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PubMed2003

Itch.

Itch is a common skin sensation, with substantial effects on behaviour. Neurophysiological research has permitted accurate definition of neural pathways of itch, and has confirmed the distinctiveness of itch pathways in comparison with pain. A clinical classification of itch, based on such improved understanding, describes the difference between peripheral (pruritoceptive) and central (neurogenic or neuropathic) itch. New specific and sensitive investigational methods in people and animals enable us to better understand this bothersome symptom, and have important clinical implications. We describe the clinical classification of itch, new findings on neuropathophysiology of itch, methods for assessment, and improved treatments.

Animals↗

PubMed2001

Corticosteroids in relation to fear, anxiety and psychopathology.

Corticosteroids play extremely important roles in fear and anxiety. The mechanisms by which corticosteroids exert their effects on behavior are often indirect, because, although corticosteroids do not regulate behavior, they induce chemical changes in particular sets of neurons making certain behavioral outcomes more likely in certain contexts as a result of the strengthening or weakening of particular neural pathways. The timing of corticosteroid increase (before, during or after exposure to a stressor) determines whether and how behavior is affected. The present review shows that different aspects of fear and anxiety are affected differentially by the occupation of the mineralocorticoid receptor (MR) or glucocorticoid receptor (GR) at different phases of the stress response. Corticosteroids, at low circulating levels, exert a permissive action via brain MRs on the mediation of acute freezing behavior and acute fear-related plus-maze behavior. Corticosteroids, at high circulating levels, enhance acquisition, conditioning and consolidation of an inescapable stressful experience via GR-mechanisms. Brain GR-occupation also promotes processes underlying fear potentiation. Fear potentiation can be seen as an adjustment in anticipation of changing demands. However, such feed-forward regulation may be particularly vulnerable to dysfunction. MR and/or GR mechanisms are involved in fear extinction. Brain MRs may be involved in the extinction of passive avoidance, and GRs may be involved in mediating the extinction of active avoidance. In the developing brain, corticosteroids play a facilitatory role in the ontogeny of freezing behavior, probably via GRs in the dorsal hippocampus, and their influence on the development of the septo-hippocampal cholinergic system. Corticosteroids can exert maladaptive rather than adaptive effects when their actions via MRs and GRs are chronically unbalanced due to chronic stress. Both mental health of humans and animal welfare is likely to be seriously threatened after psychosocial stress, prolonged stress, prenatal stress or postnatal stress, especially when maternal care or social support is absent, because these can chronically dysregulate the central MR/GR balance. In such circumstances the normally adaptive corticosteroid responses can become maladaptive.

Adrenal Cortex Hormones↗

PubMed2001

Neurogenic inflammation and particulate matter (PM) air pollutants.

Exposure to a class of airborne pollutants known as particulate matter (PM) is an environmental health risk of global proportions. PM is thought to initiate and/or exacerbate respiratory disorders, such as asthma and airway hyper-responsiveness and is epidemiologically associated with causing death in the elderly and those with pre-existing respiratory, or cardiopulmonary disease. Plausible mechanisms of action to explain PM inflammation and its susceptible sub-population component are lacking. This review describes a series of published studies which indicate that PM initiates airway inflammation through sensory neural pathways, specifically by activation of capsaicin-sensitive vanilloid (e.g. VRI) irritant receptors. These acid-sensitive receptors are located on the sensory C nerve fibers that innervate the airways as well as on various immune and non-immune airway target cells. The activation of these receptors results in the release of neuropeptides from the sensory terminals that innervate the airways. Their interactions with airway target cells, result in signs of inflammation (e.g. bronchoconstriction, vasodilation, histamine release, mucous secretion etc.). Our data have linked the activation of the VR1 receptors to the surface charge carried on the colloidal particulates which constitute PM pollution. Related studies have examined how genetic and non-genetic factors modify the sensitivity of these irritant receptors and enhance the inflammatory responsiveness to PM. In summary, this review proposes a mechanism by which neurogenic elements initiate and sustain PM-mediated airway inflammation. Although neurogenic influences have been appreciated in normal airway homeostasis, they have not, until now, been associated with PM toxicity. The sensitivity of the sensory nervous system to irritants and its interactions with pulmonary target tissues, should encourage neuroscientists to explore the relevance of neurogenic influences to toxic disorders involving other peripheral target systems.

