TY - JOUR
T1 - Nitric oxide contributes to functional hyperemia in cerebellar cortex
AU - Iadecola, C.
AU - Li, J.
AU - Ebner, Timothy J
AU - Xu, X.
PY - 1995
Y1 - 1995
N2 - We used the parallel fibers (PF) system of the cerebellar cortex as a model to investigate the role of nitric oxide (NO) in the increases in blood flow elicited by neural activation. Rats were anesthetized with halothane and ventilated. The vermis was exposed, and the site was superfused with Ringer (37°C; pH 7.3-7.4). PF were stimulated electrically (100 μA; 30 Hz), and the associated changes in cerebellar cortex blood flow (BF(erb)) were monitored by laser-Doppler flowmetry. The field potentials evoked by PF stimulation were recorded using microelectrodes. During Ringer superfusion (n = 7), PF stimulation increased BF(erb) (+52 ± 4%). Topical application of the NO synthase (NOS) inhibitor N(ω)-nitro-L-arginine (L-NNA; 0.1-1 mM) attenuated the increases in BF(crb) dose dependently and by 50 ± 4% at 1 mM (n = 9; P < 0.001; analysis of variance and Tukey's test). L-NNA (1 mM) inhibited NOS catalytic activity, assessed ex vivo using the citrulline assay, by 95 ± 9% (P < 0.001). L-NNA did not influence the field potentials evoked by PF stimulation. D-NNA (1 mM; n = 6), the inactive stereoisomer of nitroarginine, did not attenuate the BF(crb) response (P > 0.05). Methylene blue (1 mM; n = 7) reduced the response by 41 ± 9% (P < 0.01) without affecting NOS catalytic activity (P < 0.05). The increases in BF(crb) were not affected by lesioning the NOS-containing nerve fibers innervating cerebral vessels, indicating that these nerves are not the source of NO. Thus the increases in BF(crb) elicited by activation of PF are, in part, mediated by NO produced in the molecular layer during neural activity. The results indicated that NO participates in the coupling of function activity to blood flow and support the hypothesis that NO is one of the mediators responsible for functional hyperemia in the central nervous system.
AB - We used the parallel fibers (PF) system of the cerebellar cortex as a model to investigate the role of nitric oxide (NO) in the increases in blood flow elicited by neural activation. Rats were anesthetized with halothane and ventilated. The vermis was exposed, and the site was superfused with Ringer (37°C; pH 7.3-7.4). PF were stimulated electrically (100 μA; 30 Hz), and the associated changes in cerebellar cortex blood flow (BF(erb)) were monitored by laser-Doppler flowmetry. The field potentials evoked by PF stimulation were recorded using microelectrodes. During Ringer superfusion (n = 7), PF stimulation increased BF(erb) (+52 ± 4%). Topical application of the NO synthase (NOS) inhibitor N(ω)-nitro-L-arginine (L-NNA; 0.1-1 mM) attenuated the increases in BF(crb) dose dependently and by 50 ± 4% at 1 mM (n = 9; P < 0.001; analysis of variance and Tukey's test). L-NNA (1 mM) inhibited NOS catalytic activity, assessed ex vivo using the citrulline assay, by 95 ± 9% (P < 0.001). L-NNA did not influence the field potentials evoked by PF stimulation. D-NNA (1 mM; n = 6), the inactive stereoisomer of nitroarginine, did not attenuate the BF(crb) response (P > 0.05). Methylene blue (1 mM; n = 7) reduced the response by 41 ± 9% (P < 0.01) without affecting NOS catalytic activity (P < 0.05). The increases in BF(crb) were not affected by lesioning the NOS-containing nerve fibers innervating cerebral vessels, indicating that these nerves are not the source of NO. Thus the increases in BF(crb) elicited by activation of PF are, in part, mediated by NO produced in the molecular layer during neural activity. The results indicated that NO participates in the coupling of function activity to blood flow and support the hypothesis that NO is one of the mediators responsible for functional hyperemia in the central nervous system.
KW - N(ω)-nitro-L-arginine
KW - cerebral circulation
KW - field potentials
KW - laser Doppler
KW - nitric oxide synthase
KW - parallel fibers
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U2 - 10.1152/ajpregu.1995.268.5.r1153
DO - 10.1152/ajpregu.1995.268.5.r1153
M3 - Article
C2 - 7539595
AN - SCOPUS:0029065907
SN - 0363-6119
VL - 268
SP - R1153-R1162
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 5 37-5
ER -