Persistence of a defective tuberoinfundibular dopaminergic function in rats after long-term removal of oestrogen treatment. An in vivo study

1985 ◽  
Vol 109 (3) ◽  
pp. 309-314 ◽  
Author(s):  
D. Cocchi ◽  
A. Peñalva ◽  
R. Torpia ◽  
G. L. Rossi ◽  
E. E. Müller
Keyword(s):  
Neuronal Function ◽  
Oestrogen Treatment ◽  
Clear Cut ◽  
Long Time ◽  
Previously Treated ◽  
Neuroactive Drugs ◽  
Plasma Prl

Abstract. The function of the tuberoinfundibular dopaminergic (TIDA) neurons of 49 rats bearing oestradiolvalerate (EV)-induced prolactin (Prl) secreting tumours (prolactinomas) was evaluated in vivo, 7 months after discontinuation of EV-treatment, with neuroactive drugs acting via stimulation or inhibition of DA neurotransmission. Based on the size and morphologic appearance of the pituitary and on determination of plasma Prl levels, rats previously treated with EV could be divided into those bearing macro- (31/49) and those bearing microprolactinomas (18/49). Administration of the indirect DA agonist drug nomifensine (10 mg/kg iv) lowered plasma Prl levels in control rats, but failed to do so in rats bearing either macro- or microprolactinomas. Administration of the DA receptor antagonist domperidone (50 μg/kg ip) or the synthetic enkephalin analogue FK 33-824 (1 mg/kg ip) failed to induce a rise in plasma Prl in rats with macro-, but induced a clear-cut rise in plasma Prl in those with microprolactinomas. Prl unresponsiveness to all three neuroactive drugs indicates that long time after EV withdrawal TIDA neuronal function is still highly impaired in rats bearing EVinduced macroprolactinomas. The impairment of TIDA neuronal function would be of lesser extent in rats bearing microprolactinomas as revealed by a defective response to only one of the three applied neuroendocrine probes.

scholarly journals Persistence Dynamics of Antimicrobial-Resistant Neisseria in the Pharynx of Rhesus Macaques

2020 ◽  
Vol 64 (8) ◽  
Author(s):  
Eliza Thapa ◽  
Hanna M. Knauss ◽  
Benjamin A. Colvin ◽  
Benjamin A. Fischer ◽  
Nathan J. Weyand
Keyword(s):  
Rhesus Macaques ◽  
Fluoroquinolone Resistance ◽  
Host Animal ◽  
Content Type ◽  
Host Tropism ◽  
Animal Modeling ◽  
Neisseria Mucosa ◽  
Previously Treated

ABSTRACT Pharyngeal infections by Neisseria gonorrhoeae are often asymptomatic, making them difficult to treat. However, in vivo animal modeling of human pharyngeal infections by pathogenic Neisseria species is challenging due to numerous host tropism barriers. We have relied on rhesus macaques to investigate pharyngeal persistence of naturally occurring Neisseria species in response to antibiotics. These species include Neisseria mucosa, Neisseria oralis, and a species unique to macaques. Four animals previously treated intramuscularly with the fluoroquinolone enrofloxacin for 2 weeks were monitored for persistence of their preexisting Neisseria populations for a period of 10 weeks. Enrofloxacin exposure did not eliminate preexisting flora from two of the four animals. Characterization of a collection of macaque Neisseria isolates supported the hypothesis that pharyngeal persistence was linked to reduced enrofloxacin susceptibility conferred by mutations in either gyrA or parC. Interestingly, we observed a change in neisserial population dynamics for several weeks following enrofloxacin exposure. Enrofloxacin appeared to promote competition between strains for dominance in the pharyngeal niche. Specifically, following enrofloxacin treatment, strains bearing single gyrA mutations and low MICs persisted long-term. In contrast, strains with both gyrA and parC mutations and high MICs became culturally undetectable, consistent with the hypothesis that they were less fit. Our study has provided insight into pharyngeal persistence dynamics of Neisseria species bearing fluoroquinolone resistance determinants. The rhesus macaque provides a valuable host animal that may be used in the future to simulate treatment failures associated with the presence of antimicrobial-resistant Neisseria spp. in the human pharynx.

