Contribution of Ih to neuronal damage in the hippocampus after traumatic brain injury in rats

Ping Deng, Zao C. Xu

Research output: Contribution to journalArticle

11 Scopus citations


Traumatic brain injury (TBI) causes selective neuronal damage in the hippocampus; however, the underlying mechanisms are still unclear. Post-traumatic alterations of ion channel activity, which actively regulate neuronal excitability and thus impact on excitotoxicity, may be involved in TBI-induced neuronal injury. Here we report that hyperpolarization-activated cation current (Ih) contributes to the distinct vulnerability of hippocampal neurons in TBI. In a rat model of controlled cortical injury, moderate TBI produced neuronal death of both hippocampal CA3 neurons and mossy cells in the hilus, but not CA1 pyramidal cells. Treatment with lamotrigine, which enhances dendritic Ih, ameliorated TBI-induced neuronal damage to CA3 neurons and mossy cells. In contrast, intraventricular administration of Ih channel blocker caused cell death in the CA1 region after TBI. Whole-cell recordings revealed that, differently from CA3 neurons, CA1 pyramidal cells expressed larger Ih and exhibited a post-traumatic increase of Ih amplitude. Moreover, blocking Ih led to an increase of neuronal excitability, with greater effects seen in post-traumatic CA1 pyramidal cells than in CA3 neurons. In addition, the Ih in mossy cells was dramatically inhibited early after TBI. Our findings indicate that differential changes of Ih in hippocampal neurons may be one of the mechanisms of selective cell death, and that an enhancement of functional Ih may protect hippocampal neurons against TBI.

Original languageEnglish (US)
Pages (from-to)1173-1183
Number of pages11
JournalJournal of neurotrauma
Issue number7
StatePublished - Jul 1 2011


  • HCN channel
  • hilar cell
  • neuronal excitability
  • neuroprotection
  • trauma

ASJC Scopus subject areas

  • Clinical Neurology

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