wound healing model #3

Migraine Animal Models

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Model Introduction

Migraine is a chronic disabling neurological disorder characterized by periodic episodes of moderate-to-severe throbbing headache. Our center provides mature models built on various core hypotheses, covering the entire pathological process from electrophysiological abnormalities to vasomotor dysfunction:

  1. Cortical Spreading Depression (CSD) Model: Simulates the pathogenesis of migraine aura.
  2. Vasogenic Model (Nitroglycerin-induced): Uses NO donors to induce extra- and intracranial vasodilation and nociceptor activation.
  3. Trigeminovascular System Model: Simulates the transmission of pain information via electrical stimulation of the dura mater or trigeminal ganglion.
  4. Genetically Engineered Mouse Models: Targets ion channel gene mutations related to Familial Hemiplegic Migraine (FHM).

Research Applications

  • Pathogenesis Exploration: Studying cortical electrical activity, trigeminal system activation, and neuropeptide release mechanisms.
  • Drug Screening and Evaluation: Assessing the efficacy of analgesics, vasoconstrictors, and CGRP receptor antagonists.
  • Preventive Treatment Research: Targeted at long-term intervention experiments for chronic migraine.

Key Points of Experimental Design

  • Animal Selection: CSD models prefer adult SD rats (>2 months old, weight >300g); Nitroglycerin models can use rats or mice.
  • Modeling Keys:
    • CSD Method: Requires precise stereotaxic localization based on Bregma coordinates; prevent brain tissue damage during drilling; maintain electrical stimulation parameters (e.g., 1mA, 300ms).
    • Nitroglycerin Method: Choose subcutaneous or intraperitoneal injection based on acute/chronic needs; control dosage to maintain symptom stability.
    • Electrical Stimulation: Requires a stereotaxic apparatus and dental cement to fix electrodes; ensure constant stimulation frequency (20Hz) and intensity (2.5-3.5mA).

Key Monitoring Indicators

  • Behavioral Indicators: Frequent head scratching, ear redness, piloerection, increased cage climbing, and decreased periorbital mechanical pain threshold.
  • Electrophysiological Indicators: Cortical steady potential, electrocorticogram (recording CSD duration, amplitude, and frequency).
  • Biochemical Indicators: Determination of CGRP (Calcitonin Gene-Related Peptide) and Substance P levels in plasma.

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