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PubMed1999

Small intensely fluorescent cells of the rat paracervical ganglion synthesize adrenaline, receive afferent innervation from postganglionic cholinergic neurones, and contain muscarinic receptors.

In the paracervical ganglion (PCG) of the rat, double-labelling immunofluorescence for catecholamine-synthesizing enzymes and HPLC measurement of catecholamine contents were first performed to evaluate whether intraganglionic small intensely fluorescent (SIF) cells are capable of synthesizing adrenaline. Immunolabelling for tyrosine hydroxylase (TH), dopamine beta-hydroxylase and phenylethanolamine-N-methyl transferase (PNMT) occurred in all SIF cells of the PCG, thus demonstrating the presence of all the enzymes required for adrenaline biosynthesis. Adrenaline levels were undetectable in the PCG but to test the hypothesis that PNMT is active in SIF cells, catecholamines were measured in ganglia of rats pretreated with pargyline, an inhibitor of the monoamine oxidase, the major enzyme involved in the catecholamine degradation. Pargyline treatment increased adrenaline levels in the PCG, thus demonstrating that SIF cells are capable of adrenaline synthesis. The undetectable levels of adrenaline in the PCG of untreated rats suggested a slow rate of biosynthesis of adrenaline in the ganglion. Furthermore, the use of double-labelling showed that SIF cells of the PCG were stained for muscarinic receptors and were approached by varicose ChAT-immunoreactive nerve fibres. Nerve fibres immunoreactive for ChAT were also observed associated with nerve cell bodies of ganglion neurones. Following deafferentation of the PCG, the ChAT-immunoreactive nerve fibres surrounding nerve cell bodies totally disappeared indicating their preganglionic origin, while those associated with SIF cells did not degenerate, which demonstrate that they derived from intraganglionic cholinergic neurones. Taken together, the results show that adrenaline may be a transmitter for SIF cells in the PCG and suggest that cholinergic neurones of the parasympathetic division of the PCG can modulate the SIF cell activity through the activation of muscarinic receptors.

Afferent Pathways↗
PubMed1999

Acute pain mechanisms.

The systems activated by tissue-injuring stimuli are complex. The nociceptive primary afferents have little spontaneous activity under normal conditions; however, after tissue injury, they display longlasting, ongoing activity. This results, in part, because the injury elicits the release of active factors that sensitize or excite the peripheral nerve terminal. A threshold that is lowered to the extent that body temperature and the pressure of edema are adequate stimuli results in spontaneous pain. This phenomenon is mediated by a variety of blood-borne active factors released during plasma extravasation, by agents released from local inflammatory cells, and by neurotransmitters released from the peripheral terminals of the primary afferent fibers themselves. Well-defined projections into the dorsal horn convey the "pain message" to at least two well-defined populations of neurons: those that are nociceptive specific and those that display an intensity-linked discharge over a range of stimuli from innocuous to noxious. Convergence from various fiber types, modalities, and end organs permits the encoding of afferent traffic with respect to intensity and location. The convergence of axons from somatic and visceral structures reflects the mechanism for the so-called "referred pain state." Most importantly, these dorsal horn systems have a dynamic component in addition to the hard-wiring; their output can be regulated both up and down. The up-regulation provides the basis for much of the facilitated processing that is believed to account for a significant percentage of the postinjury pain state. The facilitated state has a unique pharmacology, with the underlying mechanisms reflecting a cascade of actions that starts with the NMDA receptor and proceeds through the spinal release of intermediaries, such as prostaglandins and nitric oxide. Conversely, the ability to down-regulate the dorsal horn stimulus response function accounts for the powerful control exerted by a wide variety of diverse factors, including the spinal delivery of opioid and nonopioid analgesics and the "endogenous analgesia system." These linkages reflect the complexity of the encoding mechanisms that transduce the tissue injury into the behavioral sequela known as pain. This article also emphasizes that, although considerable progress has been made in the past decade, the current pace of research promises greater insights.

Afferent Pathways↗
PubMed1998

Influences of neck afferents on sympathetic and respiratory nerve activity.

