Properties of the specific binding of 125I-nerve growth factor to responsive peripheral neurons.
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Animals↗
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Results for “peripheral response”
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Conditioned eyelid response, peripheral vasoconstriction, and attention in retarded and nonretarded individuals.
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Arousal↗
[Role of the chemical mediators of neural transmission on the central and peripheral responses of behavior to pain].
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Acetylcholine↗
Receptors for nerve growth factor in responsive peripheral neurons.
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Animals↗
Vagal-central nervous system interactions modulate the feeding response to peripheral enterostatin.
Enterostatin selectively inhibits the intake of dietary fat after both peripheral and central administration. We have investigated the role of the hepatic vagus nerve in modulating the peripheral response to enterostatin in Sprague-Dawley rats adapted to a high fat (HF) diet. Intraperitoneal (ip) enterostatin reduced intake of HF diet after overnight starvation. This response was abolished by selective vagal hepatic branch transection. Immunohistochemical techniques were used to identify the location of Fos protein in brain nuclei after ip enterostatin. Fos protein was evident in the nucleus tractus solitarius (NTS), parabrachial, paraventricular and supraoptic nuclei. The pattern of expression of Fos-like immunoreactivity differed from that induced by the lipoprivic agent beta-mercaptoacetate. Transection of the hepatic vagus blocked the central Fos responses to ip enterostatin. We conclude that afferent hepatic vagal nerve activity is required for the feeding response to peripheral enterostatin.
Animals↗
Central vasopressin blockade enhances its peripheral release in response to peripheral osmotic stimulation in conscious rats.
Increased plasma osmolality results in increased central as well as peripheral release of vasopressin. Experiments were carried out to determine whether, in this circumstance, vasopressin can act centrally to modulate its peripheral release. Prior to the start of a thirty-min i.v. infusion of 2.5 M or 0.15 M NaCl, the rats were given an intracerebroventricular (i.c.v.) injection of a peptide V1/V2 vasopressin antagonist (2 micrograms), OPC-31260 (60 micrograms), a non-peptide V2 antagonist, or 1-desamino-8-D-arginine vasopressin (dDAVP, 5 ng), a V2 agonist. Experiments with the peptide antagonist were carried out in male and non-estrous female rats. Since there were no differences between males and females in the measured responses, experiments with the other two drugs were carried out only in males. Pretreatment with either the V1/V2 antagonist or the V2 antagonist enhanced the increase in plasma vasopressin levels in response to the hypertonic saline infusion by about 50% at the end of 30 min. dDAVP, on the other hand, had no effect. None of the i.c.v. drugs had an affect on either the pressor or bradycardic responses to hypertonic saline infusion. These observations suggest that vasopressin can act centrally in a negative feedback fashion to attenuate its own release into the peripheral circulation in response to increased plasma osmolality.
Animals↗
Phosphorylated MAP1B is induced in central sprouting of primary afferents in response to peripheral injury but not in response to rhizotomy.
A peripheral nerve lesion induces sprouting of primary afferents from dorsal root ganglion (DRG) neurons into lamina II of the dorsal horn. Modifications of the environment in consequence to the axotomy provide an extrinsic stimulus. A potential neuron-intrinsic factor that may permit axonal sprouting is microtubule-associated protein 1B (MAP1B) in a specific phosphorylated form (MAP1B-P), restricted to growing or regenerating axons. We show here that both in rat and mouse, a sciatic nerve cut is rapidly followed by the appearance of MAP1B-P expression in lamina II, increasing to a maximum between 8 and 15 days, and diminishing after three months. Evidence is provided that sprouting and induction of MAP1B-P expression after peripheral injury are phenomena concerning essentially myelinated axons. This is in accordance with in situ hybridization data showing especially high MAP1B-mRNA levels in large size DRG neurons that give rise to myelinated fibers. We then employed a second lesion model, multiple rhizotomy with one spared root. In this case, unmyelinated CGRP expressing fibers do indeed sprout, but coexpression of MAP1B-P and CGRP is never observed in lamina II. Finally, because a characteristic of myelinated fibers is their high content in neurofilament protein heavy subunit (NF-H), we used NF-H-LacZ transgenic mice to verify that MAP1B-P induction and central sprouting were not affected by perturbing the axonal organization of neurofilaments. We conclude that MAP1B-P is well suited as a rapidly expressed, axon-intrinsic marker associated with plasticity of myelinated fibers.
