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Enhancement of intrinsic neuronal excitability‐mediated by a reduction in hyperpolarization‐activated cation current (I h ) in hippocampal CA1 neurons in a rat model of traumatic brain injury
Author(s) -
Karimi Seyed Asaad,
Hosseinmardi Narges,
Sayyah Mohammad,
Hajisoltani Razieh,
Janahmadi Mahyar
Publication year - 2021
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.23270
Subject(s) - neuroscience , traumatic brain injury , hippocampal formation , hyperpolarization (physics) , chemistry , rheobase , electrophysiology , current clamp , ionotropic effect , patch clamp , hippocampus , psychology , nmda receptor , receptor , biochemistry , organic chemistry , psychiatry , nuclear magnetic resonance spectroscopy
Traumatic brain injury (TBI) is associated with epileptiform activity in the hippocampus; however, the underlying mechanisms have not been fully determined. The goal was to understand what changes take place in intrinsic neuronal physiology in the hippocampus after blunt force trauma to the cortex. In this context, hyperpolarization‐activated cation current (I h ) currents may have a critical role in modulating the neuronal intrinsic membrane excitability; therefore, its contribution to the TBI‐induced hyperexcitability was assessed. In a model of TBI caused by controlled cortical impact (CCI), the intrinsic electrophysiological properties of pyramidal neurons were examined 1 week after TBI induction in rats. Whole‐cell patch‐clamp recordings were performed under current‐ and voltage‐clamp conditions following ionotropic receptors blockade. Induction of TBI caused changes in the intrinsic excitability of pyramidal neurons, as shown by a significant increase and decrease in firing frequency and in the rheobase current, respectively ( p < .05). The evoked firing rate and the action potential time to peak were also significantly increased and decreased, respectively ( p < .05). In the TBI group, the amplitude of instantaneous and steady‐state I h currents was both significantly smaller than those in the control group ( p < .05). The I h current density was also significantly decreased ( p < .001). Findings indicated that TBI led to an increase in the intrinsic excitability in CA1 pyramidal neurons and changes in I h current could be, in part, one of the underlying mechanisms involved in this hyperexcitability.