Abstract
Changes in glutamatergic system by neonatal brain infusion of quinolinic acid (QUIN) and/or N-acetyl-L-aspartyl-L-glutamate (NAAG) are supposed to be important in animal models of schizophrenia. As schizophrenic patients exhibited decreased pain sensitivity, we have hypothesized that the neonatal brain injury induced by bilateral infusion of 0,25 umol QUIN or NAAG (0,25 uL phosphate-buffered saline/ventricle) on PND 12 might modify the nociceptive transmission.
NAAG-injured rats exhibited increased withdrawal latencies of the tail flick and plantar test whereas QUIN-injured animals decreased their latencies only marginally. Nociceptive responses of the sham-operated rats paralleled their littermates neonatally treated with QUIN and/or NAAG.
The responses were decreased and/or increased, respectively. No significant changes in nociception were observed in intact animals, irrespective of their housing.
From our results it can be concluded that nociceptive sensitivity may be influenced by social factors. Sham-operated rats exhibit similar nociceptive sensitivity as their cagamates with the neonatally iduced dysfunction of the brain glutamatergic system.
The sham operation may have a long-term nonspecific impact on nociceptive behavior, which is able to mimic the behavior of other animals