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  • 1
    Electronic Resource
    Electronic Resource
    Role of calcium and calmodulin in the regulation of the rabbit ileal brush-border membrane Na+/H+ antiporter (1989)
    Springer
    The journal of membrane biology 108 (1989), S. 207-215 
    Details
    ISSN: 1432-1424
    Keywords: calcium ; calmodulin ; absorption ; ileum ; brush-border vesicle ; phosphorylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary In rabbit ileum, Ca2+/calmodulin (CaM) appears to be involved in physiologically inhibiting the linked NaCl absorptive process, since inhibitors of Ca2+/CaM stimulate linked Na+ and Cl− absorption. The role of Ca2+/CaM-dependent phosphorylation in regulation of the brush-border Na+/H+ antiporter, which is believed to be part of the neutral linked NaCl absorptive process, was studied using purified brush-border membrane vesicles, which contain both the Na+/H+ antiporter and Ca2+/CaM-dependent protein kinase(s) and its phosphoprotein substrates. Rabbit ileal villus cell brush-border membrane vesicles were prepared by Mg precipitation and depleted of ATP. Using a freezethaw technique, the ATP-depleted vesicles were loaded with Ca2+, CaM, ATP and an ATP-regenerating system consisting of creatine kinase and creatine phosphate. The combination of Ca2+/CaM and ATP inhibited Na+/H+ exchange by 45±13%. This effect was specific since Ca2+/CaM and ATP did not alter diffusive Na+ uptake, Na+-dependent glucose entry, or Na+ or glucose equilibrium volumes. The inhibition of the Na+/H+ exchanger by Ca2+/CaM/ATP was due to an effect on theV max and not on theK m for Na+. In the presence of CaM and ATP, Ca2+ caused a concentration-dependent inhibition of Na+ uptake, with an effect 50% of maximum occurring at 120nm. This Ca2+ concentration dependence was similar to the Ca2+ concentration dependence of Ca2+/CaM-dependent phosphorylation of specific proteins in the vesicles. The Ca2+/CaM/ATP-inhibition of Na+/H+ exchange was reversed by W13, a Ca2+/CaM antagonist, but not by a hydrophobic control, W12, or by H-7, a protein kinase C antagonist. we conclude that Ca2+, acting through CaM, regulates ileal brush-border Na+/H+ exchange, and that this may be involved in the regulation of neutral linked NaCl absorption.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871735
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  • 2
    Electronic Resource
    Electronic Resource
    Formation of the amphibian grey crescent: Effects of colchicine and cytochalasin B (1978)
    Springer
    Development genes and evolution 185 (1978), S. 99-104 
    Details
    ISSN: 1432-041X
    Keywords: Amphibian ; Grey crescent ; Colchicine ; Cytochalasine B
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The effects of colchicine and cytochalasin B on grey crescent formation in frog (Rana pipiens) and toad (Bufo arenarum) eggs were determined. Colchicine prevented the appearance of the grey crescent, but this inhibition was not due to the absence of an aster. Cytochalasin B did not inhibit grey crescent formation, nor did it inhibit certain activation events such as cortical granule breakdown or cortical contraction. Cytochalasin B caused a detachment of the cortex from the cytoplasm and induced the formation of a morphological grey crescent in non-activated eggs. The results suggest that microtubules may play several roles in grey crescent formation and that a change in the attachment of the cortex to the cytoplasm may also be involved.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00848218
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  • 3
    Electronic Resource
    Electronic Resource
    Ultraviolet light inhibits grey crescent formation on the frog egg (1980)
    Springer
    Development genes and evolution 189 (1980), S. 73-76 
    Details
    ISSN: 1432-041X
    Keywords: Ultraviolet irradiation ; Amphibian ; Grey crescent ; Embryology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Work by others has shown that ultraviolet (UV) irradiation of the vegetal half of the uncleaved frog egg causes defects in neural development. We find that the earliest effect of irradiation ofRana pipiens eggs is to prevent grey crescent formation, the first indication of dorso-ventral polarization of the egg. The UV effect on the grey crescent and on neural development shows similarities in timing, dose-responses, and reversal by cold. We suggest that the UV effect on neural morphogenesis may be caused by the inhibition of cortical-cytoplasmic movement involved in grey crescent formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00848569
