Effects of temperature and acid-base state on hippocampal population spikes in hamsters

1990 ◽  
Vol 258 (5) ◽  
pp. R1140-R1146 ◽  
Author(s):  
P. Eckerman ◽  
K. Scharruhn ◽  
J. M. Horowitz
Keyword(s):  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Effect Of Temperature ◽  
Acid Base ◽  
Bathing Medium ◽  
Maximal Stimulation ◽  
Synchronous Firing ◽  
Acid Base Status ◽  
Effects Of Temperature ◽  
Induced Changes

Previous studies have shown that changes in temperature, within the range encountered by hamsters entering hibernation, alter the evoked response of hippocampal pyramidal cells to stimulation of an afferent pathway. The present study was designed to determine whether these alterations are due to changes in the acid-base status of the neural tissue brought about by changes in temperature. Extracellular-evoked responses were recorded from hamster hippocampal slices after Schaffer collateral stimulation. The pH was changed by varying the concentration of CO2 aerating the bathing medium. Buffers contained either 26 or 40 mM bicarbonate ion. The width of the population spike (the synchronous firing of pyramidal cells) was measured as pH was varied between 7.5 and 7.1, with slice temperature set at either 25 or 20 degrees C. There was a significant increase in spike width as temperature was lowered to 20 degrees C, but no significant change in spike width or amplitude as pH or bicarbonate was varied. The effect of temperature (20 degrees C for half-maximal stimulation, and from 20 to 25 degrees C for just maximal stimulation) on spike width and amplitude thus does not appear to be due to pH- or bicarbonate-induced changes.

Effect of temperature on intracellular pH in crayfish neurons and muscle fibers

1984 ◽  
Vol 246 (1) ◽  
pp. C45-C49 ◽  
Author(s):  
J. L. Rodeau
Keyword(s):  
Intracellular Ph ◽  
Muscle Fibers ◽  
Effect Of Temperature ◽  
Cellular Regulation ◽  
Acid Base ◽  
Astacus Leptodactylus ◽  
Acid Base Status ◽  
Effects Of Temperature ◽  
Ph Microelectrodes

Intracellular pH microelectrodes were used to determine the effects of temperature (13-26 degrees C) on the in vitro regulation of intracellular acid-base status of neurons and muscle fibers of the crayfish Astacus leptodactylus. The values of the temperature coefficients delta pH/delta T (pH unit/degrees C) were -0.019 and -0.026 for muscles and neurons, respectively, values which are close to the temperature coefficient (-0.019) of the pK' of protein imidazole buffer groups. When temperature varies, the dissociation ratio of imidazole groups is thus maintained by the cellular regulation of cytoplasmic pH. According to the alphastat regulation hypothesis, this constancy would minimize the temperature effects on enzymic systems.

Group I mGluRs Increase Excitability of Hippocampal CA1 Pyramidal Neurons by a PLC-Independent Mechanism

2002 ◽  
Vol 88 (1) ◽  
pp. 107-116 ◽  
Author(s):  
David R. Ireland ◽  
Wickliffe C. Abraham
Keyword(s):  
Metabotropic Glutamate Receptors ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Receptor Subtypes ◽  
Ca1 Pyramidal Neurons ◽  
Group I ◽  
Hippocampal Ca1 ◽  
Group I Mglurs ◽  
Induced Changes