Air Pollutants↗

PubMed1987

Hyperphagia resulting from gut denervation in the sea slug, Pleurobranchaea.

Previous research suggests that gut distension by ingested bulk plays an important role in the regulation of food intake in gastropod molluscs. The present study tested whether the bilateral stomatogastric nerves which innervate the esophagus and crop in Pleurobranchaea form a neural pathway carrying information about gut distension to the central nervous system. The posterior branches of the paired stomatogastric nerves were surgically exposed and sectioned in seven experimental animals while the nerves were simply exposed and not sectioned in seven sham-operated control animals. In three, subsequent, daily feeding sessions, the experimental subjects consumed a greater amount of food in terms of percentage of body weight than the control subjects. The experimental animals also gained a greater percentage of body weight and later were found to contain much more food within their guts. The results support the hypothesis that stretch receptors which innervate the gut and which have axons in the stomatogastric nerves form an important negative feedback pathway for the control of feeding in the sea slug.

Animals↗

PubMed2002

Cannabinoid analgesia.

During the last decade, rigorous scientific methods have been applied to determine the effects of cannabinoids on nociceptive neurotransmission. Cannabinoids have been observed to markedly decrease signalling in specific neural pathways that transmit messages about pain. These effects were found to be due to the suppression of spinal and thalamic nociceptive neurons, and independent of any actions on either the motor system or sensory neurons that transmit messages related to non-nociceptive stimulation. Spinal, supraspinal, and peripheral sites of cannabinoid analgesia have been identified. The discovery of endocannabinoids raised the question of their natural role in pain. Multiple lines of evidence indicate that endocannabinoids serve naturally to suppress pain. While it is now clear that cannabinoids suppress nociceptive neurotransmission, more work is needed to establish the clinical utility of these compounds. The few human studies conducted to date produced mixed results, with more promising findings coming from studies of clinical pain as compared with experimental pain. The therapeutic potential of cannabinoids remains an important topic for future investigations.

Analgesics↗

PubMed1997

Tachykinins in the gut. Part I. Expression, release and motor function.

The preprotachykinin-A gene-derived peptides substance P and neurokinin (NK) A are expressed in distinct neural pathways of the mammalian gut. When released from intrinsic enteric or extrinsic primary afferent neurons, tachykinins have the potential to influence both nerve and muscle by way of interaction with three different types of tachykinin receptor, termed NK1, NK2 and NK3 receptors. Most prominent among the effects of tachykinins is their excitatory action on gastrointestinal motor activity, which is seen in virtually all regions and layers of the mammalian gut. This action depends not only on a direct activation of the muscle through NK1 and/or NK2 receptors, but also on stimulation of excitatory enteric motor pathways through NK3 and/or NK1 receptors. In addition, tachykinins can inhibit motor activity by stimulating either inhibitory neuronal pathways or interrupting excitatory relays. A synopsis of the available data indicates that endogenous substance P and NKA interact with other enteric transmitters in the physiological control of gastrointestinal motor activity. Derangement of the regulatory roles of tachykinins may be a factor in the gastrointestinal dysmotility associated with infection, inflammation, stress and pain. In a therapeutic perspective, it would seem conceivable, therefore, that tachykinin agonists and antagonists are adjuncts to the treatment of motor disorders that involve pathological disturbances of the gastrointestinal tachykinin system.

Animals↗

PubMed2003

Evaluation of methods for eliciting somatosensory-evoked potentials in the awake, freely moving rat.

