ADRENAL CORTICAL HORMONES AND RESISTANCE TO HISTAMINE STRESS IN THE INFANT RAT

1965 ◽  
Vol 48 (2) ◽  
pp. 249-252 ◽  
Author(s):  
Shawn Schapiro

ABSTRACT The adrenal gland corticosterone concentration in the infant rat is similar to that found in the intact unstressed normal adult. 1–2 day old rats did not respond to histamine administration with an increase in adrenal cortical hormone content while adults exhibited the expected increase. The 90 minute dose-mortality relationship for histamine was determined on these stress-non-responsive infant rats. Prior treatment with cortisone, cortisol, corticosterone or ACTH did not significantly influence the number of deaths occurring at a given dose of histamine. These results are compatible with the hypothesis that, in the otherwise normal animal, the abrupt secretion of ACTH and the adrenal cortical hormones in response to acute stress may not contribute stress resistance to contemporaneous insults, at least to those allied to histamine administration.

2019 ◽  
Vol 17 (3) ◽  
pp. 39-49
Author(s):  
Sergey V. Kuznetsov ◽  
Nataliya N. Kuznetsova ◽  
Polina A. Gaydukova

The effects of calcium-channel blockers (CCBs) (verapamil, nifedipine) on heart rate, respiration rate and motor activity were studied in 3-30-day-old rats. The role of calcium channels in development of disturbances of a heart and respiratory rhythms after introduction to newborn rats of acetylcholinesterase (AChE) inhibitor of physostigmine was revealed. Parameters of functional activity of heart, respiratory and somatomotor systems in case of blockade of calcium channels were studied also under conditions of the activation of cholinoceptive structures caused by an injection to infant rats of AChE inhibitor after premedication by CCBs. It is shown that use of calcium channels blockers leads to development of bradycardia, and verapamil causes more expressed disturbance of a heart rhythm in rats of younger age, while blockade of dihydropyridinic receptors by nifedipine has no ontogenetic specifics. Similar ontogenetic dynamics concerns also reaction of respiratory system. Verapamil have a detrimental effect on respiration, up to a stop, in 3-7-day-old and to a lesser extent in 16-30-day-old infant rats. Nifedipine slightly reduces a respiration rate at younger infant rats, but raises it at the mature rats. The nifedipine injection more in comparison with verapamil changes the level and a pattern of motor activity. Preliminary blockade of calcium channels does not render significant change of reaction at the subsequent introduction of physostigmin.


1988 ◽  
Vol 254 (5) ◽  
pp. E617-E624 ◽  
Author(s):  
M. R. Odio ◽  
A. Brodish

The effect of age on the capacity of an organism to mobilize glucose and free fatty acids during stress and to adapt these responses from an acute to a chronic stress situation is not known. The purpose of this study was to determine whether aging impaired the capacity to 1) raise glucose and free fatty acid levels and suppress insulin release in acute stress situations and 2) develop adaptation of these responses to exposure to chronic stress. Our results indicate that 6-mo-old rats (young) trained to escape electric shock (short-term modulation) showed greater acute stress-induced hyperglycemic, hypoinsulinemic, and lipolytic responses than untrained young rats. By contrast, in 22-mo-old rats (old), responses of trained and untrained animals were not different. In the chronic stress (long-term adaptation) experiments, it was found that 1) adaptation of stress-induced hyperglycemia occurred at a faster rate in young than in old animals; 2) in young but not in aged rats, a strong positive correlation was observed between adaptation of stress-induced hyperglycemia and hypoinsulinemia; and 3) in young rats, stress-induced lipolytic responses declined proportionately to the duration of chronic stress exposure, whereas by contrast in chronically stressed aged rats steady-state levels of free fatty acids were not raised during exposure to stress. Thus we conclude that 1) glucose intolerance may play a key role in the altered stress-induced metabolic responses of aged rats; 2) with age, there is a loss of plasticity in physiological adaptive response mechanisms associated with metabolic responses to stress.


2006 ◽  
Vol 74 (11) ◽  
pp. 6213-6225 ◽  
Author(s):  
Thomas W. Seale ◽  
Daniel J. Morton ◽  
Paul W. Whitby ◽  
Roman Wolf ◽  
Stanley D. Kosanke ◽  
...  

