In order to understand the neuronal mechanisms involved in acute and chronic pain, we studied the thalamic and cortical control action, which allows the suppression of the neuronal responses to noxious stimulation. As an experimental pain model we used carrageenin injected in the paw of male Wistar rats. The tonic facilitatory cortical control on centralis lateralis thalamic nuclei (CL) activity is described at different times after carrageenin-produced inflammation. Simultaneous extracellular unit recordings were carried out at CL and medial prefrontal cortex (PCx) cells in anesthetized male Wistar rats. The PCx control was 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 unit activity in PCx and CL cells. Thalamic cells recorded in acute and subacute stages (24-72 h after carrageenin administration) were activated 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 progressive and significant increase (p < 0.001, ANOVA test) of their spontaneous firing rate when compared with control cell activity. Lidocaine reduced the enhanced activity induced by carrageenin in thalamic neurones (p < 0.001, Student t test). In PCx neurones were also recorded in acute and subacute stages. Cortical cells from acute and subacute group were activated by nociceptive and non-nociceptive stimulation. In acute stage, cortical cells increased their firing rate after carrageenin and we could not observe modifications upon their firing rate due to Lidocaine. The CSD blocked all cortical activity in acute and subacute stages. During the CSDs, overall thalamic activity was suppressed in neurones from acute (91%) and subacute (87%) stages. The blockage was observed when the propagated wave produced by CSD arrived into the medial prefrontal cortex. The CSD also suppressed the PCx and the CL noxious responses evoked by pressure in the receptive field. This study shows the tonic facilitatory control of the PCx upon intralaminar thalamic noxious responses, during acute and subacute stages of carrageenin produced-inflammation. In the literature, it has been proposed that the CL thalamic nuclei and the prefrontal cortex are involved in processing the affective component of pain. It may be possible to suppress the thalamic activity during chronic pain, using the transient and reversible blockage of CSD, giving rise to a reduction in the affective reactions to pain. This could also be a therapeutic alternative in chronic pain treatment.