[Abstract Title]. - Society for Neuroscience

connections between early-life stress and visceral hypersensitivity remain unresolved. A growing
body of evidence suggests that an alteration in spinal sensory neurotransmission is critically
involved in visceral pain. In this regard, glial cells, in particular astrocytes, are of particular
interest as they play pivotal functions in glutamate and gamma-amino butyric acid (GABA)
reuptake and are strongly implicated in various chronic pain states. Here, we investigate the
influence of early life stress on astrocytic markers in the rat spinal cord. We study the expression
of GFAP, the astrocytic glutamate transporters EAAT1 and EAAT2 as well as GABA
transporters GAT1 and GAT3. Adult male Sprague-Dawley rats (250-300g) exposed to maternal
separation (MS) between post-natal day 2 and 12 were used for the study. Immunofluorescence
and western-blot were used to evaluate the spinal protein expression. Visceral hypersensitivity
was quantified by counting abdominal contractions during colorectal distension (CRD, 10
minutes, 40 mm/Hg). We show that rats submitted to MS present a visceral hypersensitivity to
colorectal distnsion. Additionally, the basal expression of GFAP, GAT1, GAT3 and EAAT2
appears to be unaltered by MS. However, a significant reduction in the expression of glutamate
transporter EAAT1 is reported in MS rats. The reactivity of EAAT1 expression to a noxious
visceral stimulus was studied following CRD. No change in EAAT1 expression was observed in
non-separated rats; however, a significant increase in EAAT1 immunoreactivity was present in
the spinal cord of MS animals two hours post-CRD. Taken together, our results represent a key
insight into understanding the influence of early-life stress on visceral hypersensitivity.
Moreover, it has direct implications for understanding pain states associated with a variety of
stress-related psychiatric disorders and irritable bowel syndrome (IBS).
This work was funded by Science Foundation Ireland, IDA Ireland and GlaxoSmithKline.
Disclosures: R.D. Gosselin , GlaxoSmithKline, C. Other Research Support (receipt of drugs,
supplies, equipment or other in-kind support); N. Dwyer, None; P. Fitzgerald,
GlaxoSmithKline, C. Other Research Support (receipt of drugs, supplies, equipment or other inkind
support); T.G. Dinan, GlaxoSmithKline, B. Research Grant (principal investigator,
collaborator or consultant and pending grants as well as grants already received); J.F. Cryan,
GlaxoSmithKline, B. Research Grant (principal investigator, collaborator or consultant and
pending grants as well as grants already received).
Poster
269. Pain: Visceral Pain II
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 269.4/GG19
Topic: D.08.n. Visceral pain
Support: BBSRC