Modification of activity-dependent increases in cerebellar blood flow by extracellular potassium in anaesthetized rats.
1. The hypothesis that potassium ions mediate activity-dependent increases of cerebral blood flow was examined in rat cerebellar cortex using ion-selective microelectrodes and laser-Doppler flowmetry. Increases of cerebellar blood flow (CeBF) and extracellular potassium concentration ([K+]o) were evoked by stimulation of parallel fibres and climbing fibres, and by microinjection of KCl into the cortex. 2. For parallel fibre stimulation, there was a maximal increase in [K+]o to 6.3 +/- 0.5 mM and in CeBF of 122 +/- 11 %. Climbing fibre stimulation gave a maximal increase in [K+]o to 4.4 +/- 0.2 mM and in CeBF of 157 +/- 20 %. This indicates different maxima for [K+]o and CeBF, dependent on the afferent system activated. 3. [K+]o and CeBF responses evoked by parallel or climbing fibre stimulation increased rapidly at the onset of stimulation, but exhibited different time courses during the remainder of the stimulation period and during return to baseline. 4. Microinjections of KCl into the cortex increased [K+]o to levels comparable to those evoked by parallel fibre stimulation. The corresponding CeBF increases were the same as, or smaller than, for parallel fibre stimulation, and much smaller than for climbing fibre stimulation. This suggests that mediators other than [K+]o are important for activity-dependent cerebral blood flow increases. 5. The present study showed that increased [K+]o is involved in CeBF regulation in the parallel fibre system, but is of limited importance for CeBF regulation in the climbing fibre system. The hypothesis that K+ is a major mediator of activity-dependent blood flow increases is probably not generally applicable to all brain regions and all types of neuronal stimulation.
Caesar
K
K
Department of Medical Physiology, University of Copenhagen, 2200 Copenhagen N, Denmark. kcaesar@mfi.ku.dk
Akgören
N
N
Mathiesen
C
C
Lauritzen
M
M
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000758:Anesthesia; D000818:Animals; D002531:Cerebellum / Q000098:blood supply* / Q000166:cytology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D003712:Dendrites / Q000502:physiology; D004558:Electric Stimulation; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005110:Extracellular Space / Q000502:physiology; D017078:Laser-Doppler Flowmetry; D008839:Microelectrodes; D009847:Olivary Nucleus / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000494:pharmacology*; D011689:Purkinje Cells / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D018091:Receptors, AMPA / Q000037:antagonists & inhibitors; D013569:Synapses / Q000502:physiology
D018691:Excitatory Amino Acid Antagonists; D018091:Receptors, AMPA; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D011188:Potassium