Altered local cerebral glucose utilization induced by electrical stimulations of the thalamic sensory and parafascicular nuclei in rats.

Alterations in local cerebral glucose utilization (LCGU) induced by electrical stimulation of the sensory relay nucleus (VPL) or parafascicular nucleus (Pf) of the thalamus in conscious rats were measured by the [14C]2-deoxyglucose method, the objective being to assess the mechanism of analgesia induced by electrical stimulations of these structures. Stimulation of the VPL induced an ipsilateral increase in LCGU in the sensory thalamic nucleus itself, the sensory cortex and substantia nigra. Stimulation of the Pf induced bilateral increases in LCGU in the Pf and central medial nucleus of the thalamus, sensory cortex, ventral areas of the striatum and substantia nigra, and ipsilateral increase in LCGU in the periaqueductal gray, parabrachial pontine nucleus and deep layers of the superior colliculus. No significant change in LCGU was detected in the raphe dorsalis, raphe magnus and spinal dorsal horn, in both groups. Our observations coincide with clinical findings that unilateral electrical stimulation of the Pf leads to amelioration of intractable pain bilaterally, while that of the VPL induces an analgesia restricted to the contralateral side.