BASAL FOREBRAIN AND CEREBRAL CORTICAL MUSCARINIC RECEPTORS MEDIATE INCREASE IN CORTICAL BLOOD-FLOW PROVOKED BY PERIAQUEDUCTAL GRAY-MATTER
Citation
M. Nakai et al., BASAL FOREBRAIN AND CEREBRAL CORTICAL MUSCARINIC RECEPTORS MEDIATE INCREASE IN CORTICAL BLOOD-FLOW PROVOKED BY PERIAQUEDUCTAL GRAY-MATTER, Neuroscience, 79(2), 1997, pp. 571-579
Categorie Soggetti
Neurosciences
SICI code
0306-4522(1997)79:2<571:BFACCM>2.0.ZU;2-C
Abstract
The midbrain periaqueductal gray matter has been identified as a refle
x centre located uppermost in the central organization of diverse defe
nsive reactions. We recently found that when activated, the caudal thi
rd of the lateral periaqueductal gray was also capable of provoking a
marked increase in cortical blood flow. The response may be the combin
ed outcome of a flow increase of nitrergic origin and that coupled to
a possible concomitant cortical activation. In the present study, we a
ttempted to clarify the neural substrates for mediation of the increas
e in flow (observed by laser-Doppler flowmetry), in 49 anaesthetized,
artificially ventilated, and cervically cordotomized rats. The flow in
crease provoked by stimulation of the particular subdivision of the pe
riaqueductal gray with N-methyl-D-aspartate (1 mM, 100 nl) was unaffec
ted by i.v. pentolinium tartrate (10 mg/kg), suggesting little contrib
ution by the cerebrovasodilator parasympathetic nervous system to the
response. The response was abolished by i.v. or topical cortical admin
istration of scopolamine hydrobromide (3.16 mg/kg or 1.0 mM, respectiv
ely). Placement of bilateral lesions in the basal forebrain with alpha
-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (15 mM) impaired
the cortical choline acetyltransferase activity and attenuated the flo
w response. Overall, we suggest that the cholinergic corticopetal neur
ons of the nucleus basalis of Meynert and cortical muscarinic receptor
s may form a principal efferent arm of a central circuitry emanating f
rom the subdivision of the periaqueductal gray, in the mediation of th
e increase in cortical blood flow and possible cortical activation. (C
) 1997 IBRO.