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|Title:||Dorsal hippocampus field CA1 pyramidal cell responses to a persistent versus an acute nociceptive stimulus and their septal modulation|
medial septal-vertical limb of diagonal band of Broca
pyramidal cell depression
selective cell excitation
|Source:||Khanna, S. (1997). Dorsal hippocampus field CA1 pyramidal cell responses to a persistent versus an acute nociceptive stimulus and their septal modulation. Neuroscience 77 (3) : 713-721. ScholarBank@NUS Repository. https://doi.org/10.1016/S0306-4522(96)00456-3|
|Abstract:||In urethane anaesthetized rats subcutaneous formalin injection in the right hind paw, a model of persistent pain, produced (i) a prolonged increase in the period of field rhythmic sinusoidal (or theta) activity, (ii) a depression of dorsal hippocampal field CA1 pyramidal cell synaptic excitabilitv (mean peak depression of population spike amplitude being 50 ± 6%) observed to the 60th min post injection, and (iii) a persistent decrease in extracellular activity of the majority of CA1 pyramidal cells (15/20 or 75%) with only a small percentage excited (5/20 or 25%). In contrast an intense noxious heat stimulus applied briefly to the distal end of the tail evoked a short duration increase in period of theta activation and suppression of pyramidal cell responses. With this acute stimulus the proportion of CA1 pyramidal cells excited (8/16) were similar to that suppressed (7/16). Finally, electrolytic lesions centred in the medial septal-vertical limb of diagonal band of Broca (or septal region) prevented a noxious stimulus-induced theta and depression of CA1 pvramidal cell responses. Rather, in such lesioned animals noxious stimulation excited the majority CA1 complex spike cells studied (8/10). The above data are consistent with the notion that septohippocampal inputs are involved in noxious stimulus-induced CA1 pyramidal cell suppression. The formalin injection-induced selective activation of CA1 complex spike cells against a background of widespread pyramidal cell suppression might produce a 'signal to noise' contributory to nociceptive processing in limbic structures. Such a processing might be involved in the affective-motivational component of pain.|
|Appears in Collections:||Staff Publications|
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