Carbon dioxide and pH effects on temperature-sensitive and -insensitive hypothalamic neurons

2007 ◽  
Vol 102 (4) ◽  
pp. 1357-1366 ◽  
Author(s):  
Chadwick L. Wright ◽  
Jack A. Boulant
Keyword(s):  
Heat Stroke ◽  
Ph Effects ◽  
Temperature Sensitive ◽  
Sprague Dawley ◽  
Tissue Slices ◽  
Hypothalamic Neurons ◽  
Electrophysiological Recordings ◽  
Sprague Dawley Rats ◽  
Hypothalamic Tissue ◽  
Solution Bathing

The preoptic-anterior hypothalamus (POAH) controls body temperature, and thermoregulatory responses are impaired during hypercapnia. If increased CO2 or its accompanying acidosis inhibits warm-sensitive POAH neurons, this could provide an explanation for thermoregulatory impairment during hypercapnia. To test this possibility, extracellular electrophysiological recordings determined the effects of CO2 and pH on the firing rates of both temperature-sensitive and -insensitive neurons in hypothalamic tissue slices from 89 male Sprague-Dawley rats. Firing rate activity was recorded in 121 hypothalamic neurons before, during, and after changing the CO2 concentration aerating the tissue slice chamber or changing the pH of the solution bathing the tissue slices. Increasing the aeration CO2 concentration from 5% (control) to 10% (hypercapnic) had no effect on most (i.e., 69%) POAH temperature-insensitive neurons; however, this hypercapnia inhibited the majority (i.e., 59%) of warm-sensitive neurons. CO2 affected similar proportions of (non-POAH) neurons in other hypothalamic regions. These CO2 effects appear to be due to changes in pH since the CO2-affected neurons responded similarly to isocapnic acidosis (i.e., normal CO2 and decreased pH) but were not responsive to isohydric hypercapnia (i.e., increased CO2 and normal pH). These findings may offer a neural explanation for some heat-related illnesses (e.g., exertional heat stroke) where impaired heat loss is associated with acidosis.

Temperature-sensitive properties of rat suprachiasmatic nucleus neurons

2001 ◽  
Vol 281 (3) ◽  
pp. R706-R715 ◽  
Author(s):  
Penny W. Burgoon ◽  
Jack A. Boulant
Keyword(s):  
Membrane Potential ◽  
Firing Rate ◽  
Suprachiasmatic Nucleus ◽  
Interspike Interval ◽  
Slow Component ◽  
Resting Membrane Potential ◽  
Temperature Sensitive ◽  
Tissue Slices ◽  
Hypothalamic Tissue ◽  
Potential Threshold

The hypothalamic suprachiasmatic nucleus (SCN) contains a heterogeneous population of neurons, some of which are temperature sensitive in their firing rate activity. Neuronal thermosensitivity may provide cues that synchronize the circadian clock. In addition, through synaptic inhibition on nearby cells, thermosensitive neurons may provide temperature compensation to other SCN neurons, enabling postsynaptic neurons to maintain a constant firing rate despite changes in temperature. To identify mechanisms of neuronal thermosensitivity, whole cell patch recordings monitored resting and transient potentials of SCN neurons in rat hypothalamic tissue slices during changes in temperature. Firing rate temperature sensitivity is not due to thermally dependent changes in the resting membrane potential, action potential threshold, or amplitude of the fast afterhyperpolarizing potential (AHP). The primary mechanism of neuronal thermosensitivity resides in the depolarizing prepotential, which is the slow depolarization that occurs prior to the membrane potential reaching threshold. In thermosensitive neurons, warming increases the prepotential's rate of depolarization, such that threshold is reached sooner. This shortens the interspike interval and increases the firing rate. In some SCN neurons, the slow component of the AHP provides an additional mechanism for thermosensitivity. In these neurons, warming causes the slow AHP to begin at a more depolarized level, and this, in turn, shortens the interspike interval to increase firing rate.

scholarly journals Posttraumatic therapeutic hypothermia alters microglial and macrophage polarization toward a beneficial phenotype

2016 ◽  
Vol 37 (8) ◽  
pp. 2952-2962 ◽  
Author(s):  
Jessie S Truettner ◽  
Helen M Bramlett ◽  
W Dalton Dietrich
Keyword(s):  
Brain Injury ◽  
Therapeutic Hypothermia ◽  
Macrophage Polarization ◽  
Temperature Sensitive ◽  
Sprague Dawley ◽  
Rt Pcr ◽  
M2 Microglia ◽  
Sprague Dawley Rats ◽  
Inflammatory Processes ◽  
Clinical Models

