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PubMed2004

Pharmacological evidence that multiple phospholipid signaling pathways link Rhizobium nodulation factor perception in Medicago truncatula root hairs to intracellular responses, including Ca2+ spiking and specific ENOD gene expression.

Rhizobium nodulation (Nod) factors are specific lipochito-oligosaccharide signals essential for initiating in root hairs of the host legume developmental responses that are required for controlled entry of the microsymbiont. In this article, we focus on the Nod factor signal transduction pathway leading to specific and cell autonomous gene activation in Medicago truncatula cv Jemalong in a study making use of the Nod factor-inducible MtENOD11 gene. First, we show that pharmacological antagonists that interfere with intracellular ion channel and Ca2+ pump activities are efficient blockers of Nod factor-elicited pMtENOD11-beta-glucuronidase (GUS) expression in root hairs of transgenic M. truncatula. These results indicate that intracellular Ca2+ release and recycling activities, essential for Ca2+ spiking, are also required for specific gene activation. Second, pharmacological effectors that inhibit phospholipase D and phosphoinositide-dependent phospholipase C activities are also able to block pMtENOD11-GUS activation, thus underlining a central role for multiple phospholipid signaling pathways in Nod factor signal transduction. Finally, pMtENOD11-GUS was introduced into all three Nod-/Myc- dmi M. truncatula mutant backgrounds, and gene expression was evaluated in response to the mastoparan peptide agonist Mas7. We found that Mas7 elicits root hair MtENOD11 expression in dmi1 and dmi2 mutants, but not in the dmi3 mutant, suggesting that the agonist acts downstream of DMI1/DMI2 and upstream of DMI3. In light of these results and the recently discovered identities of the DMI gene products, we propose an integrated cellular model for Nod factor signaling in legume root hairs in which phospholipids play a key role in linking the Nod factor perception apparatus to downstream components such as Ca2+ spiking and ENOD gene expression.

Calcium↗
PubMed2006

Noradrenergic and cholinergic neural pathways mediate stress-induced reactivation of colitis in the rat.

Evidence to date suggests that stress-induced exacerbation or relapse of intestinal inflammation in inflammatory bowel disease requires both activation of the autonomic nervous system and the activation of the immune system by the presence of previously encountered luminal antigens. The aim of the present study was to further explore these associations and to determine the role of the autonomic nervous in modulating the intestinal inflammatory response to stress. Rats healed from an initial dinitrobenzene sulfonic acid-induced colitis were given a non-colitic dose of dinitrobenzene sulfonic acid (dissolved in saline) or 0.9% saline intra-rectally and then subjected to restraint stress. Cardiac sympathovagal balance was assessed by power spectral analysis of heart rate variability data collected from telemetric electrocardiogram recordings before, during and post stress. Only rats that were stressed and received dinitrobenzene sulfonic acid showed an inflammatory relapse characterized by significant macroscopic damage and elevated myeloperoxidase activity associated with a significant infiltration of mucosal and submucosal T lymphocytes. No difference in inflammatory markers was observed in animals that received intra-rectal saline and restraint stress. Rats subjected to stress and intra-rectal dinitrobenzene sulfonic acid demonstrated an increase in sympathetic activity with a nearly four fold increase in LF:HF ratio during stress and a significant increase in heart rate. Shortly after cessation of stress, the LF:HF ratio decreased significantly, returning to baseline levels, however the heart rate remained significantly elevated over baseline levels following stress, but decreased to a level that was significantly lower than during stress. The stress/dinitrobenzene sulfonic acid-induced relapses were preventable by pre-treating rats with hexamethonium (a nicotinic cholinergic ganglion blocking agent) or the co-administration of atropine (a muscarinic cholinoceptor antagonist) and bretylium (a noradrenergic ganglion blocking agent), but was not prevented when either atropine or bretylium were administered alone. This study utilizes an established model of chemically induced colitis that when integrated with stress results in relapsing inflammatory bowel disease. Moreover, this study demonstrates that noradrenergic and cholinergic neural pathways mediate the stress response critical for the relapse of colitis.