Determination of apoplastic Na+ in intact leaves of cotton by in vivo fluorescence ratio-imaging

2002 ◽  
Vol 29 (12) ◽  
pp. 1491 ◽  
Author(s):  
Karl H. Mühling ◽  
André Läuchli
Keyword(s):  
Mature Leaves ◽  
Fluorescence Ratio Imaging ◽  
Ratio Imaging ◽  
Compatible Osmolytes ◽  
Concentration Changes ◽  
Sodium Binding ◽  
Leaf Apoplast

Salinity may reduce plant growth via Na+-toxicity symptoms in mature leaves after long-term exposure. It has been suggested by other authors that Na+ accumulates in the leaf apoplast and leads to dehydration of leaves, wilting, and finally to death of these leaves. Two methods were employed to determine the Na+ concentration in the leaf apoplast of salt-tolerant cotton plants under salinity. The ratio imaging of sodium-binding benzofuran isophthalate (SBFI) fluorescence was used to detect in vivo concentration changes and gradients of Na+ within the leaf apoplast under salinity stress, and results were compared with the infiltration–centrifugation method. A�significant increase in Na+ concentration was found in the leaf apoplast under salinity (75 mM NaCl), but no further significant increase was determined when NaCl supply was increased from 75 to 150 mM. Both methods revealed that Na+ concentrations remained relatively low, and thus could not be responsible for the decline in yield under salinity. The ratio images showed changes in Na+ concentration and gradients within the leaf apoplast under salt stress, and demonstrated the validity of the method. However, SBFI fluorescence was also influenced by pH, proteins and salt-induced compatible osmolytes.

scholarly journals Plasticity of Neuron-Glial Transmission: Equipping Glia for Long-Term Integration of Network Activity

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Wayne Croft ◽  
Katharine L. Dobson ◽  
Tomas C. Bellamy
Keyword(s):  
Long Term Potentiation ◽  
Brain Regions ◽  
Neuronal Firing ◽  
Network Activity ◽  
Neuronal Function ◽  
Term Potentiation ◽  
Bidirectional Communication ◽  
Long Time ◽  
Activity Dependent

The capacity of synaptic networks to express activity-dependent changes in strength and connectivity is essential for learning and memory processes. In recent years, glial cells (most notably astrocytes) have been recognized as active participants in the modulation of synaptic transmission and synaptic plasticity, implicating these electrically nonexcitable cells in information processing in the brain. While the concept of bidirectional communication between neurons and glia and the mechanisms by which gliotransmission can modulate neuronal function are well established, less attention has been focussed on the computational potential of neuron-glial transmission itself. In particular, whether neuron-glial transmission is itself subject to activity-dependent plasticity and what the computational properties of such plasticity might be has not been explored in detail. In this review, we summarize current examples of plasticity in neuron-glial transmission, in many brain regions and neurotransmitter pathways. We argue that induction of glial plasticity typically requires repetitive neuronal firing over long time periods (minutes-hours) rather than the short-lived, stereotyped trigger typical of canonical long-term potentiation. We speculate that this equips glia with a mechanism for monitoring average firing rates in the synaptic network, which is suited to the longer term roles proposed for astrocytes in neurophysiology.

After the Dance is over: Some Issues and Suggestions for Follow-up Assessment in Behavior Therapy

1977 ◽  
Vol 41 (3_suppl) ◽  
pp. 1287-1308 ◽  
Author(s):  
Eric J. Mash ◽  
Leif G. Terdal
Keyword(s):  
Behavior Therapy ◽  
Intervention Programs ◽  
Long Term Effects ◽  
Long Time ◽  
Time Periods ◽  
Research Recommendations ◽  
Selection Of

