Abstract
Sensory mismatch between actual motion information and anticipated sensory patterns (internal model) is the etiology of motion sickness (MS). Some evidence supports that hippocampus might involve the neural storage of the “internal model”. This study established an “internal model” acquisition-retention behavioral model using a repeated habituation rotation training protocol. We tried to identify the hippocampal subregion involved in “internal model” retention using chemical lesion methods. Hippocampal kinases (CaMK, CaMKIV, CREB and ERK1/2) phosphorylation in the target subregion was assayed and the effects of kinase inhibitors (KN93 or U0126) on “internal model” retention were investigated. The activities of potential kinases (CaMKII and CREB) were also examined in otoliths deficit het/het mice. In habituated rats, CA1 lesion reproduced MS-related behavioral responses on “internal model” retention day. Habituation training increased CaMKII and CREB activity but had no effect on CaMKIV and ERK1/2 activity in the CA1, while inhibition of CaMKII but not ERK1/2 impaired “internal model” retention. In het/het mice, CaMKII and CREB were not activated in the CA1 on the retention day. These results suggested that CaMKII/CREB pathway might potentially contribute to the storage of the “internal model” in the hippocampal CA1 after motion sickness induced by vestibular stimulation.
Highlights
During forward–backward translocation and passive rotation in rats
The current study confirmed that repeated passive motion stimulation induced a progressive and almost linear decrease in these behavioral responses which gradually reappeared at least 4 days after the habituation training stopped
Data are represented as mean ±SEM. *P < 0.05, **P < 0.01 compared with the corresponding solvent control group. ∆P < 0.05, ∆∆P < 0.01 compared with the corresponding Hab-Sta group. #P < 0.05 compared with the Hab-Rot animals receiving 10 μM KN93 injection
Summary
During forward–backward translocation and passive rotation in rats. Electrical stimulation of these regions at theta rhythm (8 Hz) increased heart rate[10]. In addition to CaMKII, genetic deletion or the inhibition of CaMKIV impaired synaptic plasticity leading to the deficits in fear memory formation and spatial memory retention[21,22]. Both αCaMKII and CaMKIV are responsible for phosphorylation of cAMP-response element-binding protein (CREB) which is a gene transcription factor required for for plasticity-related stimulation of gene transcription[23]. The B6Ei.GL-Nox3het (het/het) mouse strain absent of otoliths was used to investigate the contribution of vestibular afference to the “internal model” retention-related alterations in kinase activity in the hippocampus
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