The selective 5-HT(1A) receptor agonist repinotan HCl attenuates histopathology and spatial learning deficits following traumatic brain injury in rats

Neuroscience. 2001;106(3):547-55. doi: 10.1016/s0306-4522(01)00300-1.

Abstract

The selective 5-HT(1A) receptor agonist Repinotan HCl (BAY x3702) has been reported to attenuate cortical damage and improve functional performance in experimental models of cerebral ischemia and acute subdural hematoma. Using a clinically relevant contusion model of traumatic brain injury, we tested the hypothesis that a 4-h continuous infusion of Repinotan HCl (10 microg/kg/h i.v.) commencing 5 min post-injury would ameliorate functional outcome and attenuate histopathology. Forty isoflurane-anesthetized male adult rats were randomly assigned to receive either a controlled cortical impact (2.7 mm tissue deformation, 4 m/s) or sham injury (Injury/Vehicle=10, Injury/MK-801=10, Injury/Repinotan HCl=10, Sham/Vehicle=10), then tested for vestibulomotor function on post-operative days 1-5 and for spatial learning on days 14-18. Neither Repinotan HCl nor the non-competitive N-methyl-D-aspartate receptor antagonist MK-801, which served as a positive control, improved vestibulomotor function on beam balance and beam walk tasks relative to the Injury/Vehicle group, but both did significantly attenuate spatial learning and memory deficits on a water maze task. Repinotan HCl also reduced hippocampal CA(1) and CA(3) neuronal loss, as well as cortical tissue damage, compared to the Injury/Vehicle group at 4 weeks post-trauma. No significant difference in histological outcome was revealed between the Repinotan HCl- and MK-801-treated groups.These findings extend the therapeutic efficacy of Repinotan HCl to a contusion model of experimental brain injury and demonstrate for the first time that 5-HT(1A) receptor agonists confer neuroprotection and attenuate spatial learning deficits following controlled cortical impact injury. This treatment strategy may be beneficial in a clinical context where memory impairments are common following human traumatic brain injury.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Benzopyrans / pharmacology*
  • Body Temperature / drug effects
  • Body Temperature / physiology
  • Brain / drug effects
  • Brain / pathology
  • Brain / physiopathology
  • Brain Injuries / drug therapy*
  • Brain Injuries / pathology
  • Brain Injuries / physiopathology
  • Cognition / drug effects
  • Cognition / physiology
  • Cognition Disorders / drug therapy
  • Cognition Disorders / etiology
  • Cognition Disorders / physiopathology
  • Dizocilpine Maleate / pharmacology
  • Drug Administration Schedule
  • Excitatory Amino Acid Antagonists / pharmacology
  • Hippocampus / drug effects
  • Hippocampus / pathology
  • Hippocampus / physiopathology
  • Male
  • Maze Learning / drug effects
  • Maze Learning / physiology
  • Nerve Degeneration / drug therapy*
  • Nerve Degeneration / pathology
  • Nerve Degeneration / physiopathology
  • Neurons / drug effects
  • Neurons / metabolism
  • Neurons / pathology
  • Neuroprotective Agents / pharmacology*
  • Postural Balance / drug effects
  • Postural Balance / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Serotonin / drug effects*
  • Receptors, Serotonin / metabolism
  • Receptors, Serotonin, 5-HT1
  • Serotonin Receptor Agonists / pharmacology*
  • Thiazoles / pharmacology*
  • Vestibular Nuclei / drug effects
  • Vestibular Nuclei / pathology
  • Vestibular Nuclei / physiopathology

Substances

  • Benzopyrans
  • Excitatory Amino Acid Antagonists
  • Neuroprotective Agents
  • Receptors, Serotonin
  • Receptors, Serotonin, 5-HT1
  • Serotonin Receptor Agonists
  • Thiazoles
  • repinotan hydrochloride
  • Dizocilpine Maleate