Acute Disease↗
PubMed2001

The biological functions of A-kinase anchor proteins.

cAMP-dependent protein kinase is targeted to discrete subcellular locations by a family of specific anchor proteins (A-kinase anchor proteins, AKAPs). Localization recruits protein kinase A (PKA) holoenzyme close to its substrate/effector proteins, directing and amplifying the biological effects of cAMP signaling.AKAPs include two conserved structural modules: (i) a targeting domain that serves as a scaffold and membrane anchor; and (ii) a tethering domain that interacts with PKA regulatory subunits. Alternative splicing can shuffle targeting and tethering domains to generate a variety of AKAPs with different targeting specificity. Although AKAPs have been identified on the basis of their interaction with PKA, they also bind other signaling molecules, mainly phosphatases and kinases, that regulate AKAP targeting and activate other signal transduction pathways. We suggest that AKAP forms a "transduceosome" by acting as an autonomous multivalent scaffold that assembles and integrates signals derived from multiple pathways. The transduceosome amplifies cAMP and other signals locally and, by stabilizing and reducing the basal activity of PKA, it also exerts long-distance effects. The AKAP transduceosome thus optimizes the amplitude and the signal/noise ratio of cAMP-PKA stimuli travelling from the membrane to the nucleus and other subcellular compartments.

A Kinase Anchor Proteins↗
PubMed1984

Subcortical efferent projections of the medial geniculate nucleus mediate emotional responses conditioned to acoustic stimuli.

The purpose of this study was to identify the afferent link in the neural pathway which mediates emotional responses coupled to auditory stimuli. We evaluated whether autonomic and behavioral responses elicited by acoustic conditioned emotional stimuli are based on afferent information derived from the auditory cortex or from the auditory thalamic relay station, the medial geniculate nucleus (MG), in rats. The rat auditory cortex was defined through anterograde neuroanatomical tracing studies involving the injection of HRP into MG. Lesions were then placed in the auditory cortex or in MG. After 10 to 20 days the rats were subjected to classical fear conditioning trials involving the pairing of a pure tone with electric footshock. Changes in mean arterial pressure and heart rate and the duration of immobilization ("freezing") and drink suppression elicited by presentation during extinction trials (no footshock) of the acoustic conditioned emotional stimulus were measured. Auditory cortex lesions did not affect the magnitude of the mean arterial pressure or heart rate conditioned responses nor the duration of freezing or drink suppression. In contrast, lesions of MG suppressed the magnitude of both the autonomic and somatomotor (behavioral) conditioned emotional responses but did not affect either autonomic or somatic responses elicited by the footshock unconditioned stimulus. Lesions of the inferior colliculus, the primary source of afferent input to MG, replicated the effects of MG lesions. These findings demonstrate that lesions of MG and lower auditory centers, but not lesions of the auditory cortex, block autonomic and behavioral conditioned emotional responses coupled to acoustic stimuli and indicate that subcortical rather than cortical efferents of MG sustain these responses. Our concurrent observation that MG projects to several subcortical areas (central and lateral amygdala; caudate-putamen; ventromedial hypothalamus) involved in emotional behavior and autonomic function suggests hypotheses concerning subsequent links in this emotional processing pathway.

Acoustic Stimulation↗
PubMed2004

Anatomy and neurocontrol of the pelvic floor.

Neural control of pelvic organs is affected by a unique coordination of somatic and autonomic motor nervous systems. Sensory information and feedback is supplied by both visceral and somatic sensory fibers. The anatomical features of the pelvic floor and perineal muscles, and their innervation are described. Altogether more detailed information is known in humans on the peripheral innervation as compared to the central nervous system centers and connections of pelvic organ neurocontrol. Controversies in regional neuroanatomy are explained. Reports on individual variability and asymmetry - the former particularly with methods revealing structures, and the latter with functional methods - are interesting but need further validation.

Afferent Pathways↗
PubMed1990

Diabetic autonomic neuropathy in BB rats and effect of ARI treatment on heart-rate variability and vagus nerve structure.

