title: Global reduction in cerebral blood flow and metabolism elicited from intrinsic neurons of fastigial nucleus.
abstract: We sought to determine whether the global increase in regional cerebral blood flow (rCBF) produced by electrical stimulation of the rostral cerebellar fastigial nucleus (FN) is a consequence of excitation of intrinsic neurons of the FN or of axons of fibers passing through or projecting into it. Studies were conducted in rats anesthetized with chloralose, paralyzed and ventilated. rCBF was measured with [14C]iodoantipyrine as tracer and regional cerebral glucose utilization (rCGU) by [14C]2-deoxyglucose in homogenates of 11 brain regions. Neuronal perikarya in FN were excited chemically by local microinjection of the glutamate analogue kainic acid (KA) (5 nmol in 100 nl). KA elicited a transient and significant fall of arterial pressure and heart rate, the fastigial depressor response (FDR). Associated was a significant and symmetrical reduction in rCBF, to 44% of control in all regions except medulla. The response was site- and agent-specific and unrelated to the hypotension. KA also significantly and proportionally reduced, to 52% of control, rCGU in the same 10 areas of brain. In all regions the magnitudes of the reductions in rCBF and rCGU elicited by KA were linearly related. Intrinsic neurons of FN were chronically destroyed by local microinjection of the excitotoxin ibotenic acid (IBO) (10 micrograms/microliters in 0.4 microliter). Destruction of intrinsic FN neurons had no effect on resting rCBF nor on the global cerebrovascular vasodilation elicited by electrical stimulation of the FN. We conclude that: (a) excitation of intrinsic neurons of FN elicits a widespread reduction of cerebral metabolism and, secondarily, blood flow; (b) FN neurons do not exert a long-term tonic influence on brain blood flow nor metabolism; (c) the global increase in rCBF elicited by electrical stimulation of the FN is a consequence of excitation of axons projecting into or through the nucleus.
authors.affiliation: Division of Neurobiology, Cornell University Medical College, New York, NY 10021.
authors.forename: K
authors.initials: K
authors.lastname: Chida
authors.forename: C
authors.initials: C
authors.lastname: Iadecola
authors.forename: D J
authors.initials: DJ
authors.lastname: Reis
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001921:Brain / Q000378:metabolism*; D002529:Cerebellar Nuclei / Q000187:drug effects / Q000502:physiology*; D002560:Cerebrovascular Circulation; D003837:Deoxy Sugars / Q000378:metabolism*; D003847:Deoxyglucose / Q000378:metabolism*; D004558:Electric Stimulation; D004734:Energy Metabolism; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D003837:Deoxy Sugars; D003847:Deoxyglucose; D007608:Kainic Acid