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  • 4
    Electronic Resource
    Electronic Resource
    Interactions of naloxone with morphine, amphetamine and phencyclidine on fixed interval responding for intracranial self-stimulation in rats (1990)
    Springer
    Psychopharmacology 102 (1990), S. 263-268 
    Details
    ISSN: 1432-2072
    Keywords: Fixed interval: 60 s schedule ; Intracranial self-stimulation ; Naloxone ; Morphine ; d-Amphetamine ; Phencyclidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rats were implanted with stimulating electrodes aimed at the medial forebrain bundle-lateral hypothalamus (MFB-LH) and were trained to lever-press for brain self-stimulation on a fixed interval: 60 s schedule of reinforcement. The effects of graded doses of naloxone (0.1–30 mg/kg), morphine (0.3–5.6 mg/kg), naloxone plus morphine,d-amphetamine (0.03–1.0 mg/kg), naloxone plusd-amphetamine, phencyclidine (0.3–5.6 mg/kg), and naloxone plus phencyclidine were tested. Naloxone produced a significant decrease in rates at 30 mg/kg. Naloxone (0.1–1.0 mg/kg) plus morphine blocked the dose-dependent decrease produced by morphine alone. In contrast, naloxone (1.0–10 mg/kg) plusd-amphetamine attenuated the graded increase in response rates produced byd-amphetamine. Naloxone (1.0–10 mg/kg) plus phencyclidine did not reliably change the increase in response rates produced by phencyclidine alone. The use of the fixed interval schedule of brain self-stimulation to study these drug interactions is novel, and further demonstrates that the highly reinforcing aspects of brain stimulation, known to be influenced by dopamine, may also be modulated by the endogenous opiate system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02245931
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  • 5
    Electronic Resource
    Electronic Resource
    Threshold differences for naloxone and naltrexone in the hypothalamus and midbrain using fixed ratio brain self-stimulation in rats (1981)
    Springer
    Psychopharmacology 74 (1981), S. 17-22 
    Details
    ISSN: 1432-2072
    Keywords: Brain self-stimulation ; Fixed ratio reinforcement ; Morphine ; Naloxone ; Naltrexone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rats were implanted with stimulating electrodes aimed either at the medial forebrain bundle-lateral hypothalamus (MFB-LH) or the midbrain-central gray (MID-GG), and were trained to lever-press for brain self-stimulation on a fixed ratio: 15 schedule of reinforcement. The dose-dependent effects of morphine (0.1–3.0 mg/kg), naloxone (0.1–30 mg/kg), and naltrexone (0.1–30 mg/kg) were then determined during 1 h test sessions. Both naloxone and naltrexone decreased the rate of responding in the MFB-LH as well as in the MID-CG. However, decrements in response rates were produced in the MID-CG by both naloxone and naltrexone at one tenth the doses required to produce similar decrements with electrodes in the MFB-LH. Dose-dependent decreases in response rates produced by morphine occurred at the same doses in the two electrode sites. At both sites, the decreases in response rates produced by the highest dose of morphine were antagonized completely by a low dose of naloxone (0.1 mg/kg). At an intermediate dose of naloxone (1.0 mg/kg), antagonism occurred in the MFB-LH but not in the MID-CG. At a high dose of naloxone (10 mg/kg), a depression in lever-pressing occurred at both sites in the morphine-treated animal indicating that the depressive action predominated over antagonism. These data explain the lack of consistency of the effects of naloxone on brain self-stimulation previously reported by different laboratories, and demonstrate that the use of partial reinforcement schedules in a rational approach to the evaluation of opioid effects on brain self-stimulation behavior.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00431750
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  • 6
    Electronic Resource
    Electronic Resource
    The discriminative stimulus properties and detection thresholds of intracranial self-stimulation: Effects of d-amphetamine, morphine, and haloperidol (1985)
    Springer
    Psychopharmacology 85 (1985), S. 289-294 
    Details