To standardise the method of eliciting somatosensory-evoked potentials (SEPs), SEPs were generated by electrical stimulation of different stimulus sites and recorded bilaterally from the primary somatosensory cortex (S1) and from midline in awake, freely moving rats. Increasing stimulus intensity enhanced amplitudes of all SEPs. At supramaximal stimulation, SEPs following vibrissae and tail stimulation (V-SEP and Ta-SEP, respectively) but not following trunk stimulation (Tr-SEP), fulfilled our criterion of signal-to-noise ratio >or=4. The first V-SEP component coincided with a stimulus artefact, disqualifying these recordings for a standard stimulation protocol. The Ta-SEP generated stable and reproducible recordings and was considered to be the preferred technique. Early components of the contralateral S1 recorded V-SEP and Tr-SEP occurred at latencies different from the other recordings. Increasing stimulus repetition rate (SRR) decreased amplitudes of all SEPs. At the highest obtainable SRR, the amplitude between the V-SEP second positive and second negative components in all recordings was 70-80% of the amplitude at 0.1 Hz, whereas peak amplitudes of subsequent components and those of the Tr-SEP and Ta-SEP were 20-50%. These results indicate that the different SEP components might be generated by different ascending neural pathways.

Animals↗

PubMed1997

Neurophysiological methods for studies of the motor system in freely moving human subjects.

In this paper, the following experimental methods for studies of the motor system in freely moving human subjects will be considered: (i) eliciting the H-reflex and understanding its use as a test response, (ii) methods to measure reciprocal inhibition between antagonist muscles, (iii) methods to measure presynaptic inhibition of Ia-afferent terminals in the spinal cord, (iv) certain aspects of the interpretation of peri-stimulus time histograms (PSTH) of single motor unit discharge, and finally, (v) stimulation of the motor cortex and the measurement of response parameters that may reflect task dependent changes. Two closely related ideas bearing directly on these methods will be emphasized--the influence of the background level of motor activity on input output properties of the neural pathway investigated and the operating point on the input-output curves at which the experimental variable is measured. Finally, in the discussion a simple model that is easily understandable in geometric terms is presented to help predict and interpret the outcome of these sorts of experiments.

Electromyography↗

PubMed2000

P2 receptors in the central and peripheral nervous systems modulating sympathetic vasomotor tone.

Arterial pressure depends on the level of activity of sympathetic vasoconstrictor outflow to blood vessels. This activity is generated in the central nervous system, and involves inputs from a variety of brain regions projecting to sympathetic preganglionic neurones. Of especial interest are a group of neurones in the rostral ventrolateral medulla (RVLM), as they have been demonstrated to have a fundamental role in reflex regulation of the cardiovascular system, and in generation of tonic drive to sympathetic outflow. Sympathetic outflow to blood vessels is additionally modulated at sympathetic ganglia, and at the peripheral terminals of sympathetic nerves. This review considers the role of P2 purine receptors in this neural pathway. Ionotropic P2X receptors are expressed in the RVLM, in sympathetic ganglia, and at the sympathetic neuromuscular junction, and mediate fast excitatory neurotransmission, indicating a general role for ATP as a regulator of sympathetic vasomotor tone. P2Y receptors couple to G proteins and mediate slower signalling to ATP; they have been reported to inhibit prejunctionally neurotransmission at the peripheral terminals of sympathetic nerves, but little is known about their possible role in the central nervous system and in sympathetic ganglia.

Adenosine Triphosphate↗

PubMed1997

Methods of sympathetic degeneration and alteration.

The role of the sympathetic nervous system in health and disease has often been elucidated by inducing changes in, or degeneration of sympathetic neural pathways. Several methods of inducing peripheral lesions have been created from surgical removal, NGF depletion, auto-immune and chemical destruction to novel approaches using immunotoxins and transgenic animals. This review compares these methods in terms of their mechanism and specificity. The advantages and disadvantages of these techniques are discussed.

Animals↗

PubMed1997

Esophageal distension induced gastric relaxation is mediated in part by vagal peripheral reflex mechanism in rats.

The effect of short-term lower esophageal distension on intragastric pressure (IGP) and the related neural pathways involved were investigated in urethane-anesthetized rats in which enteric nervous system connections were interrupted by ligations of the pylorus and the gastroesophageal junction while keeping the gastric vagus nerve trunks intact. Under these conditions, lower esophageal distension with a bolus of 0.2 to 0.5 ml saline in 0.1 ml step increments, raised the inside esophagus balloon pressure from 1.89 +/- 0.17 to 4.21 +/- 0.13 cm H2O and reduced IGP from -0.42 +/- 0.08 to -0.77 +/- 0.12 cm H2O, respectively. Bilateral cervical vagotomy partly blocked the gastric relaxation induced by 0.5 ml esophageal distension from -0.77 +/- 0.12 to -0.34 +/- 0.02 cm H2O; in contrast, a further bilateral splanchnectomy partly rebounded the effect of 0.5 ml esophageal distension from -0.34 +/- 0.02 to -0.46 +/- 0.05 cm H2O. These results suggest that the enteric nervous system may not play a prominent role in acute esophageal distension induced-gastric relaxation. However, more than 50% of this effect is central nervous system mediated (via the long vago-vagal reflex). The other 40% can be maintained without central and enteric nervous systems involvement, probably via a proposed gastric vagal afferent-esophageal collateral reflex.

