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Nitric oxide and adenosine mediate vasodilation during functional activation in cerebellar cortex
1Department of Neurology, University of Minnesota Medical School, Minneapolis 55455.
Neuropharmacology
|November 1, 1994
Summary
Cerebellar parallel fiber stimulation increases blood flow via glutamate and adenosine pathways. Blocking glutamate receptors stops this increase, while blocking adenosine receptors partially reduces it, indicating their roles in regulating cerebellar blood flow.
Area of Science:
- Neuroscience
- Cerebrovascular Physiology
Background:
- Cerebellar parallel fiber (PF) activation triggers glutamate release, depolarizing Purkinje cells and interneurons, which then release GABA.
- The interplay of neurotransmitters and neuromodulators in regulating cerebellar cortex blood flow (BFcrb) following PF stimulation is not fully understood.
Purpose of the Study:
- To investigate the roles of glutamate, GABA, nitric oxide (NO), and adenosine in mediating the increase in cerebellar cortex blood flow (BFcrb) induced by PF stimulation.
Main Methods:
- Electrically stimulated cerebellar parallel fibers in anesthetized rats.
- Recorded BFcrb using laser-Doppler flowmetry and field potentials with glass microelectrodes.
- Superfused the cerebellum with various agents: glutamate receptor antagonist (kynurenic acid), adenosine receptor antagonist (8-SPT), and NO synthase inhibitor (L-NA).
Main Results:
- PF stimulation increased BFcrb by 58%.
- Kynurenic acid blocked the BFcrb increase, indicating glutamate's essential role.
- 8-SPT reduced the BFcrb elevation by 45%, and combined with L-NA, attenuated it by 82%, highlighting adenosine's contribution and interaction with NO pathways.
Conclusions:
- Glutamate is critical for the BFcrb increase evoked by PF stimulation.
- Adenosine significantly contributes to this vasodilation, acting possibly in concert with nitric oxide pathways.