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  • Erlichman, Joseph S.  (5)
  • Leiter, J. C.  (5)
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  • 1
    Online Resource
    Online Resource
    Heterogeneous patterns of pH regulation in glial cells in the dorsal and ventral medulla
    American Physiological Society ; 2004
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 286, No. 2 ( 2004-02), p. R289-R302
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 286, No. 2 ( 2004-02), p. R289-R302
    Abstract: We examined pH regulation in two chemosensitive areas of the brain, the retrotrapezoid nucleus (RTN) and the nucleus tractus solitarius (NTS), to identify the proton transporters involved in regulation of intracellular pH (pH i ) in medullary glia. Transverse brain slices from young rats [postnatal day 8 (P8) to P20] were loaded with the pH-sensitive probe 2′,7′-bis (2-carboxyethyl)-5,6-carboxyfluorescein after kainic acid treatment removed neurons. Cells were alkalinized when they were depolarized (extracellular K + increased from 6.24 to 21.24 mM) in the RTN but not in the NTS. This alkaline shift was inhibited by 0.5 mM DIDS. Removal of [Formula: see text] or Na + from the perfusate acidified the glial cells, but the acidification after Na + removal was greater in the RTN than in the NTS. Treatment of the slice with 5-( N-ethyl- N-isopropyl)amiloride (100 μM) in saline containing [Formula: see text] acidified the cells in both nuclei, but the acidification was greater in the NTS. Restoration of extracellular Cl - after Cl - depletion during the control condition acidified the cells. Immunohistochemical studies of glial fibrillary acid protein demonstrated much denser staining in the RTN compared with the NTS. We conclude that there is evidence of [Formula: see text] cotransport and Na + /H + exchange in glia in the RTN and NTS, but the distribution of glia and the distribution of these pH-regulatory functions are not identical in the NTS and RTN. The differential strength of glial pH regulatory function in the RTN and NTS may also alter CO 2 chemosensory neuronal function at these two chemosensitive sites in the brain stem.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00245.2003
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2004
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Chemosensory Responses to CO 2 in Multiple Brain Stem Nuclei Determined Using a Voltage-Sensitive Dye in Brain Slices From Rats
    American Physiological Society ; 2009
    In:  Journal of Neurophysiology Vol. 102, No. 3 ( 2009-09), p. 1577-1590
    Details
    In: Journal of Neurophysiology, American Physiological Society, Vol. 102, No. 3 ( 2009-09), p. 1577-1590
    Abstract: We used epifluorescence microscopy and a voltage-sensitive dye, di-8-ANEPPS, to study changes in membrane potential during hypercapnia with or without synaptic blockade in chemosensory brain stem nuclei: the locus coeruleus (LC), the nucleus of the solitary tract, lateral paragigantocellularis nucleus, raphé pallidus, and raphé obscurus and, in putative nonchemosensitive nuclei, the gigantocellularis reticular nucleus and the spinotrigeminal nucleus. We studied the response to hypercapnia in LC cells to evaluate the performance characteristics of the voltage-sensitive dye. Hypercapnia depolarized many LC cells and the voltage responses to hypercapnia were diminished, but not eradicated, by synaptic blockade (there were intrinsically CO 2 -sensitive cells in the LC). The voltage response to hypercapnia was substantially diminished after inhibiting fast Na + channels with tetrodotoxin. Thus action potential–related activity was responsible for most of the optical signal that we detected. We systematically examined CO 2 sensitivity among cells in brain stem nuclei to test the hypothesis that CO 2 sensitivity is a ubiquitous phenomenon, not restricted to nominally CO 2 chemosensory nuclei. We found intrinsically CO 2 sensitive neurons in all the nuclei that we examined; even the nonchemosensory nuclei had small numbers of intrinsically CO 2 sensitive neurons. However, synaptic blockade significantly altered the distribution of CO 2 -sensitive cells in all of the nuclei so that the cellular response to CO 2 in more intact preparations may be difficult to predict based on studies of intrinsic neuronal activity. Thus CO 2 -sensitive neurons are widely distributed in chemosensory and nonchemosensory nuclei and CO 2 sensitivity is dependent on inhibitory and excitatory synaptic activity even within brain slices. Neuronal CO 2 sensitivity important for the behavioral response to CO 2 in intact animals will thus be determined as much by synaptic mechanisms and patterns of connectivity throughout the brain as by intrinsic CO 2 sensitivity.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    URL: Article
    DOI: 10.1152/jn.00381.2009
    RVK:
    XA 10000 ; XA 552555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 3
    Online Resource
    Online Resource
    Ventilatory effects of gap junction blockade in the RTN in awake rats
    American Physiological Society ; 2004
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 287, No. 6 ( 2004-12), p. R1407-R1418
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 287, No. 6 ( 2004-12), p. R1407-R1418