Afferent Pathways↗

PubMed1997

Preliminary evidence for the evolution in complexity of heart rate dynamics during autonomic maturation in neonatal swine.

Previous studies suggest that the autonomic nervous system plays an important role in the generation of complex heart rate dynamics. Therefore, we hypothesized that the complexity (irregularity) of cardiac interbeat intervals would evolve with the maturation of autonomic innervation to the heart. Twelve healthy newborn piglets were implanted with ECG transmitters and studied at one or more different ages up to 33 days of age, the period during which pigs develop functional sympathetic innervation of the heart from the stellate ganglia. Three animals underwent right stellate ganglionectomy, two a left stellate ganglionectomy, two a right cardiac vagotomy and five a sham procedure. The statistic, approximate entropy (ApEn), was used to quantify the regularity of interbeat interval fluctuations. Sham-operated animals showed an increase in the standard deviation (SD) and irregularity (ApEn) of cardiac interval fluctuations with increasing age. Right stellate ganglionectomized piglets had lower interbeat interval ApEn values, but similar SD's by 26-27 days of age compared to sham-operated animals. Left stellate ganglionectomy, which affects cardiac inotropy rather than chronotropy, had no effect on cardiac interval irregularity, while vagotomy had an indeterminant effect. The increasing irregularity of interbeat interval dynamics during autonomic maturation and the apparent attenuation of heartbeat irregularity when right stellate ganglion innervation is interrupted, provides empirical support for the notion that complex heartbeat dynamics in the mature animal are the result of a network of autonomic neural pathways that enables an organism to adapt to stress.

Aging↗

PubMed2001

delta-opioid receptors inhibit neurogenic intestinal secretion evoked by mast cell degranulation and type I hypersensitivity.

Histamine and the mast cell degranulator, compound 48/80 produced elevations in short-circuit current, an electrical measure of active anion secretion, across porcine ileal mucosa sheets mounted in Ussing chambers. Luminally-applied beta-lactoglobulin produced similar effects in mucosal sheets from cow's milk-sensitized pigs. Their secretory effects were attenuated by blockers of H(1)-histamine receptors, neuronal conduction or epithelial Na(+)/K(+)/Cl(-) cotransport. The delta-opioid agonist [D-Pen(2), D-Pen(5)]enkephalin suppressed mucosal responses to these substances in a naltrindole-reversible manner. Furthermore, submucosal mast cells and delta-opioid receptor-immunoreactive nerve fibers were observed in close juxtaposition. Intestinal neural pathways linking immediate hypersensitivity to secretory host defense appear to express inhibitory delta-opioid receptors.

Animals↗

PubMed2002

Cytokine-induced sickness behaviour: mechanisms and implications.

Sickness behaviour represents the expression of the adaptive reorganization of the priorities of the host during an infectious episode. This process is triggered by pro-inflammatory cytokines produced by peripheral phagocytic cells in contact with invading micro-organisms. The peripheral immune message is relayed to the brain via a fast neural pathway and a slower humoral pathway, resulting in the expression of pro-inflammatory cytokines in macrophage-like cells and microglia in the brain. The cellular and molecular components of this previously unsuspected system are being progressively identified. These advances are opening new avenues for understanding brain disorders, including depression.

Animals↗

PubMed1997

Sensorimotor stimulation to improve locomotor recovery after spinal cord injury.

