Abstract
To evaluate the contribution of extracellular H+ activity toward depression of brain electrical activity during anoxia, extracellular pH (pH(e)) and field potentials were measured in turtle and rat olfactory bulbs with ion-selective microelectodes. This study tests the hypothesis that unique regulation of pH(e) contributes to the remarkable tolerance of turtle brain to prolonged anoxia. Hypercapnea (20% CO2 ventilation) depressed olfactory bulb evoked potentials 25-30% in both rat and turtle. During anoxia, evoked potentials were completely abolished within 1 min in rat olfactory bulb but decreased to only 40% of control after 4 h in the turtle despite similar changes in brain pH(e). Anoxia-induced acidification of turtle brain was exacerbated by hypercapnea and was attenuated by hypocapnea or by hypocapnea plus intravenous infusion of sodium bicarbonate. However, these manipulations of pH(e) during anoxia in turtle brain had little effect on depression of evoked potentials. We conclude that energy failure, rather than extracellular acidification, is the major contributor toward suppression of electrical activity in mammalian brain and that preservation of energy balance, rather than unique pH regulation, is responsible for protection of turtle brain during anoxia.
| Original language | English |
|---|---|
| Journal | American Journal of Physiology - Regulatory Integrative and Comparative Physiology |
| Volume | 258 |
| Issue number | 1 27-1 |
| State | Published - Jan 1 1990 |
Fingerprint
Keywords
- Carbon dioxide
- Evoked potentials
- Hydrogen ion
- Olfactory bulb
ASJC Scopus subject areas
- Physiology
Cite this
Extracellular pH and suppression of electrical activity during anoxia in turtle and rat brain. / Feng, Z. C.; Sick, Thomas; Rosenthal, M.
In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 258, No. 1 27-1, 01.01.1990.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Extracellular pH and suppression of electrical activity during anoxia in turtle and rat brain
AU - Feng, Z. C.
AU - Sick, Thomas
AU - Rosenthal, M.
PY - 1990/1/1
Y1 - 1990/1/1
N2 - To evaluate the contribution of extracellular H+ activity toward depression of brain electrical activity during anoxia, extracellular pH (pH(e)) and field potentials were measured in turtle and rat olfactory bulbs with ion-selective microelectodes. This study tests the hypothesis that unique regulation of pH(e) contributes to the remarkable tolerance of turtle brain to prolonged anoxia. Hypercapnea (20% CO2 ventilation) depressed olfactory bulb evoked potentials 25-30% in both rat and turtle. During anoxia, evoked potentials were completely abolished within 1 min in rat olfactory bulb but decreased to only 40% of control after 4 h in the turtle despite similar changes in brain pH(e). Anoxia-induced acidification of turtle brain was exacerbated by hypercapnea and was attenuated by hypocapnea or by hypocapnea plus intravenous infusion of sodium bicarbonate. However, these manipulations of pH(e) during anoxia in turtle brain had little effect on depression of evoked potentials. We conclude that energy failure, rather than extracellular acidification, is the major contributor toward suppression of electrical activity in mammalian brain and that preservation of energy balance, rather than unique pH regulation, is responsible for protection of turtle brain during anoxia.
AB - To evaluate the contribution of extracellular H+ activity toward depression of brain electrical activity during anoxia, extracellular pH (pH(e)) and field potentials were measured in turtle and rat olfactory bulbs with ion-selective microelectodes. This study tests the hypothesis that unique regulation of pH(e) contributes to the remarkable tolerance of turtle brain to prolonged anoxia. Hypercapnea (20% CO2 ventilation) depressed olfactory bulb evoked potentials 25-30% in both rat and turtle. During anoxia, evoked potentials were completely abolished within 1 min in rat olfactory bulb but decreased to only 40% of control after 4 h in the turtle despite similar changes in brain pH(e). Anoxia-induced acidification of turtle brain was exacerbated by hypercapnea and was attenuated by hypocapnea or by hypocapnea plus intravenous infusion of sodium bicarbonate. However, these manipulations of pH(e) during anoxia in turtle brain had little effect on depression of evoked potentials. We conclude that energy failure, rather than extracellular acidification, is the major contributor toward suppression of electrical activity in mammalian brain and that preservation of energy balance, rather than unique pH regulation, is responsible for protection of turtle brain during anoxia.
KW - Carbon dioxide
KW - Evoked potentials
KW - Hydrogen ion
KW - Olfactory bulb
UR - http://www.scopus.com/inward/record.url?scp=0025099752&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025099752&partnerID=8YFLogxK
M3 - Article
C2 - 2301633
AN - SCOPUS:0025099752
VL - 258
JO - American Journal of Physiology - Cell Physiology
JF - American Journal of Physiology - Cell Physiology
SN - 0363-6143
IS - 1 27-1
ER -