Posttraumatic inflammatory processes contribute to pathological and reparative processes observed after traumatic brain injury (TBI). Recent findings have emphasized that these divergent effects result from subsets of proinflammatory (M1) or anti-inflammatory (M2) microglia and macrophages. Therapeutic hypothermia has been tested in preclinical and clinical models of TBI to limit secondary injury mechanisms including proinflammatory processes. This study evaluated the effects of posttraumatic hypothermia (PTH) on phenotype patterns of microglia/macrophages. Sprague-Dawley rats underwent moderate fluid percussion brain injury with normothermia (37℃) or hypothermia (33℃). Cortical and hippocampal regions were analyzed using flow cytometry and reverse transcription-polymerase chain reaction (RT-PCR) at several periods after injury. Compared to normothermia, PTH attenuated infiltrating cortical macrophages positive for CD11b+ and CD45high. At 24 h, the ratio of iNOS+ (M1) to arginase+ (M2) cells after hypothermia showed a decrease compared to normothermia. RT-PCR of M1-associated genes including iNOS and IL-1β was significantly reduced with hypothermia while M2-associated genes including arginase and CD163 were significantly increased compared to normothermic conditions. The injury-induced increased expression of the chemokine Ccl2 was also reduced with PTH. These studies provide a link between temperature-sensitive alterations in macrophage/microglia activation and polarization toward a M2 phenotype that could be permissive for cell survival and repair.

Halothane Modulates Thermosensitive Hypothalamic Neurons in Rat Brain Slices

1995 ◽  
Vol 83 (6) ◽  
pp. 1241-1253 ◽  
Author(s):  
Neil E. Farber ◽  
Jeffrey E. Schmidt ◽  
John P. Kampine ◽  
William T. Schmeling
Keyword(s):  
Rat Brain ◽  
Brain Slices ◽  
Anterior Hypothalamus ◽  
Spontaneous Firing ◽  
Preoptic Region ◽  
Tissue Slices ◽  
Hypothalamic Neurons ◽  
Hypothalamic Tissue

Abstract Background In vivo, halothane alters spontaneous firing in and thermosensitivity of neurons in the preoptic region of the anterior hypothalamus. To better understand the mechanisms by which halothane specifically disrupts normal thermoregulation, this investigation examined the effects of halothane on thermosensitive preoptic region neurons in isolated hypothalamic tissue slices.

Cyclic GMP alters the firing rate and thermosensitivity of hypothalamic neurons

2008 ◽  
Vol 294 (5) ◽  
pp. R1704-R1715 ◽  
Author(s):  
Chadwick L. Wright ◽  
Penny W. Burgoon ◽  
Georgia A. Bishop ◽  
Jack A. Boulant
Keyword(s):  
Firing Rate ◽  
Cyclic Nucleotide ◽  
Temperature Sensitive ◽  
Tissue Slices ◽  
Hypothalamic Neurons ◽  
Ambient Temperatures ◽  
Thermoregulatory Responses ◽  
Gated Channel ◽  
Cgmp Analog ◽  
Rostral Hypothalamus

The rostral hypothalamus, especially the preoptic-anterior hypothalamus (POAH), contains temperature-sensitive and -insensitive neurons that form synaptic networks to control thermoregulatory responses. Previous studies suggest that the cyclic nucleotide cGMP is an important mediator in this neuronal network, since hypothalamic microinjections of cGMP analogs produce hypothermia in several species. In the present study, immunohistochemisty showed that rostral hypothalamic neurons contain cGMP, guanylate cyclase (necessary for cGMP synthesis), and CNG A2 (an important cyclic nucleotide-gated channel). Extracellular electrophysiological activity was recorded from different types of neurons in rat hypothalamic tissue slices. Each recorded neuron was classified according to its thermosensitivity as well as its firing rate response to 2–100 μM 8-bromo-cGMP (a membrane-permeable cGMP analog). cGMP has specific effects on different neurons in the rostral hypothalamus. In the POAH, the cGMP analog decreased the spontaneous firing rate in 45% of temperature-sensitive and -insensitive neurons, an effect that is likely due to cGMP-enhanced hyperpolarizing K+ currents. This decreased POAH activity could attenuate thermoregulatory responses and produce hypothermia during exposures to cool or neutral ambient temperatures. Although 8-bromo-cGMP did not affect the thermosensitivity of most POAH neurons, it did increase the warm sensitivity of neurons in other hypothalamic regions located dorsal, lateral, and posterior to the POAH. This increased thermosensitivity may be due to pacemaker currents that are facilitated by cyclic nucleotides. If some of these non-POAH thermosensitive neurons promote heat loss or inhibit heat production, then their increased thermosensitivity could contribute to cGMP-induced decreases in body temperature.