Functional recovery after CNS injury may depend, in part, upon reorganization of undamaged neural pathways. Spinal cord circuits are capable of significant reorganization, in the form of both activity-dependent and injury-induced plasticity. This plasticity is manifest behaviourally in the ability of spinal animals to learn new locomotor tasks. Recent work with spinal-injured humans demonstrates that training can improve functional locomotor abilities. New methodologies to enhance limb movement are designed to exploit further the plastic capabilities of the spinal cord by reinforcing appropriate connections in an activity-dependent manner. In the future, these methods might also prove useful in guiding and strengthening functional synaptogenesis of regenerating axons to maximize their contribution towards restoration of function.

Animals↗

PubMed1999

The dopamine hypothesis of reward: past and current status.

Mesolimbic dopaminergic neurons are thought to serve as a final common neural pathway for mediating reinforcement processes. However, several recent findings have challenged the view that mesolimbic dopamine has a crucial role in the maintenance of reinforcement processes, or the subjective rewarding actions of natural rewards and drugs of abuse. Instead, there is growing evidence that dopamine is involved in the formation of associations between salient contextual stimuli and internal rewarding or aversive events. This evidence suggests that dopaminergic-neuron activation aids the organism in learning to recognize stimuli associated with such events. Thus, mesolimbic dopaminergic neurons have an important function in the acquisition of behavior reinforced by natural reward and drug stimuli. Furthermore, long-lasting neuroadaptive changes in mesolimbic dopamine-mediated transmission that develop during chronic drug use might contribute to compulsive drug-seeking behavior and relapse.

Dopamine↗

PubMed2003

The dorsal raphe nucleus exerts opposed control on generalized anxiety and panic-related defensive responses in rats.

It has been proposed that the ascending dorsal raphe (DR)-serotonergic (5-HT) pathway facilitates conditioned avoidance responses to potential or distal threat, while the DR-periventricular 5-HT pathway inhibits unconditioned flight reactions to proximal danger. Dysfunction on these pathways would be, respectively, related to generalized anxiety (GAD) and panic disorder (PD). To investigate this hypothesis, we microinjected into the rat DR the benzodiazepine inverse receptor agonist FG 7142, the 5-HT(1A) receptor agonist 8-OH-DPAT or the GABA(A) receptor agonist muscimol. Animals were evaluated in the elevated T-maze (ETM) and light/dark transition test. These models generate defensive responses that have been related to GAD and PD. Experiments were also conducted in the ETM 14 days after the selective lesion of DR serotonergic neurons by 5,7-dihydroxytriptamine (DHT). In all cases, rats were pre-exposed to one of the open arms of the ETM 1 day before testing. The results showed that FG 7142 facilitated inhibitory avoidance, an anxiogenic effect, while impairing one-way escape, an anxiolytic effect. 8-OH-DPAT, muscimol, and 5,7-DHT-induced lesions acted in the opposite direction, impairing inhibitory avoidance while facilitating one-way escape from the open arm. In the light/dark transition, 8-OH-DPAT and muscimol increased the time spent in the lighted compartment, an anxiolytic effect. The data supports the view that distinct DR-5-HT pathways regulate neural mechanisms underlying GAD and PD.

5,7-Dihydroxytryptamine↗

PubMed2002

Facilitation of motor evoked potentials and H-reflexes of flexor carpi radialis muscle induced by voluntary teeth clenching.

In order to examine the effects of remote facilitation on cortical and spinal sites, we recorded motor evoked potentials (MEPs) and H-reflexes from the flexor carpi radialis muscle of 13 healthy subjects. The H-reflex was used to assess excitability changes at the spinal level, while the MEP following transcranial magnetic stimulation was used to study excitability changes at the cortical level. We induced remote facilitation by means of voluntary teeth clenching (VTC), the so-called Jendrassik maneuver, because this procedure is known to be effective and reliable. Although the facilitation induced by VTC was observed in both evoked potentials (i.e., H-reflex and MEP), which is consistent with previous reports, MEP onset latencies were shortened by VTC in proportion to an increased MEP amplitude, whereas the latencies of the H-reflex were not. Furthermore, statistically significant relationships between MEP latencies and amplitudes were observed in all subjects, whereas no such relationships were observed for the H-reflex. On the basis of these results, two neural pathways are presumed: one involving a release of pre-synaptic inhibition at the spinal level and the other involving an unmasking of lateral excitatory projections at the cortical level.

Adult↗