It is well established that the vestibular system influences the sympathetic nervous system and the respiratory system; presumably, vestibulosympathetic and vestibulorespiratory responses participate in maintaining stable blood pressure and blood oxygenation during movement and changes in posture. Many brainstem neurons that generate vestibulospinal reflexes integrate signals from the labyrinth and neck muscles to distinguish between head movements on a stable body and whole body movements. In the present study, responses were recorded from the splanchnic (sympathetic), hypoglossal (inspiratory) and abdominal (expiratory) nerves during stimulation of the C2 dorsal root ganglion or C2 or C3 nerve branches innervating dorsal neck muscles. Stimulation of neck afferents using low current intensities, in many cases less than twice the threshold for producing an afferent volley recordable from the cord dorsum, elicited changes in sympathetic and respiratory nerve activity. These data suggest that head rotation on a stable body would elicit both cervical and vestibular inputs to respiratory motoneurons and sympathetic preganglionic neurons. The effects of cervical afferent stimulation on abdominal, splanchnic and hypoglossal nerve activity were not abolished by transection of the brainstem caudal to the vestibular nuclei; thus, pathways in addition to those involving the vestibular nuclei are involved in relaying cervical inputs to sympathetic preganglionic neurons and respiratory motoneurons. Transection of the C1-3 dorsal roots enhanced responses of the splanchnic and abdominal nerves to pitch head rotations on a fixed body but diminished responses of the hypoglossal nerve. Thus, neck and vestibular afferent influences on activity of respiratory pump muscles and sympathetic outflow appear to be antagonistic, so that responses will occur during whole body movements but not head movements on a stationary trunk. In contrast, neck and vestibular influences on tongue musculature are complementary, presumably to produce tongue protrusion either during movements of the head alone or of the whole body.

Afferent Pathways↗
PubMed2003

Matrix metalloproteinase inhibitors--an emphasis on gastrointestinal malignancies.

Gastrointestinal malignancies are the commonest sites of human cancer collectively. Improved understanding of tumour biology in the last few decades has allowed the identification of cellular pathways responsible for the autonomous growth and replication in cancer cells. There is considerable preclinical evidence implicating matrix metalloproteinases (MMPs) in cancer dissemination and tumour angiogenesis. Effective MMP inhibitors (MMPIs) may, therefore, hold an important key in the treatment of gastrointestinal cancers. MMPIs are cytostatic agents and traditional values of tumour regression may not be the best measures of treatment efficacy. Biological correlation studies are increasingly being incorporated into the early development of these agents, but many of these studies lack preclinical validation and are often chosen on availability rather than biological plausibility. Disappointing results with many MMPIs that have entered phase III testing so far would prompt for identification of reliable surrogate biomarkers and incorporation of functional imaging in the clinical development of matrix metalloproteinase inhibitors in gastrointestinal malignancies. In this review, the integral part in which MMPs are involved in cancer growth and metastases will be presented. This is then followed by a discussion of the challenges that clinicians are facing in assessing the efficacy of MMPIs and finally a review of the clinical studies of the synthetic MMPIs in development.

Gastrointestinal Neoplasms↗
PubMed1999

The electrical and magnetical cerebral responses evoked by electrical stimulation of the esophagus and the location of their cerebral sources.

OBJECTIVES: After electrical stimulation of the esophagus cerebral responses are recordable, their cortical source is under discussion. Brain mapping using electroencephalography recordings demonstrated partially controversial results. Sources of evoked responses can be localized more easily using magnetoencephalography than electroencephalography. METHODS: We examined 22 volunteers by recording electrical somatosensory potentials after electrical stimulation of the esophagus. In 9 of these 22 subjects additional recording of magnetic fields was performed and the sources of the evoked magnetic fields were computed. RESULTS: The evoked potentials after electrical stimulation of the esophagus had a similar latency as the previously published data. The source localization done by magnetoencephalography suggest that first a region of the postcentral gyrus is activated which is temporo-lateral to the primary somatosensory cortex of the pharynx. This region is suggested to be the primary somatosensory region of the esophagus. This source was followed by a source in the parietal operculum thought being part of the secondary somatosensory cortex. Simultaneously the insular cortex was activated pointing to a parallel neuronal pathway to the central autonomic nervous system. CONCLUSION: After electrical stimulation of the esophagus somatosensory cortical areas of the temporal postcentral gyrus and the operculum are activated. In parallel activation of the insular cortex as part of the central autonomic network was found.