The preventive effect of the aldose reductase inhibitor (ARI) ponalrestat on heart-rate variability and the development of autonomic neuropathy in the vagus nerve was investigated in the spontaneously diabetic BB rat. ARI treatment completely prevented the characteristic decrease in heart-rate variability and axonal atrophy of the vagus nerve for 4 mo in hyperglycemic BB rats. After 6 mo of treatment, the preventive effect on heart-rate variability was partial, and the vagus nerve demonstrated an increase in regenerating myelinated and unmyelinated fibers. These data suggest that autonomic neuropathy involving the vagus nerve is metabolically induced by demonstrating that inhibition of the polyol pathway significantly delays the occurrence of functional and structural autonomic neuropathy despite the presence of hyperglycemia.

Aldehyde Reductase↗
PubMed1999

Cholinergic inputs to the rat medial prefrontal cortex mediate potentiation of the cardiovascular defensive response by the anxiogenic benzodiazephine receptor partial inverse agonist FG 7142.

Consistent with its putative anxiogenic actions, administration of the benzodiazepine receptor partial inverse agonist FG 7142 has been shown to potentiate defensive-like cardiovascular reactivity to an acoustic stimulus in the rat, an effect that appears to be mediated by the basal forebrain cholinergic system. The present studies tested the hypothesis that the basal forebrain cholinergic projections to the medial prefrontal cortex, an area that has been implicated in both anxiety and autonomic control, may be a relevant pathway underlying this response potentiation. Infusions of the muscarinic receptor agonist carbachol into the medial prefrontal cortex, but not into the lateral prefrontal cortex or the basolateral amygdala, mimicked the effects of systemically administered FG 7142 on the cardioacceleratory response. Infusions of the muscarinic antagonist atropine blocked this effect, as well as the response-potentiating actions of FG 7142. The effects of FG 7142 were also blocked by lesions of the cholinergic inputs to the medial prefrontal cortex produced by local infusions of the immunotoxin 192 immunoglobulin G-saporin into this area. These findings indicate that cholinergic activation of the medial prefrontal cortex is sufficient to enhance the cardioacceleratory defensive response, and that cholinergic inputs to the medial prefrontal cortex are necessary for the response-potentiating effects of FG 7142. These results are consistent with a recent neurobiological model of anxiety and autonomic control that attributes the enhanced processing of anxiety-related stimuli and contexts to increases in activity in cortical cholinergic inputs.

Animals↗
PubMed1995

Effects of the autonomic ganglion blocking agent hexamethonium on vasodilator responses mediated by the parasympathetic ganglion on the chorda tympani pathway of the cat.

We investigated the pharmacological properties of a parasympathetic ganglion (a chorda tympani ganglion) that mediates vasodilator responses in the lower lip induced by electrical stimulation of the distal cut end of the chorda tympani or facial nerve root of the cat. These responses were suppressed by prior treatment with the autonomic ganglion blocking agent hexamethonium. We compared the effects of three doses of hexamethonium (1, 3 and 10 mg/kg, i.v.) on the chorda tympani ganglion with their effects on three large ganglia; the otic, submandibular and pterygopalatine ganglia that mediate vasodilator responses. Experiments were conducted on 20 cats weighing 1-3 kg which had been anesthetized with a mixture of urethane (100 mg/kg, i.v.) and chloralose (50 mg/kg, i.v.) then artificially ventilated (pancuronium bromide 0.2 mg/kg per h, i.v.). The chorda tympani ganglion's sensitivity to hexamethonium was similar to that of the otic ganglion but differed from the sensitivities of submandibular and pterygopalatine ganglia. We speculate that transmission through the chorda tympani ganglion is pharmacologically similar to the otic ganglion, although its precise location has yet to be determined.

Animals↗
PubMed2005

Towards a neural basis of music perception.

Music perception involves complex brain functions underlying acoustic analysis, auditory memory, auditory scene analysis, and processing of musical syntax and semantics. Moreover, music perception potentially affects emotion, influences the autonomic nervous system, the hormonal and immune systems, and activates (pre)motor representations. During the past few years, research activities on different aspects of music processing and their neural correlates have rapidly progressed. This article provides an overview of recent developments and a framework for the perceptual side of music processing. This framework lays out a model of the cognitive modules involved in music perception, and incorporates information about the time course of activity of some of these modules, as well as research findings about where in the brain these modules might be located.

