Premium
Effect of Dopamine‐3 receptor Knockout and Iron Deficiency on Pain Threshold Using a Mouse Model
Author(s) -
Weissmiller Sandra J,
Hue Gillian,
Rye David
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a777
Subject(s) - restless legs syndrome , dopamine , hyperalgesia , medicine , endocrinology , spinal cord , inhibitory postsynaptic potential , neuropathic pain , receptor , psychology , neuroscience , nociception , anesthesia , neurology
Restless Legs Syndrome (RLS) is a sensorimotor disorder characterized by unusual sensations in the legs that peak at night. RLS patients exhibit hyperalgesia and RLS symptoms are relieved by dopamine (DA) agonists and worsened with iron deficiency. Our goal was to measure pain at the spinal cord level to examine the roles of the DA D3 receptor and iron deficiency. Pain was measured using a tail flick latency apparatus in male and female mice of 3 groups: wild‐type (WT), D3 knock out (D3KO), and iron deficient (ID). WT female mice had a lower latency than D3KO female mice, while D3KO males had a lower latency than female D3KOs in the afternoon. WT & ID mice did not show significant differences in pain threshold at 28 days. We suspect that the degree of ID in the mice at 28 days might not be great enough to distinguish between control mice. We will therefore re‐test the ID & control mice at 12 weeks. Our D3KO mice did not support the believed notion that the D3 receptor has an inhibitory effect upon spinal sensorimotor circuits. We conclude that using a tail as proxy to lower limbs might be insufficient, other pain mediating systems may be involved, and measuring pain alone may not be enough to clarify the role of the D3 in symptoms of RLS.