Adult↗
PubMedDate not supplied

The pupillary and ciliary components of the cat Edinger-Westphal nucleus: a transsynaptic transport investigation.

The distribution of preganglionic motoneurons supplying the ciliary ganglion in the cat was defined both qualitatively and quantitatively. These cells were retrogradely labeled directly, following injections of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) into the ciliary ganglion, or were transsynaptically labeled following injections of WGA into the vitreous chamber. Almost half of the cells are distributed rostral to the oculomotor nucleus, both in and lateral to the anteromedian nucleus. Of the remaining preganglionic motoneurons, roughly 20% of the total are located dorsal to the oculomotor nucleus. Strikingly few of these neurons are actually found within the Edinger-Westphal nucleus proper. Instead, the majority are found in the adjacent supraoculomotor area or along the midline between the two somatic nuclei. An additional population, roughly 30% of the total, is located ventral to the oculomotor nucleus. This study also provides evidence for a functional subdivision of this preganglionic population. Pupil-related preganglionic motoneurons were transsynaptically labeled by injecting WGA into the anterior chamber, while lens-related preganglionic motoneurons were transsynaptically labeled by injecting WGA into the ciliary muscle. The results suggest that the pupil-related preganglionic motoneurons, that is, those controlling the iris sphincter pupillae muscle, are located rostrally, in and lateral to the anteromedian nucleus. In contrast, lens-related preganglionic motoneurons, that is, those controlling the ciliary muscle are particularly prevalent caudally, both dorsal and ventral to the oculomotor nucleus. Thus, the cat intraocular muscle preganglionic innervation is spatially organized with respect to function, despite the dispersed nature of its distribution.

Afferent Pathways↗
PubMed2001

Distribution and action of some putative neurotransmitters in the stomatogastric nervous system of the earthworm, Eisenia fetida (Oligochaeta, Annelida).

The chemical neuroanatomy of the stomatogastric nervous system of the earthworm, Eisenia fetida, has been investigated, using antibodies raised against serotonin, tyrosine hydroxylase, octopamine, GABA, FMRFamide, proctolin, Eisenia tetradecapeptide and neuropeptide Y. Neurons immunoreactive to these antibodies can be observed in the stomatogastric ganglia. The labelled cells comprise altogether 95.4% of the total number of neurons in the ganglion. Immunoreactive projections were followed between stomatogastric individual ganglia as well as towards the enteric plexus. Intrinsic neurons containing the different signal molecules examined are present along the entire length of the enteric plexus, but serotonin immunoreactive perikarya were only found in the hindgut. The density of the different immunoreactive neurons, except the serotonin ones, is highest in the pharyngeal plexus, and the number of labelled neurons decreases along the alimentary canal towards the hindgut. A number of epithelial cells also reveal tyrosine hydroxylase, octopamine, GABA and Eisenia tetradecapeptide immunoreactivity. The action of some putative neurotransmitters, such as dopamine, octopamine, serotonin and proctolin was tested on foregut preparations. Dopamine and octopamine (10(-6)-10(-4) M) have an excitatory effect on the musculature, whereas the effect of serotonin depends on the actual muscle tension. Following precontraction evoked by acetylcholine, serotonin in low concentrations (10(-7)-10(-6) M) causes relaxation, whereas in higher (10(-4) M) concentration it evokes slight contractions. In preparations at basal tone, serotonin (10(-7)-10(-6) M) evokes contractions of the foregut. Atropine strongly inhibits the action of acetylcholine but is ineffective against serotonin, dopamine and octopamine. Similarly, the Na+ channel blocker tetrodotoxin fails to influence the contractile effect of dopamine, octopamine and serotonin. These results suggest that dopamine, octopamine and serotonin act directly on the muscle cells of the alimentary tract. Proctolin do not evoke any significant effect on the foregut.

Animals↗
PubMed2006

Integrative control of the lower urinary tract: preclinical perspective.