Arousal↗
PubMed1971

Central autonomic effects of prostaglandin F2 alpha on the cardiovascular system of the dog.

1. Prostaglandin F(2alpha) infused into the vertebral artery of the anaesthetized greyhound in doses which had no effect when given intravenously ((8-64 ng/kg)/min) caused an increase in blood pressure and heart rate.2. This response was not significantly altered by beta-adrenoceptor blockade with propranolol (10 mg i.v.) or by cervical cord section at C(4-6).3. The tachycardia was abolished and the pressor response greatly reduced by vagotomy or atropine (250 mug/kg i.v.).4. The pressor response which remained after vagotomy was abolished by subsequent sympathetic blockade with bethanidine (2-3 mg/kg i.v.) or bretylium (10 mg/kg i.v.).5. In contrast to the effects of propranolol or cervical cord section bethanidine (4-5 mg/kg i.v.) or bretylium (10 mg/kg i.v.) significantly reduced blood pressure and heart rate responses to intravertebral prostaglandin F(2alpha). This result suggests that bethanidine and bretylium have some central actions.6. It is concluded that the cardiovascular effects of intravertebral infusions of prostaglandin F(2alpha) are mediated by the autonomic nervous system and that the preferential pathway is withdrawal of vagal tone to the heart.

Animals↗
PubMed1996

Central and primary visceral afferents to nucleus tractus solitarii may generate nitric oxide as a membrane-permeant neuronal messenger.

An anatomical basis was sought for the postulated roles of nitric oxide (NO) as a labile transcellular messenger in the dorsal vagal complex (NTS-X). The diaphorase activity of NO synthase was used as a marker of neurons in NTS-X that are presumed to convert L-arginine to L-citrulline and NO. Nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) staining patterns in the nucleus tractus solitarii (NTS) were spatially related to terminal sites of primary visceral afferents from 1) orosensory receptors (e.g., rostral-central nucleus); 2) soft palate, pharynx, larynx, and tracheobronchial tree (e.g., dorsal, intermediate, and interstitial nuclei); 3) esophagus (nucleus centralis); 4) stomach (nucleus gelatinosus); 5) hepatic and coeliac nerves (nucleus subpostrema); and 6) carotid body and baroreceptors (medial commissural and dorsal-lateral nuclei). Primary visceral afferents were identified as sources of NADPHd-stained fiber plexuses in the NTS-X based on three findings: 1) the presence of NADPHd in nodose ganglion cells with morphological features of first-order sensory relay neurons; 2) retrograde transport of Fluoro-Gold (FG) or cholera toxin B (CT-B) from NTS-X to NADPHd-positive nodose ganglion neurons; and 3) striking reductions of NADPHd-stained processes within primary vagal projection fields ipsilateral to unilateral nodose ganglionectomy. A central origin of NADPHd-stained processes in NTS-X was identified in the medial parvicellular subdivision of the paraventricular hypothalamic nucleus. We conclude that NO of peripheral and central origin may modulate viscerosensory signal processing in the NTS-X and autonomic reflex function.

Afferent Pathways↗
PubMed1983

Central autonomic effects of dermorphin in conscious rats.

Central cardiovascular and respiratory effects of dermorphin were studied in conscious rats. Intracerebroventricular administration (0.1 or 1 nM) of dermorphin increased the systolic and diastolic blood pressure whereas a high dose (50 nM) decreased blood pressure. Dermorphin at 1 nM increased respiratory rate but caused hypoxia, acidosis and hypercapnia; at 50 nM, respiratory rate was suppressed. Both of these doses produced catalepsy. Stimulation of the sympathoadrenomedullary axis at the pressor period elicited by 1 nM dermorphin was evident by high circulating levels of epinephrine and norepinephrine. N-methyl-atropine reversed the severe bradycardia induced by dermorphin and completely prevented this phenomenon if given as pretreatment. Neither blood pressure nor respiratory depression was altered by the muscarinic blocker. Naloxone (1 mg/kg) reversed the respiratory, cardiovascular and sympathetic effects of dermorphin as well as the catalepsy. These data show that dermorphin has central autonomic effects which are naloxone reversible and mediated by both sympathetic and parasympathetic pathways.