Behavioral intervention programs have thus far failed to provide sufficient follow-up information for the evaluation of long-term effects. This omission is believed to be related to an inadequate conceptualization of follow-up assessment, as well as to the methodological and practical difficulties inherent in assessing behavior over long time periods. A framework for follow-up assessment that is consistent with current behavioral efforts to program generalization is described and is contrasted with traditional views of follow-up that look for effects following the termination of treatment. Several methodological features of follow-up assessment are discussed, along with research recommendations, including the determination of length of appropriate follow-up intervals, the frequency of follow-up assessments, the need for standardization of measures both within and between studies, reactivity of follow-up assessment, the selection of follow-up measures and attrition of subjects.

scholarly journals In Vivo Assessment of Thromboresistant Materials by Determination of Platelet Survival

1977 ◽  
Author(s):  
N. Coe ◽  
R. Collins ◽  
A. Jagoda ◽  
D. Brier ◽  
J. Lindon ◽  
...  
Keyword(s):  
Silicone Rubber ◽  
Needle Puncture ◽  
Polydimethyl Siloxane ◽  
Artificial Surface ◽  
Long Term Behavior ◽  
Shunt Control ◽  
Free Plasma

The reactivity of potentially thromboresistant polymers was determined in sheep by measurement of the lifespan of Cr51-labelled platelets. Materials were tested as tubing (90-125 cm × 2.5-3 mm I.D.) interposed in a 7 cm silicone rubber carotid A.-ext. jugular V. shunt.Platelet lifespan decreased as the length of the basic silicone rubber shunt increased from 7 cm (“shunt control”, T½ 78.3 ± 11.6 S.D. hrs.; n = 18) to 50 cm (T½ 62.0 ± 7.5 hrs.; n=7; p< 0.001 vs. shunt control) but was longer than in sheep without a shunt (T½ 63.1 ± 11.2 hrs.; n=21; p<0.001 vs. shunt control), probably because of artifactual activation of platelets in blood sampling by needle puncture in the absence of a shunt. Of sixteen polymers studied in 42 sheep (n=117), all significantly shortened platelet lifespan except polyurethane (T½ 72.8 ± 12.1 hrs.; n=12) and non-cross-linked silica-free polydimethyl siloxane (T½ 69.8 ± 13.9 hrs.; n = 9). Polymethyl acrylate (PMA) (T½ 71.2 ± 5.4 hrs.; n=ll; p<0.04 vs. shunt control) was passivated by exposure to platelet free plasma before whole blood (T½ 90.3 ± 3.6 hrs.; n=5; ρ <0.05 vs. untreated PMA). Thus, the adsorbed film of plasma constituents has a lasting and decisive effect on thromboresistance of the surface. The long term behavior of an artificial surface may be dictated by the events of the first few seconds of blood-surface contact.

scholarly journals Discoidin domain receptor regulates ensheathment, survival, and caliber of peripheral axons

2021 ◽  
Author(s):  
Megan M. Corty ◽  
Alexandria P. Lassetter ◽  
Jo Q. Hill ◽  
Amy E. Sheehan ◽  
F. Javier Bernardo-Garcia ◽  
...  
Keyword(s):  
Peripheral Nerves ◽  
Motor Behavior ◽  
Genetic Interaction ◽  
Neuronal Function ◽  
Term Survival ◽  
Discoidin Domain Receptor ◽  
And Function ◽  
Circuit Function

Invertebrate axons and small caliber axons in mammalian peripheral nerves are unmyelinated but still ensheathed by glia. How this type of ensheathment is controlled and its roles in supporting neuronal function remain unclear. We performed an in vivo RNAi screen in Drosophila to identify glial genes required for axon ensheathment and identified the conserved receptor tyrosine kinase Discoidin domain receptor (Ddr). In larval peripheral nerves, loss of Ddr resulted in incomplete ensheathment of axons. We found a strong dominant genetic interaction between Ddr and the fly type XV/XVIII collagen Multiplexin (Mp), suggesting Ddr functions a collagen receptor to drive wrapping of axons during development. Surprisingly, while ablation of glia that wrap axons severely impaired larval motor behavior, incomplete wrapping in Ddr mutants was sufficient to support basic circuit function. In adult nerves, loss of Ddr from glia decreased long-term survival of sensory neurons and significantly reduced axon caliber without overtly affecting ensheathment. Our data establish a crucial role for non-myelinating glia in peripheral nerve development and function across the lifespan, and identify Ddr as a key regulator of axon-glia interactions during ensheathment.