Storage and periodic expulsion of urine is regulated by a neural control system in the brain and spinal cord that coordinates the reciprocal activity of two functional units in the lower urinary tract (LUT): (a) a reservoir (the urinary bladder) and (b) an outlet (bladder neck, urethra and striated muscles of the urethral sphincter). Control of the bladder and urethral outlet is dependent on three sets of peripheral nerves: parasympathetic, sympathetic and somatic nerves that contain afferent as well as efferent pathways. Afferent neurons innervating the bladder have A-delta or C-fibre axons. Urine storage reflexes are organized in the spinal cord, whereas voiding reflexes are mediated by a spinobulbospinal pathway passing through a coordination centre (the pontine micturition centre) located in the brainstem. Storage and voiding reflexes are activated by mechanosensitive A-delta afferents that respond to bladder distension. Many neurotransmitters including acetylcholine, norepinephrine, dopamine, serotonin, excitatory and inhibitory amino acids, adenosine triphosphate, nitric oxide and neuropeptides are involved in the neural control of the LUT. Injuries or diseases of the nervous system as well as disorders of the peripheral organs can produce LUT dysfunctions including: (1) urinary frequency, urgency and incontinence or (2) inefficient voiding and urinary retention. Neurogenic detrusor overactivity is triggered by C-fibre bladder afferent axons, many of which terminate in the close proximity to the urothelium. The urothelial cells exhibit 'neuron-like' properties that allow them to respond to mechanical and chemical stimuli and to release transmitters that can modulate the activity of afferent nerves.

Afferent Pathways↗
PubMed1987

Autocrine stimulation after transfer of the granulocyte/macrophage colony-stimulating factor gene and autonomous growth are distinct but interdependent steps in the oncogenic pathway.

Autocrine stimulation of cells by aberrant synthesis of growth factor may lead to malignant transformation, either as a direct consequence of endogenous factor production or as a first step of a series of successive events. Introduction of the granulocyte/macrophage colony-stimulating factor (GM-CSF) cDNA clone into a vector based on the myeloproliferative sarcoma virus allowed efficient transfer and expression of GM-CSF in factor-dependent myeloid cell lines (FDC-P1 and FDC-P2). Factor-independent growth was acquired when the vector was introduced into the GM-CSF-responsive FDC-P1 cell line but not the multi-CSF-dependent FDC-P2 line. Nonlinear clonability in the absence of exogenous growth factor and growth inhibition by GM-CSF antiserum support a model of autocrine stimulation that requires interaction of factor and receptor at the outer membrane. However, many, but not all, infected FDC-P1 cells acquired subsequently a second mutation that abrogated the requirement of GM-CSF secretion and external interaction. The nature of the second step, which presumably leads to tumorigenicity of these cells, is not well understood, but its frequency could be correlated with the level of GM-CSF released by an individual cell clone.

Animals↗
PubMed1996

Cross talk between cell death and cell cycle progression: BCL-2 regulates NFAT-mediated activation.

BCL-2-deficient T cells demonstrate accelerated cell cycle progression and increased apoptosis following activation. Increasing the levels of BCL-2 retarded the G0-->S transition, sustained the levels of cyclin-dependent kinase inhibitor p27Kip1, and repressed postactivation death. Proximal signal transduction events and immediate early gene transcription were unaffected. However, the transcription and synthesis of interleukin 2 and other delayed early cytokines were markedly attenuated by BCL-2. In contrast, a cysteine protease inhibitor that also blocks apoptosis had no substantial affect upon cytokine production. InterleUkin 2 expression requires several transcription factors of which nuclear translocation of NFAT (nuclear factor of activated T cells) and NFAT-mediated transactivation were impaired by BCL-2. Thus, select genetic aberrations in the apoptotic pathway reveal a cell autonomous coregulation of activation.

Apoptosis↗
PubMed2000

Review of immune function, healing of pressure ulcers, and nutritional status in patients with spinal cord injury.