Animals↗
PubMed2001

Immunohistochemical profiles of spinal lamina I neurones retrogradely labelled from the nucleus tractus solitarii in rat suggest excitatory projections.

Three morphologically distinct types of lamina I neurones, fusiform, flattened and pyramidal, project from the spinal cord to the caudal part of the nucleus tractus solitarii in the rat, and may represent a pathway whereby peripheral stimuli can modify autonomic functions. The neurochemistry of these three types of projection neurones was investigated using retrograde neuronal tracing with cholera toxin B-subunit combined with dual and triple immunofluorescence labelling for different neuroactive substances. None of the lamina I neurones with immunoreactivity for GABA or glycine were found to project to the nucleus tractus solitarii, whereas high levels of glutamate immunoreactivity, which may indicate a glutamatergic phenotype, were found in 18.4% of fusiform, 9.6% of pyramidal and 2.1% of flattened projection neurones. Immunoreactivity for calbindin-D28K was present in 34.9% of fusiform cells, 18.3% of pyramidal cells and 10.5% of flattened cells, and nitric oxide synthase immunoreactivity was detected in 13.8% of fusiform cells, 1.1% of pyramidal cells and 4.2% of flattened cells that had projections to the nucleus tractus solitarii. Calbindin immunoreactivity was co-localised in major subpopulations of projection neurones of each morphological type that contained glutamate immunoreactivity, whereas co-localisation of nitric oxide synthase immunoreactivity in these neurones was relatively uncommon. The pyramidal cell was the only retrogradely labelled cell type found to be immunoreactive for substance P, but few (<5%) of these neurones were immunolabelled. These data are consistent with the hypothesis that lamina I neurones projecting to the dorsal vagal complex are not inhibitory, and that some of them, belonging mostly to the fusiform and pyramidal types, may exert excitatory, glutamate- or substance P-mediated effects upon inhibitory interneurones in the nucleus tractus solitarii. Such excitatory pathways could be involved in the attenuation of the reflex control of blood pressure by both painful and innocuous peripheral stimuli, such as those arising in injury and exercise.

Afferent Pathways↗
PubMed2000

Neurotransmission of autonomic components of aortic baroreceptor afferents in the NTS of awake rats.

The effect of sequential blockade of N-methyl-D-aspartic acid (NMDA) receptors with DL-2-amino-5-phosphonopentanoic acid (AP-5) and non-NMDA receptors with 6,7-dinitroquinoxaline-2,3 dione (DNQX) in the nucleus tractus solitarii (NTS) on the cardiovascular responses to electrical stimulation (ES) of the aortic depressor nerve (ADN) was evaluated in awake rats. Two protocols were used. In protocol 1, bilateral microinjection of AP-5 into the NTS (n = 7) reduced the hypotensive response to ES of the ADN; subsequent microinjection of DNQX produced additional reduction in this response. AP-5 reduced the bradycardic response, and DNQX almost abolished this response. In protocol 2, bilateral microinjection of DNQX into the NTS (n = 6) reduced the hypotensive response, and subsequent microinjection of AP-5 significantly reduced this response. DNQX produced a significant reduction in bradycardic response, and AP-5 abolished this response. The data indicate that processing of the parasympathetic component of the NTS aortic baroreceptor afferents is mediated by both NMDA and non-NMDA receptors, whereas processing of the sympathoinhibitory component seems to be only partially mediated by ionotropic receptors.

Afferent Pathways↗
PubMed1986

The development and pathogenesis of the sensory neuropathy in the mutant rat mf.

A study was made of the development of sensory pathways in the mutant rat mutilated foot (mf) which is affected by a sensory neuropathy with autosomal recessive inheritance. Microscopic abnormalities are well recognizable at the fifteenth embryonic day. By day 16, dorsal root ganglia are smaller than normal and show more numerous foci of cell necrosis which continue throughout the remainder of gestation and during the first and second postnatal days. During this period the number of ganglion cells decreases sharply. Reconstruction of cell volumes shows that the larger cells are more severely affected. The secondary sensory nuclei (gracile nuclei) are normal at birth but during the first two postnatal weeks become progressively smaller than in normal rats. The results suggest that the mutant gene acts primarily on the dorsal root ganglia causing excessive neuronal cell death. Qualitatively, the events in this mutant are closely similar to 'programmed cell death' in the normal. It is likely that neurons of second order nuclei, which are not contacted by afferent fibres, undergo a process of transneuronal degeneration as a secondary effect of excessive ganglion cell loss.