scholarly journals Spontaneous BOLD waves – A novel hemodynamic activity in Sprague-Dawley rat brain detected by functional magnetic resonance imaging

2018 ◽  
Vol 39 (10) ◽  
pp. 1949-1960 ◽  
Author(s):  
Artem Shatillo ◽  
Arto Lipponen ◽  
Raimo A Salo ◽  
Heikki Tanila ◽  
Alexei Verkhratsky ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Vascular Reactivity ◽  
Brain Activity ◽  
Lung Ventilation ◽  
Sprague Dawley ◽  
Electrophysiological Recordings ◽  
Sprague Dawley Rats ◽  
Mechanical Lung Ventilation ◽  
Adrenoceptor Blocker ◽  
Potent Agonist

We report spontaneous hemodynamic activity termed “Spontaneous BOLD Waves” (SBWs) detected by BOLD fMRI in Sprague-Dawley rats under medetomidine anesthesia. These SBWs, which lasted several minutes, were observed in cortex, thalamus and hippocampus. The SBWs’ correlates were undetectable in electrophysiological recordings, suggesting an exclusive gliovascular phenomenon dissociated from neuronal activity. SBWs were insensitive to the NMDA receptors antagonist MK-801 but were inhibited by the α1-adrenoceptor blocker prazosin. Since medetomidine is a potent agonist of α2 adrenoceptors, we suggested that imbalance in α1/α2 receptor-mediated signalling pathways alter the vascular reactivity leading to SBWs. The frequency of SBWs increased with intensity of mechanical lung ventilation despite the stable pH levels. In summary, we present a novel type of propagating vascular brain activity without easily detectable underlying neuronal activity, which can be utilized to study the mechanisms of vascular reactivity in functional and pharmacological MRI and has practical implications for designing fMRI experiments in anesthetized animals.

Effects of estrogen on thermoregulatory evaporation in rats exposed to heat

1994 ◽  
Vol 267 (3) ◽  
pp. R673-R677 ◽  
Author(s):  
M. A. Baker ◽  
D. D. Dawson ◽  
C. E. Peters ◽  
A. M. Walker
Keyword(s):  
Heat Exposure ◽  
Plasma Osmolality ◽  
Ovariectomized Rats ◽  
Body Core Temperature ◽  
Temperature Sensitive ◽  
Sprague Dawley ◽  
Evaporative Water ◽  
Sprague Dawley Rats ◽  
Body Core ◽  
Opposite Order

The purpose of this study was to determine the effects of estrogen (E2) replacement on thermoregulation in ovariectomized rats exposed to heat. Female Sprague-Dawley rats were ovariectomized and splenectomized and implanted with a temperature-sensitive transmitter. Each rat was studied when E2 treated (after an E2 pellet implant) and untreated. Animals were divided into two groups with opposite order of treatment and were studied over a 9-wk period. Measurements of body core temperature (Tc) and evaporative water loss (EWL) were made on unrestrained animals resting at 38 degrees C air temperature. E2-treated animals increased EWL at all levels of Tc, reduced the threshold Tc for onset of saliva spreading, and regulated Tc at a lower level during heat exposure. E2 treatment elevated plasma E2 and reduced hematocrit but did not affect plasma osmolality. These effects of E2 on evaporative cooling and Tc in heat-stressed rats are similar to those that have been reported in human females. The mechanisms of the thermoregulatory effects of E2 remain to be studied.

Hypoxic Augmentation of Fast-Inactivating and Persistent Sodium Currents in Rat Caudal Hypothalamic Neurons

2000 ◽  
Vol 84 (5) ◽  
pp. 2572-2581 ◽  
Author(s):  
Eric M. Horn ◽  
Tony G. Waldrop
Keyword(s):  
Sodium Current ◽  
Oxygen Electrode ◽  
Firing Frequency ◽  
Current Response ◽  
Sodium Currents ◽  
Sprague Dawley ◽  
Hypothalamic Neurons ◽  
Inward Current ◽  
Sprague Dawley Rats ◽  
Voltage Ramp