scholarly journals Ubiquitin C-terminal hydrolase L1 (UCH-L1) loss causes neurodegeneration by altering protein turnover in the first postnatal weeks

2019 ◽  
Vol 116 (16) ◽  
pp. 7963-7972 ◽  
Author(s):  
Anna T. Reinicke ◽  
Karoline Laban ◽  
Marlies Sachs ◽  
Vanessa Kraus ◽  
Michael Walden ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Protein Turnover ◽  
Neuronal Development ◽  
Postnatal Period ◽  
Neuronal Function ◽  
Neuronal Protein ◽  
Neurological Phenotype ◽  
Deficient Mice

Ubiquitin C-terminal hydrolase L1 (UCH-L1) is one of the most abundant and enigmatic enzymes of the CNS. Based on existing UCH-L1 knockout models, UCH-L1 is thought to be required for the maintenance of axonal integrity, but not for neuronal development despite its high expression in neurons. Several lines of evidence suggest a role for UCH-L1 in mUB homeostasis, although the specific in vivo substrate remains elusive. Since the precise mechanisms underlying UCH-L1–deficient neurodegeneration remain unclear, we generated a transgenic mouse model of UCH-L1 deficiency. By performing biochemical and behavioral analyses we can show that UCH-L1 deficiency causes an acceleration of sensorimotor reflex development in the first postnatal week followed by a degeneration of motor function starting at periadolescence in the setting of normal cerebral mUB levels. In the first postnatal weeks, neuronal protein synthesis and proteasomal protein degradation are enhanced, with endoplasmic reticulum stress, and energy depletion, leading to proteasomal impairment and an accumulation of nondegraded ubiquitinated protein. Increased protein turnover is associated with enhanced mTORC1 activity restricted to the postnatal period in UCH-L1–deficient brains. Inhibition of mTORC1 with rapamycin decreases protein synthesis and ubiquitin accumulation in UCH-L1–deficient neurons. Strikingly, rapamycin treatment in the first 8 postnatal days ameliorates the neurological phenotype of UCH-L1–deficient mice up to 16 weeks, suggesting that early control of protein homeostasis is imperative for long-term neuronal survival. In summary, we identified a critical presymptomatic period during which UCH-L1–dependent enhanced protein synthesis results in neuronal strain and progressive loss of neuronal function.

RETARDED BIOSYNTHESIS OF THYROGLOBULIN SUBUNITS AND THEIR POLYMERIZATION IN VITRO AFTER SUPPRESSION OF TSH SECRETION IN RATS BY CHRONIC ADMINISTRATION OF EXCESS THYROXINE IN THE FORM OF IODINATED CASEIN

1978 ◽  
Vol 89 (1) ◽  
pp. 108-121
Author(s):  
J. Sinadinović ◽  
M. Krainčanić ◽  
G. Kostić ◽  
M. Jovanović
Keyword(s):  
Chronic Administration ◽  
Thyroxine Treatment ◽  
Time Period ◽  
Tsh Secretion ◽  
Long Time ◽  
Pre Treatment ◽  
Reduced Rate

ABSTRACT The effects of short- and long-term (from 3 days to 28 weeks) administration of excess thyroxine in the form of the iodinated casein "Protamone" (0.2%) to rats on the content of soluble thyroid iodoproteins and on biosynthesis and polymerization of thyroid proteins in vitro were investigated. The concentration of soluble iodoproteins significantly increased (40–80%) up to 2 weeks of treatment, and after that remained at the same level. 27S iodoprotein markedly increased during thyroxine treatment. The content of DNA in the gland and the thyroid weight were a little lower in the treated rats than in the control. The incorporation rate of [14C]leucine into soluble and microsome-bound proteins in vitro was markedly reduced in the treated animals (30–80 % of control). Thyroxine pre-treatment of rats induced retarded synthesis of thyroglobulin and its subunits in vitro. The inhibition of the synthesis of thyroid proteins in vitro and the incrrease in the soluble iodopritein content in the gland in vivo was not correlated with the duration of thyroxine treatment. The immobilization of pre-formed thyroglobulin in the follicle lumen for a long time period is probably an important factor in the enlarged conversion of thyroglobulin into 27S iodoprotein. In conclusion, the long-term suppression of endogenous TSH secretion by administration of thyroxine results in an accumulation of iodoproteins in the thyroid and a reduced rate of synthesis of iodoproteins; after 2 weeks a steady state is reached both with regard to iodoprotein accumulation and synthesis. Finally, the results obtained suggest that the thyroid-pituitary axis becomes adapted to chronic administration of excess thyroxine.