Animals↗
PubMed1994

Effects of monosodium glutamate (umami taste) with and without guanosine 5'-monophosphate on rat autonomic responses to meals.

Monosodium glutamate (MSG) is used as a food additive to improve the taste of food. The effect of MSG on sweet taste is enhanced by guanosine 5'-monophosphate (GMP). Because increased palatability is known to increase the vagally mediated preabsorptive insulin response (PIR), we hypothesized that MSG and GMP will enhance the PIR. To study this, male Wistar rats were provided with permanent cannulas for venous blood sampling and intragastric drug administration. The MSG and GMP were either added to a test meal or infused into the stomach during a test meal. Blood samples were taken to measure concentrations of glucose, insulin, epinephrine (E), and norepinephrine (NE). Addition of 56 mg MSG to a control meal markedly reduced both phases of the meal-induced increase in plasma insulin and had no effects on blood glucose and plasma E and NE responses. Infusion of 56 mg MSG into the stomach at the onset of food intake reduced the PIR with no effect on glucose, E, NE, or the second phase insulin release. Addition of 2 mg MSG in combination with GMP to the test meal or gastric administration of these drugs did not affect the changes in any of the blood components measured. It is concluded that addition of a high dose of MSG to a test meal leads to a reduction in the vagal response to food.

Administration, Oral↗
PubMed1984

The organization of projections from the central nucleus of the amygdala to brainstem sites involved in central autonomic regulation: a combined retrograde transport-immunohistochemical study.

The central nucleus of the amygdala (ACe) in the rat sends a considerable projection to, and receives projections from, the parabrachial nucleus (PB) and the dorsal vagal complex (DVC; the nucleus of the solitary tract and the dorsal motor nucleus of the vagus nerve). In each part of this 'triangle', immunohistochemical staining for the following peptides has been observed in perikarya and fibers: neurotensin, somatostatin, substance-P, Leu-enkephalin and corticotropin-releasing factor. The aim of the present study was to investigate whether any of these peptides are involved in projections to the brainstem from the ACe, and to characterize the distribution of each cell type in the ACe. The results of double retrograde tracing studies indicate that most of the ACe neurons projecting to the PB and DVC are present in the medial part of ACe (ACem), and that many of them project to both the 1 B and the DVC. The combined use of immunohistochemistry with a retrograde fluorescent tracer, True Blue, indicated that the peptide-containing perikarya are found predominantly in the lateral part of ACe (ACe1), and that only a small proportion of neurotensin, somatostatin and corticotropin-releasing factor-stained neurons contained True Blue after injections into the PB or the DVC. The results suggest that most of the fibers in the descending projection from the ACe to the brainstem do not contain the peptides examined here.

Afferent Pathways↗
PubMed1991

Stress--mechanisms of immunosuppression.

Stress, a term commonly used to describe varied phenomena, should be restricted to describe an adaptive response by an animal to threats to homeostasis. The threats to homeostasis are called stressors. Stressors include a variety of physical, psychological, chemical, or infectious causes that are modified by intrinsic and extrinsic factors. Examples of modifiers include stressor severity, duration, novelty, host genetics and immune status. What may be a stressor to an animal in one situation, when modified, may not be a stressor in another situation. Mechanisms of stress once thought to involve a single pathway described by Seyle as the General Adaptation Syndrome, have been rejected. Four pathways, some incompletely defined, have been implicated in modulation of the immune system. They include autonomic nervous system, the hypothalamic adrenal axis, extra-adrenal pathways involving neuropeptides and neurotransmitters and neuroimmunological mediators. The mechanisms of stress-induced immunosuppression resistance are poorly defined in domestic fowl and will require careful experimentation linking defined stressors with altered physiological responses that affect specific immune function and result in increased disease susceptibility.

Adaptation, Physiological↗