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Spatial recognition memory deficits without notable CNS pathology in rats following herpes simplex encephalitis
D R Beers1, J S Henkel, R P Kesner
1Program in Neuroscience, University of Utah, Salt Lake City, USA.
Journal of the Neurological Sciences
|August 1, 1995
Summary
Herpes simplex encephalitis survivors often face memory deficits. This study shows herpes simplex virus type-1 causes memory impairment in rats, even without obvious brain inflammation.
Area of Science:
- Neuroscience
- Virology
- Immunology
Background:
- Survivors of herpes simplex encephalitis (HSE) exhibit cognitive deficits, particularly in memory storage and recall.
- The temporal lobes and limbic system are crucial for memory and are often impacted in HSE.
- Previous research linked herpes simplex virus type-1 (HSV-1) intranasal inoculation in rats to limbic system lesions.
Purpose of the Study:
- To investigate if rats recovered from HSE exhibit memory impairments.
- To determine the relationship between HSV-1 infection, limbic system function, and behavioral deficits.
Main Methods:
- Rats recovered from experimentally induced HSE were assessed using an eight-arm radial maze.
- Behavioral testing included allocentric-spatial location and egocentric-spatial discrimination tasks.
- In situ hybridization was used to detect HSV-1 nucleic acids in neural tissues.
Main Results:
- HSV-1 infected rats performed at chance levels in allocentric-spatial memory tasks, indicating impaired acquisition and retention.
- Infected rats performed similarly to controls in egocentric-spatial discrimination tasks.
- HSV-1 was detected in hippocampal and entorhinal cortex neurons, yet some rats with deficits showed no clear histopathological evidence of infection.
Conclusions:
- HSV-1 infection can lead to significant learning and memory impairments in rats.
- These behavioral deficits can occur without apparent inflammatory injury to the temporal lobe memory system.
- This study provides the first experimental evidence of HSV-1 causing behavioral impairments in the absence of overt CNS inflammation.