EFFECTS OF CONTRACTILE STIMULI ON EXCHANGES OF ELECTROLYTES BETWEEN UTERINE TISSUES AND A SALINE–BICARBONATE MEDIUM

1959 ◽  
Vol 37 (1) ◽  
pp. 127-148
Author(s):  
Edwin E. Daniel ◽  
Betty N. Daniel
Keyword(s):  
Smooth Muscle ◽  
Glycogen Content ◽  
Concomitant Increase ◽  
Sodium Permeability ◽  
Potassium Loss ◽  
Clear Cut ◽  
Long Term Experiments ◽  
Tissue Sodium

(1) Evidence has been presented suggesting that progesterone pretreatment in vivo increases the rate of leakage of potassium from rabbit uterine segments into a saline–bicarbonate medium.(2) Various types of evidence indicate that in uterine tissues, the loss of potassium from cells into potassium-free solutions is increased during the contractile actions of drugs. There was no clear-cut concomitant increase in tissue sodium concentrations. The results tend to confirm previous findings indicating that increases in potassium (but not in sodium) permeability are associated with contraction of smooth muscle.(3) Epinephrine effects on potassium loss occurred only in uteri which contracted in response to epinephrine. Norepinephrine, but not iproterenol, had a similar effect. Dibenamine, alone, decreased potassium loss and partly blocked the effects of epinephrine. Direct measurement of glycogen content suggested that these findings were not related to a glycogenolytic action of the epinephrine. Rather, the effect of epinephrine to increase potassium loss seemed to be closely related to its contractile action. In long-term experiments, both epinephrine and calcium slowed the rate of K loss and of water and sodium gain. This effect also was absent in uterine tissues which were not contracted by epinephrine.

EFFECTS OF CONTRACTILE STIMULI ON EXCHANGES OF ELECTROLYTES BETWEEN UTERINE TISSUES AND A SALINE–BICARBONATE MEDIUM

1959 ◽  
Vol 37 (1) ◽  
pp. 127-148 ◽  
Author(s):  
Edwin E. Daniel ◽  
Betty N. Daniel
Keyword(s):  
Smooth Muscle ◽  
Glycogen Content ◽  
Concomitant Increase ◽  
Sodium Permeability ◽  
Potassium Loss ◽  
Clear Cut ◽  
Long Term Experiments ◽  
Tissue Sodium

(1) Evidence has been presented suggesting that progesterone pretreatment in vivo increases the rate of leakage of potassium from rabbit uterine segments into a saline–bicarbonate medium.(2) Various types of evidence indicate that in uterine tissues, the loss of potassium from cells into potassium-free solutions is increased during the contractile actions of drugs. There was no clear-cut concomitant increase in tissue sodium concentrations. The results tend to confirm previous findings indicating that increases in potassium (but not in sodium) permeability are associated with contraction of smooth muscle.(3) Epinephrine effects on potassium loss occurred only in uteri which contracted in response to epinephrine. Norepinephrine, but not iproterenol, had a similar effect. Dibenamine, alone, decreased potassium loss and partly blocked the effects of epinephrine. Direct measurement of glycogen content suggested that these findings were not related to a glycogenolytic action of the epinephrine. Rather, the effect of epinephrine to increase potassium loss seemed to be closely related to its contractile action. In long-term experiments, both epinephrine and calcium slowed the rate of K loss and of water and sodium gain. This effect also was absent in uterine tissues which were not contracted by epinephrine.

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