Cortical facilitatory action on centralis lateralis thalamic activity during the development of carrageenin-produced inflammation

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 carrgeenin-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 percent; 0.2 ml) into the plantar surface of the right hind paw, and the influence of Lidocaine (2 percent; 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 aftercarrageenin 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 when 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-nociceptives 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 subacute stages. During the CSDs, overall thalamic activity was suppressed in neurones from acute (91 percent) and subacute (87 percent) stages. The blockage was observed when the propagated weve 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 show the tonic facilitatory control of the PCx upon intralaminar thalamic noxious responses, during acute and subsacute stages of carrageenin produced inflammation. In the literature, it has been proposed that the CL thalamic...

El dolor y los mecanismos de analgesia / Pain and analgesic mechanisms

El Sistema Nervioso Central presenta una compleja especialización estructural y funcional. Entre sus propiedades funcionales destacan los sistemas sensoriales, el control motor, la regulación de la vida vegetativa, la emotividad y los procesos cognoscitivos. La integridad de estas funciones permite al organismo interaccionar con su ambiente, así, las funciones sensoriales tienen como finalidad el ponernos en contacto con el medio externo e interno. El dolor como un proceso sensorial, se integra en una serie de señales nerviosas, con importantes correlatos bio-eléctricos y bio-químicos, que nos advierten sobre un eventual o actual daño a los tejidos del cuerpo. Unas se encargan de captar los estímulos nocivos, otras acarrean las señales nerviosas a estructuras específicas, otras integran estas señales y producen una sensación consciente, otras más interconectan las señales nerviosas sensoriales con las estructuras encargadas de las respuestas motoras, y otras llevan a cabo una función reguladora de la sensación dolorosa, incluyendo a la analgesia. En este trabajo se señalan algunos aspectos generales y básicos de la actividad nerviosa y su relación con los procesos sensoriales, particularmente con el dolor. De esta forma pretendemos que el lector tenga una visión del funcionamientio de los sistemas sensoriales. Con este objetivo presentamos algunos resultados experimentales llevados a cabo pro nuestro grupo de investigación. En ellos se describen algunos correlatos electrofisiológicos implicados en la disminución de las respuestas al dolor de las alteraciones en el tamaño de los campos receptivos periféricos por la activación algógena