Animals↗
Peripheral cytokine responses to Trichuris muris reflect those occurring locally at the site of infection.
The study of human cellular immune responses to parasite infection under field conditions is very complex. Often, the only practical site from which to sample the cellular responses is the peripheral blood. Sampling peripheral blood lymphocytes (PBL) relies on the assumption that these peripheral responses accurately reflect the immune responses acting locally at the site of infection. This is a particularly important point for the human intestinal helminth Trichuris trichiura, which solely inhabits the cecum and large intestine and so will stimulate a localized immune response. Using the well-defined model of T. trichiura, T. muris in the mouse, we have demonstrated that the dominant cytokine responses of the mesenteric lymph nodes (MLN) can be detected by sampling PBL. Resistant mice which mount a type 2 cytokine response in their MLN had PBL producing interleukin-4 (IL-4), IL-5, and IL-9, with negligible levels of gamma interferon (IFN-gamma). Conversely, susceptible mice which mount a type 1 cytokine response in their MLN had PBL producing IFN-gamma and negligible levels of type 2 cytokines. We have also shown that the PBL are capable of mounting a functional immune response against T. muris. PBL from immune mice were capable of transferring immunity to T. muris-infected severe combined immunodeficient (C.B-17 scid/scid) mice. Sampling PBL responses is therefore a viable option for monitoring human intestinal immune responses during T. trichiura infection in the field.
Animals↗
Effects of acute administration of natural progesterone on peripheral vascular responsiveness in healthy postmenopausal women.
Peripheral vascular responses to acute administration of natural progesterone were studied in 12 postmenopausal women (mean +/- SD age 50.3 +/- 4.8 years) with no evidence of cardiovascular disease. According to a randomized, double-blind protocol, all subjects were given natural progesterone as a vaginal cream, able to produce a rapid peak and decay of plasma hormone concentrations, or matched placebo, with crossover after a 1-week washout period. Forearm blood flow and peak flow after ischemic stress (ml/100 ml/min), local vascular resistance (mm Hg/ml/100 ml/min), venous volume (ml/100 ml), and venous compliance (ml/100 ml/mm Hg) were measured by strain-gauge venous occlusion plethysmography at baseline and after progesterone or placebo administration. Plasma norepinephrine concentrations were determined by high-performance liquid chromatography with electrochemical detection. Progesterone sharply decreased forearm blood flow (p <0.01) through an increase in local vascular resistance (p <0.01). Measures of venous function remained unchanged. Although the hormone increased circulating norepinephrine concentrations (p <0.05), there were no significant changes in mean arterial pressure or heart rate. Furthermore, progesterone reduced the local vasodilator capacity, shown by a decrease in forearm delta flow (difference between peak flow and basal flow, p <0.05). Compared with the well-known effect of estrogen, progesterone exerted an opposite action on peripheral vascular responsiveness. Peripheral circulatory changes may be attributed to a direct activity of progesterone on the arterial wall and may in part reflect a modulation of the hormone on peripheral sympathetic tone. Consideration must be given to the hypothesis that the addition of progestin may attenuate the beneficial effects of unopposed estrogen replacement therapy in postmenopausal women.
Cardiovascular Physiological Phenomena↗
Peripheral vascular responses in the limbs. Is there a difference between the peripheral vascular responses of the upper and lower limbs?
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Arm↗
Falls in peripheral eosinophil counts parallel the late asthmatic response.
Peripheral eosinophil counts were measured at intervals before and after control and allergen inhalation in 14 asthmatic subjects. A relative fall in eosinophil counts was noted 9 h after allergen challenge, in contrast to the diurnal increase seen on the control day (p = 0.005). This fall in eosinophil count correlated strongly with the magnitude of the late asthmatic response (r = -0.72, p = 0.003) and with the changes in bronchial responsiveness to histamine at 3 and 24 h after allergen was given (r = 0.54, p = 0.044 and r = 0.82, p less than 0.001, respectively). The findings demonstrate eosinophil kinetics are related to the occurrence of late-phase reactions and to the associated worsening of bronchial hyperreactivity.
Adult↗
Hepatitis B core antigen specific CD4 response in peripheral blood.
