Electrical stimulation of the dorsal periaqueductal gray decreases volume of the brain infarction independently of accompanying hypertension and cerebrovasodilation.
We investigated whether selective stimulation of neurons of the sympathoinhibitory ventral periaqueductal gray (VPAG), or sympathoexcitatory dorsal periaqueductal gray (DPAG), differentially modulates CBF and EEG and exerts neuroprotection. Electrical stimulation of either regions of PAG comparably elevated AP and CBF, whereas chemical stimulation with the D,L-homocysteine produced either sympathoinhibition accompanied by decrease in CBF from ventral region or sympathoexcitation accompanied by increase in CBF from dorsal region in nonspinalized rats. The CBF effects evoked from DPAG and VPAG by chemical stimulation were preserved in spinalized rats supporting that the evoked CBF responses result directly from stimulation and are not secondary to AP changes. Stimulation of either region, whether chemical or electrical, synchronized the EEG. To explore whether PAG stimulation might protect the brain against ischemic injury, in other rats the VPAG or DPAG were stimulated for 1 h (50 Hz, 1 s on/1 s off, 75-100 microA) and the middle cerebral artery occluded 72 h later. Stimulation of the DPAG, but not VPAG, significantly reduced infarction volumes relative to sham-stimulated controls as determined 24 h after occlusion. Elevations of AP and CBF did not differ between groups. We conclude: (a). intrinsic neurons of D- and VPAG differentially regulate CBF; (b). neurons of DPAG are neuroprotective independently of changes in CBF and/or AP. The DPAG effect on infarct volume may be related to the central neuroprotective pathway evoked by stimulation of the cerebellar FN.
Glickstein
Sara B
SB
Departments of Psychiatry and Neuroscience, Columbia University and New York State Psychiatric Institute, 1051 Riverside Dr, Box #42, New York, NY 10032, USA.
Ilch
Christopher P
CP
Golanov
Eugene V
EV
D000704:Analysis of Variance; D000818:Animals; D001784:Blood Gas Analysis / Q000379:methods; D001786:Blood Glucose; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D020520:Brain Infarction / Q000503:physiopathology / Q000628:therapy*; D002245:Carbon Dioxide / Q000097:blood; D002560:Cerebrovascular Circulation / Q000528:radiation effects*; D004558:Electric Stimulation / Q000379:methods; D004569:Electroencephalography / Q000379:methods; D006400:Hematocrit / Q000379:methods; D006710:Homocysteine / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D006973:Hypertension / Q000503:physiopathology*; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000503:physiopathology; D017078:Laser-Doppler Flowmetry / Q000379:methods; D008297:Male; D008845:Microinjections; D010100:Oxygen / Q000097:blood; D010487:Periaqueductal Gray / Q000503:physiopathology / Q000528:radiation effects*; D051381:Rats; D011916:Rats, Inbred F344; D011918:Rats, Inbred SHR; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000502:physiology; D013119:Spinal Cord Injuries / Q000503:physiopathology; D013268:Stimulation, Chemical; D013997:Time Factors; D014664:Vasodilation / Q000502:physiology*
D001786:Blood Glucose; D006710:Homocysteine; D002245:Carbon Dioxide; D010100:Oxygen