ABSTRACT Haemophilus influenzae requires an exogenous heme source for aerobic growth in vitro. Hemoglobin or hemoglobin-haptoglobin satisfies this requirement. Heme acquisition from hemoglobin-haptoglobin is mediated by proteins encoded by hgp genes. Both Hgps and additional proteins, including those encoded by the hxu operon, provide independent pathways for hemoglobin utilization. Recently we showed that deletion of the set of three hgp genes from a nontypeable strain (86-028NP) of H. influenzae attenuated virulence in the chinchilla otitis media model of noninvasive disease. The present study was undertaken to investigate the role of the hgp genes in virulence of the wild-type serotype b clinical isolate HI689 in the infant rat model of hematogenous meningitis, an established model of invasive disease requiring aerobic growth. Bacteremia of high titer and long duration (>14 days) and histopathologically confirmed meningitis occurred in >95% of infant rats challenged at 5 days of age with strain HI689. While mutations disrupting either the Hgp- or Hxu-mediated pathway of heme acquisition had no effect on virulence in infant rats, an isogenic mutant deficient for both pathways was unable to sustain bacteremia or produce meningitis. In contrast, mutations disrupting either pathway decreased the limited ability of H. influenzae to initiate and sustain bacteremia in weanling rats. Biochemical and growth studies also indicated that infant rat plasma contains multiple heme sources that change with age. Taken together, these data indicate that both the hgp genes and the hxuC gene are virulence determinants in the rat model of human invasive disease.


2018 ◽  
Author(s):  
Didhiti Mukherjee ◽  
Greta Sokoloff ◽  
Mark S. Blumberg

AbstractIn week-old rats, somatosensory input arises predominantly from stimuli in the external environment or from sensory feedback associated with myoclonic twitches during active (REM) sleep. A previous study of neural activity in cerebellar cortex raised the possibility that the brainstem motor structures that produce twitches also send copies of motor commands (or corollary discharge, CD) to the cerebellum. Here, by recording from two precerebellar nuclei—the inferior olive and lateral reticular nucleus—we demonstrate that CD does indeed accompany the production of twitches. Within both structures, the CD signal comprises a surprisingly sharp activity peak within 10 ms of twitch onset. In the inferior olive, this sharp peak is attributable to the opening of slow potassium channels. We conclude that a diversity of neural activity is conveyed to the developing cerebellum preferentially during sleep-related twitching, enabling cerebellar processing of convergent input from CD and reafferent signals.


1998 ◽  
Vol 274 (6) ◽  
pp. R1712-R1717 ◽  
Author(s):  
Greta Sokoloff ◽  
Robert F. Kirby ◽  
Mark S. Blumberg

Previous research in infant rats suggested that brown adipose tissue (BAT), by providing warm blood to the heart during moderate cold exposure, protects cardiac rate. This protective role for BAT thermogenesis was examined further in the present study. In experiment 1, 1-wk-old rats in a warm environment were pretreated with saline or chlorisondamine (a ganglionic blocker), and then BAT thermogenesis was stimulated by injection with the β3-agonist CL-316243. In experiment 2, pups were pretreated with chlorisondamine and injected with CL-316243, and after BAT thermogenesis was stimulated the interscapular region of the pups was cooled externally with a thermode. In both experiments, cardiac rate, oxygen consumption, and physiological temperatures were monitored. Activation of BAT thermogenesis substantially increased cardiac rate in saline- and chlorisondamine-treated pups, and focal cooling of the interscapular region was sufficient to lower cardiac rate. The results of these studies support the hypothesis that BAT thermogenesis contributes directly to the modulation of cardiac rate.


1991 ◽  
Vol 131 (2) ◽  
pp. 251-257 ◽  
Author(s):  
M. Parenti ◽  
D. Cocchi ◽  
G. Ceresoli ◽  
C. Marcozzi ◽  
E. E. Müller