The proliferative response of peripheral blood CD4+ T cells to recombinant hepatitis B core antigen (rHBcAg) has been studied in patients with chronic active hepatitis (CAH) type B (CAH-B), CAH-nonA nonB, and normal volunteers. CD4+ T cells from patients with CAH-B indicated a significant proliferative response to rHBcAg in the presence of non-T antigen presenting cells. In contrast, there was no apparent T cell reaction to rHBcAg in patients with CAH-nonA nonB and healthy volunteers. We suggested the possibility of CD4-mediated HBcAg specific response even in the peripheral blood compartments of HBcAg-responsive CAH-B patients.
Adult↗
Peripheral and central ventilatory responses in central sleep apnea with and without congestive heart failure.
Given that the apnea-ventilation cycle length during central sleep apnea (CSA) with congestive heart failure (CHF) is approximately 70 s, we hypothesized that rapidly responsive peripheral CO(2) ventilatory responses would be raised in CHF-CSA and would correlate with the severity of CSA. Sleep studies and single breath and rebreathe hypercapnic ventilatory responses (HCVR) were measured as markers of peripheral and central CO(2) ventilatory responses, respectively, in 51 subjects: 12 CHF with no apnea (CHF-N), 8 CHF with obstructive sleep apnea (CHF-OSA), 12 CHF-CSA, 11 CSA without CHF ("idiopathic" CSA; ICSA), and 8 normal subjects. Single breath HCVR was equally elevated in CHF-CSA and ICSA groups compared with CHF-N, CHF-OSA, and normal groups (0.58 +/- 0.09 [mean +/- SE] and 0. 58 +/- 0.07 versus 0.23 +/- 0.06, 0.25 +/- 0.04, and 0.27 +/- 0.02 L/min/PET(CO(2)) mm Hg, respectively, p < 0.001). Similarly, rebreathe HCVR was elevated in both CHF-CSA and ICSA groups compared with CHF-N, CHF-OSA, and normal groups (5.80 +/- 1.12 and 3.53 +/- 0. 29 versus 2.00 +/- 0.25, 1.44 +/- 0.16, and 2.14 +/- 0.22 L/min/PET(CO(2)) mm Hg, respectively, p < 0.001). Furthermore, in the entire CHF group, single breath HCVR correlated with central apnea-hypopnea index (AHI) (r = 0.63, p < 0.001) and percentage central/total apneas (r = 0.52, p = 0.022). Rebreathe HCVR correlated with awake Pa(CO(2)) (r = -0.61, p < 0.001), but not with central AHI or percentage central/total apneas independent of its relationship with single breath HCVR. In conclusion, in subjects with CHF, raised central CO(2) ventilatory response predisposes to CSA promoting background hypocapnia and exposing the apnea threshold to fluctuations in ventilation, whereas raised and faster-acting peripheral CO(2) ventilatory response determines the periodicity and severity of CSA.
Analysis of Variance↗
Transcriptional profiling of the peripheral blood response during tularemia.
Tularemia is a febrile disease caused by the highly contagious bacterium Francisella tularensis. We undertook an analysis of the transcriptional response in peripheral blood during the course of ulceroglandular tularemia by use of Affymetrix microarrays comprising 14,500 genes. Samples were obtained from seven individuals at five occasions during 2 weeks after the first hospital visit and convalescent samples 3 months later. In total, 265 genes were differentially expressed, 95 of which at more than one time point. The differential expression was verified with real-time quantitative polymerase chain reaction for 36 genes (R(2)=0.590). The most prominent changes were noted in samples drawn on days 2-3 and a considerable proportion of the upregulated genes appeared to represent an interferon-gamma-induced response and also a proapoptotic response. Genes involved in the generation of innate and acquired immune responses were found to be downregulated, presumably a pathogen-induced event. A logistic regression analysis revealed that seven genes were good predictors of the early phase of tularemia. This is the first description of the transcriptional host response to ulceroglandular tularemia and the study has identified gene subsets relevant to the pathogenesis of the disease and subsets that may serve as early diagnostic biomarkers.
Aged↗
Foveal versus peripheral retinal responses: a new analysis for early diagnosis of multiple sclerosis.
