Noncholinergic, nonadrenergic cortical vasodilatation elicited by thalamic centromedian-parafascicular complex.

The centromedian-parafascicular complex (CMPf) of the intralaminar thalamus was stimulated in anesthetized, ventilated rats, and cerebral cortical perfusion was continuously measured using laser Doppler flowmetry. Stimulation led to a frequency- and intensity-dependent increase in cortical perfusion (vasodilatation). The maximum response was seen at a rate of 200/s, and studied at 150 microA, was a 120 +/- 27% (n = 6) increase in flow. The mean time from the initiation of stimulation to a change in the cerebral blood flow measured by laser Doppler flowmeter signal was 800 +/- 100 ms (n = 13). The response to electrical stimulation was not blocked after high spinal cord section. Chemical stimulation of the CMPf neurons by microinjection of carbachol led to a 98 +/- 15% (n = 4) increase in flow. The response to electrical stimulation was not blocked by the muscarinic antagonist scopolamine (1 mg/kg) or by the nicotinic antagonist mecamylamine (4 mg/kg). It was also unaffected by the beta-adrenoceptor antagonist propranolol (1.5 mg/kg). These data add to understanding of the CMPf cerebral vasodilator response by demonstrating a robust stimulus-locked change in cortical perfusion that does not involve a cholinergic or adrenergic mechanism. It is also shown to be frequency and intensity dependent, consistent with a functioning physiological system, and has a rapid onset consistent with a primarily neurally mediated phenomenon. Furthermore, it is elicited by pathways that may possibly be entirely within the central nervous system and is due to activation of cell bodies within the region.