Previous work from this laboratory has indicated that TTX-sensitive sodium channels are involved in the hypoxia-induced inward current response of caudal hypothalamic neurons. Since this inward current underlies the depolarization and increased firing frequency observed in these cells during hypoxia, the present study utilized more detailed biophysical methods to specifically determine which sodium currents are responsible for this hypoxic activation. Caudal hypothalamic neurons from ∼3-wk-old Sprague-Dawley rats were acutely dissociated and patch-clamped in the voltage-clamp mode to obtain recordings from fast-inactivating and persistent (noninactivating) whole cell sodium currents. Using computer-generated activation and inactivation voltage protocols, rapidly inactivating sodium currents were analyzed during normal conditions and during a brief (3–6 min) period of severe hypoxia. In addition, voltage-ramp and extended-voltage-activation protocols were used to analyze persistent sodium currents during normal conditions and during hypoxia. A polarographic oxygen electrode determined that the level of oxygen in this preparation quickly dropped to 10 Torr within 2 min of initiation of hypoxia and stabilized at <0.5 Torr within 4 min. During hypoxia, the peak fast-inactivating sodium current was significantly increased throughout the entire activation range, and both the activation and inactivation values ( V 1/2) were negatively shifted. Furthermore both the voltage-ramp and extended-activation protocols demonstrated a significant increase in the persistent sodium current during hypoxia when compared with normoxia. These results demonstrate that both rapidly inactivating and persistent sodium currents are significantly enhanced by a brief hypoxic stimulus. Furthermore the hypoxic-induced increase in these currents most likely is the primary mechanism for the depolarization and increased firing frequency observed in caudal hypothalamic neurons during hypoxia. Since these neurons are important in modulating cardiorespiratory activity, the oxygen responsiveness of these sodium currents may play a significant role in the centrally mediated cardiorespiratory response to hypoxia.

EFFECT OF HYPERBARIC OXYGEN ON CORTICOSTEROID SECRETION AND MORPHOLOGY OF ORGAN CULTURES OF ADULT RAT ADRENAL GLANDS

1967 ◽  
Vol 39 (2) ◽  
pp. 233-249 ◽  
Author(s):  
S. BISWAS ◽  
J. D. B. MacDOUGALL ◽  
R. E. COUPLAND
Keyword(s):  
Hyperbaric Oxygen ◽  
Adrenal Glands ◽  
Horse Serum ◽  
Unit Weight ◽  
Sprague Dawley ◽  
Tissue Slices ◽  
Microscopic Appearance ◽  
Adult Rat ◽  
Sprague Dawley Rats ◽  
Significant Difference

SUMMARY Slices of adrenal glands of 4- to 6-months-old Sprague—Dawley rats were cultured for up to 6 days under air or hyperbaric oxygen in a mixture of 80% Parker's tissue culture Medium 199 and 20% horse serum. The use of hyperbaric oxygen instead of air resulted in a marked improvement in the microscopic appearance of the adrenal slices in cultures of 3–6 days duration. There was a marked stimulation of steroid output in cultures exposed to hyperbaric oxygen during the first 24 hr. After this time, in spite of the improved histological appearance of the tissue slices, no significant difference in steroid output was observed. Female glands secrete about twice as much steroid per unit weight as male glands under similar hyperbaric conditions. Corticosterone, 18-hydroxydeoxycorticosterone and 18-hydroxycorticosterone were the most abundant steroids secreted, but smaller amounts of aldosterone and deoxycorticosterone were also identified. Hyperbaric oxygen did not materially affect the relative amounts of the various steroids. The presence of a greater quantity of adrenocortical tissue in female animals was confirmed. The absolute weight of the medulla in male animals was significantly greater than that of females of the same age, but when expressed in terms of body weight the female medulla was greater than the male medulla.

Ultrastructural Investigation of Spontaneous Pituitary Adenomas in Aging Sprague-Dawley Rats

1982 ◽  
Vol 40 ◽  
pp. 216-217
Author(s):  
D. J. McComb ◽  
J. Beri ◽  
F. Zak ◽  
K. Kovacs
Keyword(s):  
Microscopic Study ◽  
Pituitary Adenomas ◽  
Wistar Rats ◽  
Microscopic Level ◽  
Sprague Dawley ◽  
Prolactin Cells ◽  
Light Microscopic Level ◽  
Ultrastructural Investigation ◽  
Sprague Dawley Rats ◽  
Long Evans

Investigation of the spontaneous pituitary adenomas in rat have been limited mainly to light microscopic study. Furth et al. (1973) described them as chromophobic, secreting prolactin. Kovacs et al. (1977) in an ul trastructural investigation of adenomas of old female Long-Evans rats, found that they were composed of prolactin cells. Berkvens et al. (1980) using immunocytochemistry at the light microscopic level, demonstrated that some spontaneous tumors of old Wistar rats could contain GH, TSH or ACTH as well as PRL.

Early Development of Drug-Induced Hepatic Necrosis

1971 ◽  
Vol 29 ◽  
pp. 576-577
Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser
Keyword(s):  
Early Development ◽  
Hepatic Necrosis ◽  
Screening Tests ◽  
Dense Matrix ◽  
Sprague Dawley ◽  
Electron Microscopic ◽  
Drug Induced ◽  
Hepatocellular Damage ◽  
Sprague Dawley Rats ◽  
Microscopic Studies

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.

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