Visual potentials evoked by brief flashes (VEPs) were recorded in 85 patients with MS, 30 healthy controls and 25 neurological patients without demyelinating diseases. In a group of 44 patients, diffuse field stimulation was used, resutling in 15 altered responses (34%). In a second group of 41 patients with superimposable characteristics including age, sex, diagnosis of MS (definite, probable and possible) and score on the Rose's scale, the separate responses of central and peripheral retina were analysed. A total of 30 abnormal VEPs were recognized (73%) with the following distribution: 16 foveal VEPs (78%), 4 peripheral responses (13%) and 26 centreperiphery latency differences (CPLD, 60%). Twenty subjects of Group A with normal or slightly altered full field VEPs were retested with both stimulating methods with the following result: 3 altered full field VEPs (15%) and 15 abnormal CPLD (75%). With diffuse field stimulation, the correlation between the VEP scores and the results of other examinations (visual, pyramidal, etc.) were insignficant; on the contrary, the CPLD was clearly correlated with the involvement of the visual and other systems in the fluctuating clinical course of MS.
Adolescent↗
Peripheral vascular responses during acute anemia.
Peripheral vascular responses during acute anemia were studied in 19 anesthetized dogs. In one study (n = 9) hindlimb weight and venous pressures were measured prior to and during acute anemia produced by isovolemic dextran-for-blood exchange. In another series of five control and five anemic dogs (hematocrit = 14 +/- 1% (mean +/- SE)), flow to the limb was occluded and arterial and venous pressure changes in the occluded limb were measured as an index of neurally mediated alterations in limb vasomotor tone. Following reduction of the hematocrit to 14 +/- 0.3%, hindlimb weight decreased by an average of 10.0 g (P less than 0.01) at 15 min and 12.8 g (P less than 0.01) at 30 min of anemia. The decrease in limb weight was associated with a rise (P less than 0.01) in limb venous pressure. There was also a relatively greater degree of vasomotor tone in the occluded hindlimb of anemic dogs as compared with control animals. Although both arterial and venous pressure decreased in an occluded hindlimb following the production of anemia, the decreases in vascular pressures were significantly less than those observed in control experiments. It was not possible to distinguish between tone changes in arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone. arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone. arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone.
Acute Disease↗
Activity and distribution patterns of monkey pallidal neurons in response to peripheral nerve stimulation.
The response patterns of pallidal neurons to electrical stimulation of the median and tibial nerves were examined in awake monkeys. Around 30% of the recorded neurons responded to the stimulation of either the median or tibial nerve, while only 6% responded to the stimulation of both nerves. The vast majority of these pallidal neurons displayed monophasic excitation or monophasic inhibition. The latency of the excitation was shorter than that of the inhibition. In each pallidal segment, the neurons responding to the median nerve stimulation (representing the forelimb) tended to be located ventral to those responding to the tibial nerve stimulation (representing the hindlimb). The present results indicate that the somatotopical arrangement in the globus pallidus can be outlined based on the neuronal responses to peripheral nerve stimulation.
Animals↗
Influence of exogenous bovine somatotropin on the responsiveness of peripheral blood lymphocytes to mitogen.
Our objectives were to determine the effects of exogenous bovine somatotropin on peripheral blood lymphocyte responsiveness to mitogen and on concentrations of serum insulin-like growth factor-I and to determine whether a statistical relationship exists between these two variables. The cows on trial were treated with 0, 10.3, or 20.6 mg/d somatotropin, starting between wk 4 and 5 of lactation and continuing for 266 consecutive d. Lymphocyte proliferation (counts per minute) and concentration of insulin-like growth factor-I (nanograms per milliliter) were recorded from blood sampled at wk 3, 10, 26, 35, and 46 of lactation. The results showed that lymphocytes from the blood of treated cows responded to mitogen with higher proliferative responsiveness than cells from control cows, but that this effect required long-term treatment and adequate mitogen concentrations to be detected. The blood of treated cows also had elevated concentrations of insulin-like growth factor-I relative to that of control cows, but these were not statistically associated with the proliferative responsiveness of the peripheral blood lymphocytes to mitogen. Our results suggest that somatotropin has a role in the immune system of cows, but its mode of action and target tissues must be determined. Bovine somatotropin, injected at doses that increase milk yield, can augment cow immunity as judged by the proliferative responsiveness of peripheral blood lymphocytes in culture.
Analysis of Variance↗