    ISSN: 1432-2072
    Keywords: Discriminative stimulus properties ; ICSS detection thresholds ; d-Amphetamine ; Morphine ; Haloperidol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A two-choice discrimination task was used to evaluate the effects of psychoactive drugs on the discriminative stimulus properties of brain self-stimulation in rats. In these experiments, brain stimulation served both as a discriminative stimulus and as a reinforcing stimulus, but the two effects were manipulated separately. Animals were trained to a criterion of 95% correct in choosing between two levers, and when this levels of accuracy was reached, the ability to choose correctly remained stable over an 8-month period. Increasing the current strength of the discriminative stimulus from zero to 100% of the training current produced a graded increase in the number of trials completed on the appropriate lever. The discriminative effects produced by brain stimulation were evaluated pharmacologically by using three prototypical psychoactive drugs in an attempt to change the detection threshold for the discriminative stimulus. Morphine, d-amphetamine, and haloperidol, drugs that reliably alter reinforcement thresholds for brain stimulation, failed to change detection thresholds. These results demonstrated that: (1) brain stimulation produces potent and reliable discriminative effects and (2) the effects of psychoactive drugs on detection thresholds can be dissociated from their effects on reinforcement thresholds for brain stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00428189
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  • 7
    Electronic Resource
    Electronic Resource
    Local alteration of cortical actin in Xenopus eggs by the fertilizing sperm (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Molecular Reproduction and Development 35 (1993), S. 69-75 
    Details
    ISSN: 1040-452X
    Keywords: Amphibian ; Microfilaments ; Fertilization ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: Rhodamine phalloidin (Rph) staining was used to examine the microfilament organization of the Xenopus laevis egg cortex during the early stages of fertilization. Unactivated eggs possessed a cytochalasin B (CR)-insensitive Rph-stained matrix that was reorganized upon egg activation and diminished in the presence of CB. Xenopus laevis sperm caused a temporary local increase in Rph staining on the Xenopus cortex. In CB-treated eggs, the local increases of cortical Rph staining later changed to a Rph-free area. These temporary local increases of cortical Rph staining were also observed when Notophthalmus viridescens sperm fertilized Xenopus and Rana pipiens eggs, and were followed by the appearance of concentric rings of stained and unstained areas. Our data suggest that Xenopus and Notophthalmus sperm have activities that can both organize and disrupt the cortical filamentous actin of the Xenopus egg. © 1993 Wiley-Liss, Inc.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/mrd.1080350112
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  • 8
    Electronic Resource
    Electronic Resource
    Release of norepinephrine and dopamine from brain vesicular preparations: Effects of adenosine analogues (1982)
    Springer
    Cellular and molecular neurobiology 2 (1982), S. 193-204 
    Details
    ISSN: 1573-6830
    Keywords: adenosine ; catecholamines ; neurotransmission ; calcium ; brain ; striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. Adenosine analogues inhibit calcium-dependent K+-evoked release of [3H]norepinephrine from guinea pig cerebral cortical and hippocampal vesicular preparations. Inhibition requires high concentrations (100µM) of the adenosine analogues and is abolished in the presence of high concentrations (2 mM) of calcium ions. The inhibitory effect of 2-chloroadenosine is blocked by theophylline. The structure activity profile (N 6-d-phenylisopropyladenosine ≥N 6-l-phenylisopropyladenosine ≥ 2-chloroadenosine 〉N 6-cyclohexyladenosine, adenosine 5′-cyclopropylcar-boxamide) is not that expected of either A1 (high-affinity) or A2 (low-affinity) adenosine receptors. 2. Calcium-dependent K+-evoked release of [3H]dopamine from guinea pig striatal vesicular preparations is inhibited by apomorphine. However, only 2-chloroadenoine causes an inhibition of K+-evoked release of [3H]dopamine. Other adenosine analogues such asd- andl-phenylisopropyladenosine and adenosine 5′-cyclopropylcar-boxamide cause a facilitation of K+-evoked release. The facilitation is abolished or reduced in the presence of high concentrations (2 mM) of calcium ions. The sites of action of adenosine analogues do not appear to have structural requirements identical to those expected of A1 (high-affinity) or A2 (low-affinity) adenosine receptors. 3. The results indicate that adenosine analogues can have either inhibitory or facilitory effects on K+-evoked release of catecholamines from central synaptic terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00711147