Previous studies have implicated phospholipase C (PLC)-linked Group I metabotropic glutamate receptors (mGluRs) in regulating the excitability of hippocampal CA1 pyramidal neurons. We used intracellular recordings from rat hippocampal slices and specific antagonists to examine in more detail the mGluR receptor subtypes and signal transduction mechanisms underlying this effect. Application of the Group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) suppressed slow- and medium-duration afterhyperpolarizations (s- and mAHP) and caused a consequent increase in cell excitability as well as a depolarization of the membrane and an increase in input resistance. Interestingly, with the exception of the suppression of the mAHP, these effects were persistent, and in the case of the sAHP lasting for more than 1 h of drug washout. Preincubation with the specific mGluR5 antagonist, 2-methyl-6-(phenylethynyl)-pyridine (MPEP), reduced but did not completely prevent the effects of DHPG. However, preincubation with both MPEP and the mGluR1 antagonist LY367385 completely prevented the DHPG-induced changes. These results demonstrate that the DHPG-induced changes are mediated partly by mGluR5 and partly by mGluR1. Because Group I mGluRs are linked to PLC via G-protein activation, we also investigated pathways downstream of PLC activation, using chelerythrine and cyclopiazonic acid to block protein kinase C (PKC) and inositol 1,4,5-trisphosphate-(IP3)-activated Ca2+ stores, respectively. Neither inhibitor affected the DHPG-induced suppression of the sAHP or the increase in excitability nor did an inhibitor of PLC itself, U-73122. Taken together, these results argue that in CA1 pyramidal cells in the adult rat, DHPG activates mGluRs of both the mGluR5 and mGluR1 subtypes, causing a long-lasting suppression of the sAHP and a consequent persistent increase in excitability via a PLC-, PKC-, and IP3-independent transduction pathway.

Effects of temperature on muscle pHi and phosphate metabolites in newts and lungless salamanders

1993 ◽  
Vol 265 (5) ◽  
pp. R1162-R1167 ◽  
Author(s):  
D. C. Johnson ◽  
C. T. Burt ◽  
W. C. Perng ◽  
B. M. Hitzig
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscle Cell ◽  
Resonance Spectroscopy ◽  
Behavioral Regulation ◽  
Acid Base ◽  
Acid Base Status ◽  
Cell Cytosol ◽  
Effects Of Temperature ◽  
Increasing Temperature ◽  
Tail Muscle

The effect of acute alterations in body temperature (BT) on intracellular pH (pHi) and phosphate metabolites was assessed in white skeletal muscle of intact newts and lungless red-backed salamanders using 31P-nuclear magnetic resonance spectroscopy. pHi decreased with increasing BT in the tail muscle of both newts and lungless red-backed salamanders. The change in pH with change in temperature from 10 to 30 degrees C was -0.018 U/degrees C in newts and -0.041 U/degrees C in red backs. The calculated alpha-imidazole for skeletal muscle cytosol did not change (0.56) in newts from 10 to 30 degrees C but fell from 0.69 to 0.43 in red-backed salamanders. Phosphocreatine (PCr)/Pi fell and Pi/beta-ATP rose with increasing temperature in both newts and red backs; however, the change was much greater in red backs. Providing the red backs with O2 at 30 degrees C led to higher pH and alpha-imidazole, comparable to that of newts, along with increased PCr/Pi and lower Pi/beta-ATP. Thus newts maintain white skeletal muscle cell cytosol alpha-imidazole constant with changes in BT, whereas red backs apparently do not. However, at the BT of preference, red backs and newts maintain similar muscle pHi and alpha-imidazole. The method of gas exchange appears to strongly influence the ability of an animal to maintain its acid-base status over a range of temperatures, and our results suggest that behavioral regulation of BT may involve alpha-imidazole regulation as well.

scholarly journals Temperature Effects on Haemolymph Acid-Base Status In Vivo and In Vitro in the Two-Striped Grasshopper Melanoplus Bivittatus

1988 ◽  
Vol 140 (1) ◽  
pp. 421-435 ◽  
Author(s):  
JON M. HARRISON
Keyword(s):  
Body Temperature ◽  
Carbonic Acid ◽  
Temperature Shift ◽  
Effect Of Temperature ◽  
Locomotory Activity ◽  
Acid Base ◽  
Protein Dissociation ◽  
Acid Base Status

