CORTICAL FACILITATORY ACTION ON CENTRALIS LATERALIS THALAMIC ACTIVITYDURING THE DEVELOPMENT OF CARRAGEENAN-PRODUCED INFLAMMATION

In order to understand the neuronal mechanisms involved in acute and c hronic pain, we studied the thalamic and cortical control action, whic h allows the suppression of the neuronal responses to noxious stimulat ion. As an experimental pain model we used carrageenin injected in the paw of male Wistar rats. The tonic facilitatory cortical control on c entralis lateralis thalamic nuclei (CL) activity is described at diffe rent times after carrageenin-produced inflammation. Simultaneous extra cellular unit recordings were carried out at CL and medial prefrontal cortex (PCx) cells in anesthetized male Wistar rats, The PCx control w as tested by blocking in a transient and reversible manner, using the cortical spreading depression (CSD). Carrageenin injection (1%; 0.2 ml ) into the plantar surface of the right hind paw, and the influence of Lidocaine (2%; 0.2 ml) applied in the inflamed paw, was tested on uni t activity in PCx and CL cells. Thalamic cells recorded in acute and s ubacute stages (24 - 72 h after carrageenin administration) were activ ated by tactile, light pressure and joint movement stimulation yielded before the injection. After carrageenin, the thalamic cells displayed spontaneous high frequency burst discharges, also presenting a progre ssive acid significant increase (p < 0.001, ANOVA test) of their spont aneous firing rate when compared with control cell activity. Lidocaine reduced the enhanced activity induced by carrageenin in thalamic neur ones (p < 0.001, Student t test). In PCx neurones were also recorded i n acute and subacute stages. Cortical cells from acute and subacute gr oup were activated by nociceptive and non-nociceptive stimulation. In acute stage, cortical cells increased their firing rate after carragee nin and we could not observe modifications upon their firing rate due to Lidocaine. The CSD blocked all cortical activity in acute and subac ute stages. During the CSDs, overall thalamic activity was suppressed in neurones from acute (91%) and subacute (87%) stages. The blockage w as observed when the propagated wave produced by CSD arrived into the medial prefrontal cortex. The CSD also suppressed the PCx and the CL n oxious responses evoked by pressure in the receptive field. This study shows the tonic facilitatory control of the PCx upon intralaminar tha lamic noxious responses, during acute and subacute stages of carrageen in produced-inflammation. In the literature, it has been proposed that the CL thalamic nuclei and the prefrontal cortex are involved in proc essing the affective component of pain. It may be possible to suppress the thalamic activity during chronic pain, using the transient acid r eversible blockage of CSD, giving rise to a reduction in the affective reactions to pain. This could also be a therapeutic alternative in ch ronic pain treatment.