitis virus ChAT choline acetyltransferase Dopamine Central nervous system Hippocampus 5-HIAA 5-hydroxyindole acetic acid Biology Motor Activity Serotonergic Article Vesicular stomatitis Indiana virus Choline O-Acetyltransferase Norepinephrine Cognition DOPAC 3 4-dihydroxyphenylacetic acid medicine HVA homovanillic acid Animals p.i. post infection GAD glutamate decarboxylase NA noradrenaline 5-HT 5-hydroxytryptamine Neocortex Glutamate Decarboxylase General Neuroscience Brain Homovanillic Acid Rats Inbred Strains Hydroxyindoleacetic Acid Rats medicine.anatomical_structure nervous system Cerebral cortex Virus Diseases Mutation 3 4-Dihydroxyphenylacetic Acid Female DA dopamine Neuroscience Olfactory epithelium medicine.drug |
| Zdroj: | Neuroscience |
| ISSN: | 1873-7544 0306-4522 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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