The immune, neural, and endocrine systems do not act autonomously; rather, multiple communicative pathways exist among the nervous, endocrine, and immune systems that facilitate physiological immunoregulation. Patients with spinal cord injury (SCI) have decreased natural and adaptive immune responses by 2 weeks after injury. In patients with SCI, adrenocorticotropic hormone (ACTH) and urine-free cortisol levels were increased while zinc and albumin levels were decreased, respectively. In addition, the surface markers alpha 2, alpha 3, alpha 4, CD11a, CD11b, CD18, CD54, and CD8 found on lymphocytes and alpha 3, alpha 4, CD11a, CD18, and CD8 surface markers found on granulocytes were also decreased in the patient population. Finally, the adhesion molecules binding ability in the SCI group was also decreased when compared with a control group. Overall, the investigation showed that patients with SCI have a decreased immune function, especially succeeding the SCI injury, an impaired nutrition status, and a decreased number of adhesion molecules, all of which contribute to delayed wound healing.

Adult↗
PubMedDate not supplied

The spinocerebellar ataxias.

The spinocerebellar ataxias (SCAs) are diseases characterized by the progressive degeneration and subsequent loss of neurons accompanied by reactive gliosis, degeneration of fibers from the deteriorating neurons, and clinical symptoms reflecting the locations of the lost neurons. The degenerative changes affect specific neuronal groups while others remain preserved, and these diseases can therefore be viewed as system degenerations. The SCAs result from either genetically transmitted diseases with dominant inheritance or unknown causes with sporadic occurrence. Most of these disorders affect the cerebellum and its pathways, resulting in progressive deterioration of cerebellar function manifested by increasing unsteadiness of gait, incoordination of limb movements with impairment of skilled movements such as handwriting, and a distinctive dysarthria. Other neuronal systems are affected in some of these disorders, notably the corticospinal pathway, basal ganglia, and autonomic nuclei of the brain stem and spinal cord.

Humans↗
PubMed1980

Incessant reciprocating atrioventricular tachycardia. Factors playing a role in the mechanism of the arrhythmia.

The case of a patient suffering from incessant supraventricular tachycardia is presented. The electrophysiological study showed the presence of an accessory atrioventricular (A-V) bundle with nodal-like properties and long conduction times. This structure was used as the retrograde arm of the tachycardia circuit. Tachycardia was intermittent at rest, but had a sustained character during slight exercise. Administration of atropine and isoproterenol failed to sustain the arrhythmia and spontaneous initiation during sinus rhythm was no longer observed. During handgrip exercise a sustained tachycardia developed immediately. During ventricular stimulation a dual atrial response to a single paced ventricular premature beat was repeatedly observed, proving the availability of two separate A-V pathways for retrograde conduction. The case illustrates the labile nature of this type of accessory pathway, and suggests that autonomic changes can play an important role in the initiation, maintenance, termination, or even spontaneous cure of tachycardia in patients with this anomaly.

Atrioventricular Node↗
PubMed1997

The influence of cervical sympathetic neurons on parathyroid hormone and calcitonin release in the rat: independence of pineal mediation.

The objective of this study was to evaluate the involvement of the pineal gland in modulation of parathyroid hormone (PTH) and calcitonin release found in rats after changes in activity of cervical sympathetic nerves. The response of serum PTH to a hypocalcemia produced by EDTA injection, and of serum calcitonin to a hypercalcemia produced by administering calcium chloride, were studied in rats at the time of the wallerian degeneration of regional sympathetic nerves (i.e., 16 hr after superior cervical ganglionectomy, SCGx). Rats received a pinealectomy or its sham-operation 4 days before SCGx. During wallerian degeneration of nerves after SCGx, a higher hypocalcemia and a lower PTH response were found as compared to sham-SCGx rats, regardless of whether the pineal gland was present or not. When the response of calcitonin to a bolus injection of calcium chloride was assessed, rats subjected to SCGx 16 hr earlier showed a depressed calcitonin release, which was also unaffected after pinealectomy. To a similar extent in pinealectomized and sham-pinealectomized rats, a mild stress given by the subcutaneous injection of turpentine oil brought about a greater hypocalcemia after EDTA, concomitantly with a higher PTH secretory response. In turpentine oil-injected rats, the rise of serum calcitonin was significantly greater than that of vehicle-treated rats, regardless of pineal presence. The results further indicate that cervical autonomic nerves constitute a pathway through which the brain modulates calcium homeostasis and do not support the participation of the pineal gland in short term changes of PTH or calcitonin release.

