AJP - Regulatory, Integrative and Comparative Physiology, Vol 264, Issue 6 1150-R1156, Copyright © 1993 by American Physiological Society
Noncholinergic, nonadrenergic cortical vasodilatation elicited by thalamic centromedian-parafascicular complex
P. J. Goadsby, J. Seylaz and S. Mraovitch
Laboratoire de Recherche Cerebrovasculaire, Centre National de la Recherche Scientifique Unite Associee, Universite VII, Paris, France.
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.
