Format

Send to

Choose Destination
Pain. 1993 Apr;53(1):81-8.

Streptozocin-induced diabetic rats: behavioural evidence for a model of chronic pain.

Author information

1
Laboratoire de Pharmacologie Médicale, INSERM (U195), Faculté de Médecine, Clermont-Ferrand, France.

Abstract

Painful diabetic neuropathy is one of the most common complications of insulin-dependent diabetes in man. Conflicting results have been obtained in experimentally diabetic animals subjected to pain stimuli. This work aimed to systematically study the response of rats made diabetic (hyperglycemia > or = 14 mM) by injection of streptozocin (STZ) (75 mg/kg, i.p.), to various pain stimuli: mechanical, thermal (warm and cold) and chemical. The time course of the scores was followed for 4 weeks simultaneously with the clinical symptoms (weight, body and skin temperature, motility) and hyperglycemia. A decrease in reaction thresholds to noxious heat stimuli (44 degrees C and 46 degrees C) and to non-painful thermal (cold: 10 degrees C, and warm: 38-42 degrees C) and mechanical stimulation (paw pressure) was observed. This can be considered as evidence for hyperalgesia and allodynia, respectively. These troubles appeared gradually and required at least 2 weeks of diabetes to reach statistical significance. Four weeks after the induction of diabetes, the scores obtained in diabetic rats injected with formalin were greater than those in normal rats, indicating hyperalgesia. Variation in sensitivity to pain occurred at the same time as arrested weight increase, fall in skin temperature, some amyotrophy measured in terms of hind-paw volume, and the usual polyuria-polydipsia syndrome. Spontaneous motor activity of the rats was lowered. This model is thus of interest as the observed reactions to noxious and non-noxious stimuli correspond to hyperalgesia and allodynia, symptoms encountered in painful diabetic neuropathy in man. Operating conditions for this model are discussed.

PMID:
8316394
DOI:
10.1016/0304-3959(93)90059-x
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center