    Abstract: We tested the hypothesis that carbenoxolone, a pharmacological inhibitor of gap junctions, would reduce the ventilatory response to CO 2 when focally perfused within the retrotrapezoid nucleus (RTN). We tested this hypothesis by measuring minute ventilation (V E ), tidal volume (V T ), and respiratory frequency (F R ) responses to increasing concentrations of inspired CO 2 (Fi CO 2 = 0–8%) in rats during wakefulness. We confirmed that the RTN was chemosensitive by perfusing the RTN unilaterally with either acetazolamide (AZ; 10 μM) or hypercapnic artificial cerebrospinal fluid equilibrated with 50% CO 2 (pH ∼6.5). Focal perfusion of AZ or hypercapnic aCSF increased V E , V T , and F R during exposure to room air. Carbenoxolone (300 μM) focally perfused into the RTN decreased V E and V T in animals 〈 11 wk of age, but V E and V T were increased in animals 〉 12 wk of age. Glyzyrrhizic acid, a congener of carbenoxolone, did not change V E , V T , or F R when focally perfused into the RTN. Carbenoxolone binds to the mineralocorticoid receptor, but spironolactone (10 μM) did not block the disinhibition of V E or V T in older animals when combined with carbenoxolone. Thus the RTN is a CO 2 chemosensory site in all ages tested, but the function of gap junctions in the chemosensory process varies substantially among animals of different ages: gap junctions amplify the ventilatory response to CO 2 in younger animals, but appear to inhibit the ventilatory response to CO 2 in older animals.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00404.2004
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2004
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Glia modulation of the extracellular milieu as a factor in central CO 2 chemosensitivity and respiratory control
    American Physiological Society ; 2010
    In:  Journal of Applied Physiology Vol. 108, No. 6 ( 2010-06), p. 1803-1811
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 108, No. 6 ( 2010-06), p. 1803-1811
    Abstract: We discuss the influence of astrocytes on respiratory function, particularly central CO 2 chemosensitivity. Fluorocitrate (FC) poisons astrocytes, and studies in intact animals using FC provide strong evidence that disrupting astrocytic function can influence CO 2 chemosensitivity and ventilation. Gap junctions interconnect astrocytes and contribute to K + homeostasis in the extracellular fluid (ECF). Blocking gap junctions alters respiratory control, but proof that this is truly an astrocytic effect is lacking. Intracellular pH regulation of astrocytes has reciprocal effects on extracellular pH. Electrogenic sodium-bicarbonate transport (NBCe) is present in astrocytes. The activity of NBCe alkalinizes intracellular pH and acidifies extracellular pH when activated by depolarization (and a subset of astrocytes are depolarized by hypercapnia). Thus, to the extent that astrocytic intracellular pH regulation during hypercapnia lowers extracellular pH, astrocytes will amplify the hypercapnic stimulus and may influence central chemosensitivity. However, the data so far provide only inferential support for this hypothesis. A lactate shuttle from astrocytes to neurons seems to be active in the retrotrapezoid nucleus (RTN) and important in setting the chemosensory stimulus in the RTN (and possibly other chemosensory nuclei). Thus astrocytic processes, so vital in controlling the constituents of the ECF in the central nervous system, may profoundly influence central CO 2 chemosensitivity and respiratory control.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.01321.2009
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 5
    Online Resource
    Online Resource
    Response of membrane potential and intracellular pH to hypercapnia in neurons and astrocytes from rat retrotrapezoid nucleus
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 289, No. 3 ( 2005-09), p. R851-R861
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 289, No. 3 ( 2005-09), p. R851-R861
    Abstract: We compared the response to hypercapnia (10%) in neurons and astrocytes among a distinct area of the retrotrapezoid nucleus (RTN), the mediocaudal RTN (mcRTN), and more intermediate and rostral RTN areas (irRTN) in medullary brain slices from neonatal rats. Hypercapnic acidosis (HA) caused pH o to decline from 7.45 to 7.15 and a maintained intracellular acidification of 0.15 ± 0.02 pH unit in 90% of neurons from both areas ( n = 16). HA excited 44% of mcRTN (7/16) and 38% of irRTN neurons (6/16), increasing firing rate by 167 ± 75% (chemosensitivity index, CI, 256 ± 72%) and 310 ± 93% (CI 292 ± 50%), respectively. These responses did not vary throughout neonatal development. We compared the responses of mcRTN neurons to HA (decreased pH i and pH o ) and isohydric hypercapnia (IH; decreased pH i with constant pH o ). Neurons excited by HA (firing rate increased 156 ± 46%; n = 5) were similarly excited by IH (firing rate increased 167 ± 38%; n = 5). In astrocytes from both RTN areas, HA caused a maintained intracellular acidification of 0.17 ± 0.02 pH unit ( n = 6) and a depolarization of 5 ± 1 mV ( n = 12). In summary, many neurons (42%) from the RTN are highly responsive (CI 248%) to HA; this may reflect both synaptically driven and intrinsic mechanisms of CO 2 sensitivity. Changes of pH i are more significant than changes of pH o in chemosensory signaling in RTN neurons. Finally, the lack of pH i regulation in response to HA suggests that astrocytes do not enhance extracellular acidification during hypercapnia in the RTN.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00132.2005
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Location Call Number Limitation Availability
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    Online Resource
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