In this study, I examine the effect of temperature on haemolymph acid-base status in vivo and in vitro in the two-striped grasshopper Melanoplus bivittatus. Melanoplus bivittatus experience wide (up to 40 °C) diurnal body temperature fluctuations in the field, but maintain body temperature relatively constant during sunny days by behavioural thermoregulation. Haemolymph pH was statistically constant (7.12) between 10 and 25°C, but decreased by −0.017 units °C− from 25 to 40°C. Relative alkalinity and fractional protein dissociation were conserved only at body temperatures at which feeding and locomotory activity occur, above 20°C. Haemolymph total CO2 (Ctot) increased from 10 to 20°C and decreased from 20 to 40°C. Haemolymph Pco2 increased from 10 to 20°C and was statistically constant between 20 and 40°C. Carbonic acid pKapp in haemolymph was 6.122 at 35°C, and decreased with temperature by −0.0081 units°C−1. Haemolymph buffer value averaged −35mequivl−1pHunit−1. Haemolymph pH changes with temperature were small (less than −0.004 units°C−1) in vitro at constant Pco2. Therefore, passive physicochemical effects cannot account for the pattern of acid-base regulation in vivo. The temperature shift from 10 to 20°C was accompanied by a net addition of 4.2-6.2 mmoll−1 of bicarbonate equivalents to the haemolymph. The temperature shift from 20 to 40°C was accompanied by a net removal of 10–14 mmoll−1 of bicarbonate equivalents from the haemolymph. Haemolymph acid-base regulation in vivo during temperature changes is dominated by active variation of bicarbonate equivalents rather than by changes in Pco2 as observed for most other air-breathers.

The effects of hypercapnia on intracellular and extracellular acid-base status in the toad Bufo marinus

1982 ◽  
Vol 97 (1) ◽  
pp. 79-86
Author(s):  
D. P. Toews ◽  
N. Heisler
Keyword(s):  
Extracellular Space ◽  
Environmental Water ◽  
Bufo Marinus ◽  
Acid Base ◽  
Relative Preference ◽  
Base Parameters ◽  
Initial Drop ◽  
Acid Base Status ◽  
Body Compartments ◽  
Induced Changes

Toads (Bufo marinus) were exposed to environmental hypercapnia of 5% CO2 in air, and extracellular and intracellular acid-base parameters were determined 1 and 24 h after the onset of hypercapnia. The initial drop in pH was compensated by the elevation of extracellular and intracellular bicarbonate. Relating the pH compensation to the pH drop that is expected to occur by increased PCO2 at constant bicarbonate concentration, the pH compensation in the extracellular space was 30% and reached the following values for intracellular body compartments: 65% in skeletal muscle, 77% in heart muscle and 44% in skin. The additional bicarbonate was partly produced by blood and intracellular non-bicarbonate buffers; the major portion of the remainder was related to the excretion of ammonia into the environmental water. The hypercapnia-induced changes of pH were considerably smaller in all tissue cells than in the extracellular space. Thus Bufo marinus exhibits the relative preference of intracellular over extracellular acid-base regulation that has been observed in other vertebrates.

scholarly journals Interaction between temperature and hypoxia in the alligator

1993 ◽  
Vol 265 (6) ◽  
pp. R1339-R1343 ◽  
Author(s):  
L. G. Branco ◽  
H. O. Portner ◽  
S. C. Wood
Keyword(s):  
Body Temperature ◽  
Blood Gases ◽  
The Body ◽  
Plasma Lactate ◽  
Acid Base ◽  
Terrestrial Vertebrates ◽  
Beneficial Response ◽  
Acid Base Status ◽  
Induced Changes ◽  
Selected Body Temperature

Hypoxia elicits behavioral hypothermia in alligators. Under normoxic conditions, the selected body temperature is 27.8 +/- 1.2 degrees C. However, when inspired O2 is lowered to 4%, selected body temperature decreases to 15.4 +/- 1.0 degrees C. The threshold for the behavioral hypothermia is between 4 and 5% inspired O2, the lowest threshold measured so far in terrestrial vertebrates. This study assessed the physiological significance of the behavioral hypothermia. The body temperature was clamped at 15, 25, and 35 degrees C for measurements of ventilation, blood gases, metabolic rate, plasma lactate, and acid-base status. Hypoxia-induced changes in ventilation, acid-base status, oxygen consumption, and lactate were proportional to body temperature, being pronounced at 35 degrees C, less at 25 degrees C, and absent at 15 degrees C. The correlation between selected body temperature under severe hypoxia and the measured parameters show that behavioral hypothermia is a beneficial response to hypoxia in alligators.

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