Animals↗
PubMed1984

Effect of limb ischaemia on blood pressure and the blood pressure-heart rate reflex in the rat.

The effects of bilateral hind-limb ischaemia on blood pressure and on the blood pressure-heart rate reflex have been studied in the rat. Limb ischaemia increased blood pressure and decreased the elevation and slope of the regression line describing the relationship between heart period (H.P.) and mean arterial pressure (M.A.P.). Nociceptive afferents from muscle receptors using long fibre tracts in the anterolateral part of the spinal cord seem to be responsible for the changes seen. The changes in the blood pressure-heart rate reflex were mediated by a combination of vagal inhibition and sympathetic activation. The efferent pathway for the pressor effect was in the sympathetic outflow. Central catecholaminergic neurones were involved in the pressor effect of limb ischaemia but not in the changes in the blood pressure-heart rate reflex. Electrolytic lesions in the posterior hypothalamus attenuated the inhibition of the reflex and it is suggested that neurones in the defence area may be activated by limb ischaemia. The interaction between limb ischaemia and the H.P.-M.A.P. relationship was not affected by opioid antagonists. After the period of ischaemia there was an increase in the elevation of the regression line describing the relationship between H.P. and M.A.P. which was secondary to the fall in body temperature characteristic of this phase of the response to injury.

Afferent Pathways↗
PubMed1978

Studies on neural mechanisms of the gustatory-salivary reflex in rabbits.

1. Submandibular salivary secretion and the electrical activity of the parasympathetic preganglionic fibres innervating the submandibular gland were recorded in decerebrated rabbits in response to taste stimulation of the tongue. The electrical activity of a taste nerve (chorda tympani) responding to varying taste stimuli was also recorded in the deeply anaesthetized rabbits. These data representing input and output information were compared with each other. 2. Sucrose, quinine, tartaric acid, NH4Cl and KCl which induced a long-lasting response in the taste nerve evoked a continuous salivary secretion, and those chemicals such as NaCl, CaCl2 and MgCl2 which induced a transient activity of the nerve evoked a transient salivary secretion. 3. The magnitude of responses of the whole taste nerve to moderate concentrations of chemical stimuli applied to the anterior part of the tongue was statistically significantly correlated with the volume of reflex submandibular salivation. 4. Parasympathetic preganglionic fibres to the salivary gland were classified into two types according to their responsiveness to taste stimuli; taste-sensitive and taste-insensitive fibres. The magnitude of electrical activity of the taste nerve fibres was significantly correlated with that of the taste-sensitive preganglionic fibres to stimulation of the tongue with varying taste stimuli. 5. By calculating correlations between responses of the taste fibres to each of the four basic taste stimuli and all the stimuli tested, it was concluded that afferent inputs from the taste of sucrose and NaCl were different, while those of HCl and quinine were similar. On the other hand, it was found by the same procedure for the preganglionic fibres that sucrose and NaCl, and HCl and quinine produced a similar response profile, respectively. This result means that the afferent taste inputs are processed into appropriate outputs (perhaps on a hedonic basis) in the lower brain stem without involvement of higher central nervous mechanisms.

Action Potentials↗
PubMed1979

Nerve pathways in celiac plexus of the guinea pig.

In vitro preparations consisted of the right and left celiac, superior mesenteric and inferior mesenteric ganglia with attached extrinsic nerves, vasculature, mesentery, and colon. There were no systematic differences in membrane electrical properties (recorded intracellularly) between neurons in the different ganglia. Stimulation of associated nerve trunks produced graded synaptic responses in plexus neurons. Presynaptic fibers were found in splanchnic and mesenteric nerves. Input from celiac nerves dominated in the celiac galglia; input from the intermesenteric fibers dominated in the superior mesenteric ganglion. When the ganglia were attached to the entire colon, 33% of the neurons in the celiac and 54% in the superior mesenteric ganglion received a continuous excitatory synaptic input that was increased by distending the colon. This input was interrupted irreversibly by transsection of the mesenteric nerves. These results show that both the afferent and efferent pathways of a peripheral reflex arc are located in the mesenteric nerves and may mediate visceral reflexes between mechanoreceptors and sympathetic neurons in the colon.

Afferent Pathways↗