The Upregulation of L1CAM by SVHRSP Mitigates Neuron Damage, Spontaneous Seizures, and Cognitive Dysfunction in a Kainic Acid-Induced Rat Model of Epilepsy

Biomolecules. 2025 Jul 17;15(7):1032. doi: 10.3390/biom15071032.

Abstract

Temporal lobe epilepsy (TLE) is a common drug-resistant form of epilepsy, often accompanied by cognitive and emotional disturbances, highlighting the urgent need for novel therapies. Scorpion Venom Heat-Resistant Synthetic Peptide (SVHRSP), isolated and synthetically derived from scorpion venom, has shown anti-epileptic and neuroprotective potential. This study evaluated the anti-epileptic effects of SVHRSP in a kainic acid (KA)-induced TLE rat model. Our results demonstrated that SVHRSP (0.81 mg/kg/day) reduced the frequency and severity of spontaneous seizures. Behavioral tests showed improved cognitive performance in the novel object recognition, object location, and T-maze tasks, as well as reduced anxiety-like behavior in the open-field test. Moreover, SVHRSP mitigated hippocampal neuronal loss and glial activation. Transcriptomic analysis indicated that SVHRSP upregulates genes involved in adhesion molecule-triggered and axon guidance pathways. Western blotting and immunofluorescence further confirmed that SVHRSP restored dendritic (MAP2), axonal (NFL), and synaptic (PSD95) marker expression, elevated the functionally important L1CAM fragment (L1-70), and increased myelin basic protein-induced serine protease activity responsible for L1-70 generation. Blockade of L1CAM expression diminished the neuroprotective effects of SVHRSP, suggesting a critical role for L1CAM-mediated synapse functions. This study is the first to reveal the therapeutic potential of SVHRSP in TLE via L1CAM-associated mechanisms.

Keywords: L1CAM; SVHRSP; TLE; cell adhesion molecule; neuroprotection; peptide; scorpion venom.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cognitive Dysfunction* / drug therapy
  • Cognitive Dysfunction* / metabolism
  • Disease Models, Animal
  • Epilepsy* / chemically induced
  • Epilepsy* / drug therapy
  • Epilepsy* / metabolism
  • Epilepsy, Temporal Lobe* / chemically induced
  • Epilepsy, Temporal Lobe* / drug therapy
  • Epilepsy, Temporal Lobe* / metabolism
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Hippocampus / pathology
  • Kainic Acid / toxicity
  • Male
  • Neural Cell Adhesion Molecule L1* / genetics
  • Neural Cell Adhesion Molecule L1* / metabolism
  • Neurons* / drug effects
  • Neurons* / metabolism
  • Neurons* / pathology
  • Neuroprotective Agents / pharmacology
  • Peptides* / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Scorpion Venoms* / chemistry
  • Scorpion Venoms* / pharmacology
  • Seizures* / chemically induced
  • Seizures* / drug therapy
  • Seizures* / metabolism
  • Up-Regulation / drug effects

Substances

  • Kainic Acid
  • Neural Cell Adhesion Molecule L1
  • Scorpion Venoms
  • Peptides
  • Neuroprotective Agents