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

Authors

  • Anna Yamamotová,

    1. Department of Normal, Pathological and Clinical Physiology, Charles University, 3rd Faculty of Medicine, Ke Karlovu 4, 120 00 Prague 2, Czech Republic
    2. Center of Neuropsychiatric Studies,
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  • Miloslav Franĕk,

    1. Department of Normal, Pathological and Clinical Physiology, Charles University, 3rd Faculty of Medicine, Ke Karlovu 4, 120 00 Prague 2, Czech Republic
    2. Center of Neuropsychiatric Studies,
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  • Šimon Vaculín,

    1. Department of Normal, Pathological and Clinical Physiology, Charles University, 3rd Faculty of Medicine, Ke Karlovu 4, 120 00 Prague 2, Czech Republic
    2. Center of Neuropsychiatric Studies,
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  • František Št'astný,

    1. Center of Neuropsychiatric Studies,
    2. Prague Psychiatric Center and
    3. Institute of Physiology, Academy of Sciences, Prague, Czech Republic
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  • Vĕra Bubeníková-Valešová,

    1. Center of Neuropsychiatric Studies,
    2. Prague Psychiatric Center and
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  • Richard Rokyta

    1. Department of Normal, Pathological and Clinical Physiology, Charles University, 3rd Faculty of Medicine, Ke Karlovu 4, 120 00 Prague 2, Czech Republic
    2. Center of Neuropsychiatric Studies,
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Dr Anna Yamamotová, 1Department of Normal, Pathological and Clinical Physiology, as above.
E-mail: yamamoto@lf3.cuni.cz

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 μL of saline containing either 0.25 μmol quinolinic acid (QUIN) and/or 0.25 μmol 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.

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