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  • 9
    Electronic Resource
    Electronic Resource
    Release of norepinephrine from brain vesicular preparations: Effects of an adenylate cyclase activator, forskolin, and a phosphodiesterase inhibitor (1982)
    Springer
    Cellular and molecular neurobiology 2 (1982), S. 179-192 
    Details
    ISSN: 1573-6830
    Keywords: adenylate cyclase ; catecholamines ; adrenergic receptors ; cyclic AMP ; phosphodiesterase ; neurotransmission ; calcium ; brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. The calcium-dependent K+-evoked release of [3H]norepinephrine from guinea pig cerebral cortical vesicular preparations is inhibited by norepinephrine, clonidine, and epinephrine. Isoproterenol has no effect and phentolamine prevents the inhibition by norepinephrine. The results indicate that anα-adrenergic receptor mediates an inhibitory input to the calcium-dependent release process. The inhibition by norepinephrine is prevented by high concentrations (3.0 mM) of calcium ions. 2. A cyclic AMP phosphodiesterase inhibitor, ZK 62771, slightly elevates [3H]cyclic AMP levels in the guinea pig cerebral cortical preparation and potentiates the marked elevation of [3H]cyclic AMP elicited by the adenylate cyclase activator, forskolin. 3. Neither ZK 62771 nor forskolin alone has significant effects on K+-evoked release of [3H]norepinephrine from the cerebral cortical vesicular preparation; however, a combination of ZK 62771 and forskolin inhibits K+-evoked release by as much as 60%. The inhibition is reversed by high concentrations (2.0 mM) of calcium ions. The results suggest that a marked accumulation of cyclic AMP elicited via both activation of adenylate cyclase and inhibition of phosphodiesterase can be inhibitory to neurotransmitter release from central synaptic terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00711146
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  • 10
    Electronic Resource
    Electronic Resource
    Release of norepinephrine and dopamine from brain vesicular preparations: Effects of calcium antagonists (1982)
    Springer
    Cellular and molecular neurobiology 2 (1982), S. 205-213 
    Details
    ISSN: 1573-6830
    Keywords: calcium ; catecholamines ; neurotransmission ; brain ; striatum ; calcium antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. The calcium antagonists D-600 (1–10µM) and diltiazem (10–25µM) inhibit K+-evoked release of [3H]norepinephrine from guinea pig cerebral cortical vesicular preparations. The inhibition of release is partially reversed by increasing concentrations of calcium to 2 mM. Diltiazem at 100µM has no effect on K+-evoked release of [3H]norepinephrine at 0.15 mM calcium but does inhibit release at 2.0 mM calcium. 2. The calcium antagonist nifedipine and dantrolene, an agent purported to antagonize release of calcium from intracellular storage sites, have no effect on K+-evoked release of [3H]norepinephrine. 3. The calcium antagonists D-600 (1µM) and diltiazem (10µM) inhibit K+-evoked release of [3H]dopamine from guinea pig striatal vesicular preparations. Higher concentrations of drug, namely, 10µM for D-600 and 100µM for diltiazem, cause a potentiation rather than an inhibition of K+-evoked release. The potentiation is reduced in magnitude upon raising the extracellular calcium to 2.0 mM. Indeed, 10µM D-600 then inhibits K+-evoked release of [3H]dopamine. 4. The results indicate that putative calcium antagonists can have both inhibitory and facilitory effects on calcium-dependent K+-evoked release of catecholamines from central synaptic endings. Furthermore, certain peripheral calcium antagonists such as nifedipine and dantrolene may prove ineffective in central systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00711148
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