Different transfer of nociceptive sensitivity from rats with postnatal hippocampal lesions to control rats

Abstract

Hippocampal lesions in newborn rats alter the development of mechanisms involved in the processing of nociception. The hippocampal lesion was induced by the bilateral infusion, into the lateral cerebral ventricles, of 0.25 microL of saline containing either 0.25 micromol quinolinic acid (QUIN) and/or 0.25 micromol N-acetyl-L-aspartyl-L-glutamate (NAAG) on postnatal day 12. The same amount of sterile saline was injected into the sham-operated animals (group SHAM). It was expected that the QUIN- and NAAG-lesioned rats would exhibit some differences in thermal pain perception; however, we wanted to know if the control rats would exhibit, at least in part, similar changes in pain perception as their chemically lesioned siblings with which they were housed. Young adult NAAG-injured rats exhibited increased withdrawal latencies in the tail-flick and plantar tests, whereas young adult QUIN-injured animals exhibited only marginally decreased latencies. Nociceptive responses in the SHAM rats paralleled the littermates that had been neonatally treated with QUIN or NAAG, i.e. the responses in the SHAM(QUIN) group decreased, whereas the responses in the SHAM(NAAG) group increased. No significant changes in nociception were observed in intact animals, regardless of which group they were housed with. Our results show that social factors, which were originally demonstrated only for the pain behavior, may also influence basal nociceptive sensitivity in rats. We concluded that the "sham operation" may have had a long-term, nonspecific impact on nociceptive behavior by inducing behavioral mimicry of other animals.

Roles of the hippocampal formation in pain information processing

“…Consistent with this assertion, another study of neonatal chemical hippocampal lesions reported different transfer of nociceptive sensitivity from rats with postnatal hippocampal lesions to control rats, i.e. their siblings with whom they were housed [36] . [107,108] .…”

“…However, cumulating efforts from many laboratories over the past years have allowed the more clear dissection of the roles of HF in pain processing. Indeed, there have been substantial behavioral, electrophysiological, molecular/biochemical and functional imaging evidence supporting the putative relationship between the HF and affective/motivational component of pain perception [12,[27][28][29][30][31][32][33][34][35][36] .…”

Perinatal effect of methamphetamine on nociception in adult Wistar rats

“…late proestrus and early estrus) also correspond to the lowest anxiety of female rats tested in an elevated plus‐maze (Marcondes et al, 2001). Moreover, we have recently shown that the time spent in the open arms of an elevated plus‐maze was inversely related to the latency of forelimbs in the plantar test (Yamamotová et al, 2007a,b), therefore decreased latencies in our METH and S female rats should also reflect reduced anxiety. Our data are also supported by observation of Pan and Chen (2007), who found in neonatal caffeine‐treated rats hyperalgesia in hot‐plate test and lower anxiety measured by time spent in open arms of elevated plus‐maze.…”

Altered nociception in Alzheimer disease is associated with striatal-enriched protein tyrosine phosphatase signaling

“…23,24 In addition, substantial behavioral and biochemical evidence in animal studies supports a close relationship between the hippocampus and nociception perception. 2,17,28,33,34,47,48,59 It is plausible that a hippocampus lesion would greatly hinder nociceptive processing in AD.…”