ABSTRACT The mechanisms underlying the age-related decrease and increase in somatotroph responsiveness to growth hormone-releasing factor (GHRF) and somatostatin respectively were studied in rat pituitary membranes in vitro. Basal adenylate cyclase (AC) activity was similar in pituitary membranes from rats of 8 days (either sex) and male rats of 3 months, but it was almost threefold higher in membranes from male rats of 21–23 months. GHRF induced a lower percentage stimulation of AC activity in membranes from infant and old than adult rats. Somatostatin inhibited stimulation of AC induced by forskolin more effectively in membranes from adult than infant and old rats. In parallel experiments, since the tissue we used is formed by a mixed population of pituitary cells, we evaluated, for comparison, the effect on AC of neurohormones, i.e. vasoactive intestinal polypeptide (VIP) and dopamine which act primarily on lactotrophs. VIP induced a lower fold-stimulation of AC activity in membranes from infant and old than adult rats. Dopamine inhibited forskolin-induced stimulation of AC in the following rank order of magnitude: old, adult and infant rats, and was also more effective in inhibiting basal AC activity in old than in adult rats. The stimulatory and inhibitory G proteins (Gs and Gi) coupled to AC were measured indirectly by evaluating stimulatory and inhibitory effects of different concentrations of GTP on AC. GTP, at stimulatory concentrations, increased AC activity in membranes from infant and adult rats similarly whereas its effect was significantly greater in membranes from old rats. Conversely, GTP, at inhibitory concentrations, decreased AC activity similarly in membranes from adult and infant rats, whereas in old rats inhibition was apparent at more than a tenfold lower concentration of GTP. These data suggest (1) that the greater somatotroph sensitivity to GHRF in terms of GH secretion of the early postnatal period is not due to supersensitive GHRF receptors but rather may be accounted for, at least partially, by the low function of somatostatinergic receptors; (2) that the inability of GHRF to stimulate GH release in aged rats probably results from an uncoupling between the GHRF receptor and the G protein; and (3) that in aged rats the decreased ability of somatostatin to inhibit AC activity, in spite of the high Gi activity, results from a reduced number of somatotroph cells and, hence, receptors. Journal of Endocrinology (1991) 131, 251–257


2003 ◽  
Vol 71 (4) ◽  
pp. 2253-2257 ◽  
Author(s):  
Stanislav Forman ◽  
Irena Linhartova ◽  
Radim Osicka ◽  
Xavier Nassif ◽  
Peter Sebo ◽  
...  

ABSTRACT RTX cytotoxins play an important role in virulence of numerous gram-negative pathogens. Unexpectedly, however, we show here that the RTX proteins of Neisseria meningitidis are dispensable for virulence in the infant rat model of infection.


2006 ◽  
Vol 74 (5) ◽  
pp. 2803-2808 ◽  
Author(s):  
Maija Toropainen ◽  
Leena Saarinen ◽  
Gestur Vidarsson ◽  
Helena Käyhty

ABSTRACT The relative contributions of antibody-induced complement-mediated bacterial lysis and antibody/complement-mediated phagocytosis to host immunity against meningococcal infections are currently unclear. Further, the in vivo effector functions of antibodies may vary depending on their specificity and Fc heavy-chain isotype. In this study, a mouse immunoglobulin G2a (mIgG2a) monoclonal antibody (MN12H2) to meningococcal outer membrane protein PorA (P1.16), its human IgG subclass derivatives (hIgG1 to hIgG4), and an mIgG2a monoclonal antibody (Nmb735) to serogroup B capsular polysaccharide (B-PS) were evaluated for passive protection against meningococcal serogroup B strain 44/76-SL (B:15:P1.7,16) in an infant rat infection model. Complement component C6-deficient (PVG/c−) rats were used to assess the importance of complement-mediated bacterial lysis for protection. The PorA-specific parental mIgG2a and the hIgG1 to hIgG3 derivatives all induced efficient bactericidal activity in vitro in the presence of human or infant rat complement and augmented bacterial clearance in complement-sufficient HsdBrlHan:WIST rats, while the hIgG4 was unable to do so. In C6-deficient PVG/c− rats, lacking complement-mediated bacterial lysis, the augmentation of bacterial clearance by PorA-specific mIgG2a and hIgG1 antibodies was impaired compared to that in the syngeneic complement-sufficient PVG/c+ rat strain. This was in contrast to the case for B-PS-specific mIgG2a, which conferred similar protective activity in both rat strains. These data suggest that while anti-B-PS antibody can provide protection in the infant rats without membrane attack complex formation, the protection afforded by anti-PorA antibody is more dependent on the activation of the whole complement pathway and subsequent bacterial lysis.


2017 ◽  
Author(s):  
Alexandre Benedetto ◽  
Timothee Bambade ◽  
Catherine Au ◽  
Jennifer M Tullet ◽  
Hairuo Dang ◽  
...  

Caenorhabditis elegans is an excellent model for high-throughput experimental approaches, but lacks a robust, versatile and automated means to pinpoint time of death. Here we describe an automated, label-free, high-throughput method using death-associated fluorescence to monitor nematode survival, which we apply to stress and infection resistance assays. We demonstrate its use to define correlations between age, longevity and stress-resistance, and reveal an autophagy-dependent increase in acute stress resistance in early adulthood.


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