How does cisplatin scramble rat hippocampal memory circuits?
Cisplatin cut survival, impaired recognition memory, and ramped hippocampal inflammation, oxidative stress, and glutamate-receptor mRNA.
Source
Cisplatin induces hippocampal neurotoxicity and cognitive impairment in rats through neuroinflammation, oxidative stress, and overexpression of glutamatergic receptors mRNA
Study at a glance
- Design
- Animal / in-vitro — Male Wistar rats randomized to control vs cisplatin (8 mg/kg i.p. ×3) with survival, YMT/NORT, and hippocampal inflammatory/oxidative/glutamatergic assays
- N
- N=20 · 10 control + 10 cisplatin; some assays report n=6 survivors/completers
- Population
- Eight-week-old male Wistar rats
- Outcome
- Survival, body weight, memory behavior, and hippocampal inflammation/oxidative/glutamatergic markers
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How does cisplatin scramble rat hippocampal memory circuits?
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What experimental groups and sample size were used?
Two groups of eight-week-old rats (n = 10 per group) were used: control and cisplatin-treated
What cisplatin dosing regimen induced toxicity?
Cisplatin (8 mg/kg, i. p.) was administered each 2 days for three cycles
What they did
Twenty rats were split into control vs cisplatin (8 mg/kg i.p. every 2 days ×3). Investigators tracked survival/weight, ran Y-maze and novel-object tests, then assayed hippocampal cytokines, ROS/antioxidant markers, mitochondrial complex I, lipid peroxidation, and AMPAR/NMDAR mRNA.
What they found
Survival fell to 40%, weight dropped, NORT exploration declined, and NF-κB/TNF-α/IL-6 rose with oxidative stress and glutamatergic receptor overexpression—supporting a neuroinflammation–glutamate mechanism for chemo-brain.
The limits
What it doesn't show
Not a human cognitive trial; high experimental dosing and mortality limit direct clinical dose translation.
Key terms
- Chemo-brain
- Chemotherapy-associated cognitive impairment, here modeled after cisplatin.
- Y-maze / NORT
- Behavioral tests of spatial/recognition memory in rodents.
- NF-κB / TNF-α / IL-6
- Pro-inflammatory mediators elevated in cisplatin hippocampi.
- AMPAR / NMDAR
- Ionotropic glutamate receptors whose hippocampal expression was assessed.
- Mitochondrial complex I (MCI)
- Respiratory-chain activity that declined with cisplatin.
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What is the study’s primary design?
Common questions
Was this done in patients?
No—male Wistar rats only.
What dose was used?
8 mg/kg intraperitoneally every 2 days for three cycles.
Did cognition change?
Yes—novel-object exploration fell; Y-maze entries into the novel arm also declined.
Proposed mechanism?
Hippocampal neuroinflammation plus glutamatergic receptor overactivation with oxidative stress.
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