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PubMed1993

Luminal adrenergic agonists modulate ileal transport by a local mechanism.

Intestinal transport is controlled by neural pathways, hormones, and luminal agents. Luminal adrenergic agents influence water and ion transport in the jejunum. This study tested two hypotheses: (i) luminal adrenergic agents influence ileal water, ion and glucose transport, and (ii) luminal adrenergic agents exert their effects locally and selectively. Absorption studies (n = 46) were performed on dogs with two adjacent 25-cm ileal Thiry-Vella fistulas (TVF). Perfusion with [14C]polyethylene glycol was used to calculate absorption of water, ions, and glucose from the distal TVF. Experiments were composed of three 1-hr periods: basal, luminal adrenergic agonist infusion, and recovery. In group 1 the adrenergic agonists were administered to the distal TVF: norepinephrine (alpha 1 > alpha 2 and beta), phenylephrine (alpha 1), clonidine (alpha 2), and isoproterenol (beta). In group 2 the adrenergic agonists were administered to the proximal TVF, with absorption measured in the distal TVF. In group 1 norepinephrine and phenylephrine caused a significant increase in water absorption (P < 0.05). Clonidine and isoproterenol caused decreased absorption of water and ions, with clonidine causing significantly decreased absorption (P < 0.05) of water, ions, and glucose. In group 2 there were no changes in distal TVF absorption. Luminal adrenergic agents did not alter the heart rate in either group. Luminal adrenergic agonists modulate ileal transport via a local mechanism. A proabsorptive response is observed with alpha 1 agonists, while alpha 2 and beta agonists cause a prosecretory effect. Inhibition of glucose absorption appears to be selectively mediated via the alpha 2-adrenergic receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Cholinergic agents modulate transport in the isolated, perfused ileum.

The mammalian small intestine is extensively innervated by cholinergic nerve fibers, including projections to the muscular and submucosal layers. This study tested the hypothesis that cholinergic agents modulate ileal transport independent of alterations in intestinal vascular resistance and motility. Ten-centimeter segments of rabbit ileum (n = 32) were vascularly perfused ex vivo with a physiologic electrolyte solution containing red cells. The lumen was perfused with an electrolyte solution containing [14C]polyethylene glycol. Net fluxes of water, sodium, and chloride were calculated during three 20-min periods: basal, drug infusion, and recovery. Agents infused at a final arterial concentration of 10(-5) mole/liter included acetylcholine, atropine, and hexamethonium. Measured perfusion pressure reflected changes in vascular resistance. Recovery calculations controlled for motility effects. Acetylcholine caused significant secretion of water, sodium, and chloride (P < 0.05). The infusion of atropine or hexamethonium alone had no effect. Atropine but not hexamethonium prevented the prosecretory effect of acetylcholine. There were no significant changes in perfusion pressure or 14C recovery for any infused agent. Acetylcholine-induced ileal secretion is (1) mediated via atropine-sensitive muscarinic cholinergic receptors, (2) independent of extraintestinal neural pathways, and (3) independent of changes in vascular resistance or motility. These data support the hypothesis that acetylcholine influences ileal transport directly, independent of alterations in vascular resistance and motility.

Acetylcholine↗

PubMed2002

A yeast artificial chromosome containing the human preprotachykinin-A gene expresses substance P in mice and drives appropriate marker-gene expression during early brain embryogenesis.

We have produced a yeast artificial chromosome (YAC) transgenic model containing the human preprotachykinin-A gene (hPPTA) that can drive appropriate expression of beta-galactosidase within the adult mouse brain. Here, we investigate its embryonic expression to assess the transcriptional regulation of the PPTA gene during the development of several neural pathways later affected by disease in humans. We demonstrate that the human PPTA gene regulatory region is active in appropriate areas of the developing brain at significantly earlier time points than has been previously reported. Furthermore, despite replacement of most of the 3' untranslated region by the marker gene cassette, the modified human YAC is able to express substance P (SP) on a murine SP/NKA(-/-) background. This transgenic model, in addition to being valuable in examining the hPPTA regulatory region, will also prove to be important in exploring the downstream function of the gene in the adult and the embryo brain.

Amygdala↗

PubMed2002

In vivo neuronal tracing with GFP-TTC gene delivery.

The retrograde transport and transynaptic transfer properties of the nontoxic tetanus toxin C-fragment (TTC) can be used to visualize specific neural pathways or to deliver biomolecules in the central nervous system (CNS). Here we tested different delivery techniques to explore the potential use of a new GFP-TTC fusion construct for use as a genetic tracer in vivo. Plasmids encoding GFP-TTC were targeted to brain regions using intracerebral grafted transfected cells or adenoviral transduction. Transport was monitored using GFP fluorescence. We show that following GFP-TTC synthesis in grafted transfected cells, the TTC fragment alone, with no signal peptide, is necessary and sufficient to provide secretion and uptake of the fusion protein into neighboring neurons around the injection site. Using an adenoviral vector to express the fusion protein into brain neurons, we show that transduced neurons can deliver the fusion protein specifically into connected neurons, demonstrating that synaptic transfer in the CNS can be visualized with GFP-TTC.

Animals↗

PubMedDate not supplied

Overview of neural mechanisms in asthma.

There is much evidence that neural mechanisms are involved in the mechanisms and symptoms of asthma. Afferent nerves may be activated and sensitized by inflammatory mechanisms, resulting in symptoms such as cough and chest tightness, in activation of cholinergic reflexes and in the release of inflammatory neuropeptides. Cholinergic mechanisms are the predominant bronchoconstrictor neural pathway and may be enhanced in asthma, particularly during exacerbations, through several mechanisms, including impaired function of muscarinic autoreceptors on cholinergic nerve terminals. There may also be abnormalities in adrenergic control and in the function of beta-adrenoceptors, particularly in severe asthma. The neurotransmitter of bronchodilator nerves is now identified as nitric oxide and this mechanism may be impaired during asthma exacerbations. Finally, neurogenic inflammation, due to release of neuropeptides from sensory nerves, may contribute and amplify the inflammation in asthmatic airways.

Animals↗

PubMed1998

Retrograde transport of intact poliovirus through the axon via the fast transport system.

Intramuscularly inoculated poliovirus is thought to spread to the central nervous system through neural pathways in humans, monkeys, and the transgenic (Tg) mice carrying the human poliovirus receptor (PVR) gene. To gain insight into molecular mechanisms for the retrograde axonal transport of poliovirus, resulting in the expression of neurovirulence, a poliovirus-sensitive ICR-PVRTg21 mouse line (Tg21) was used as an animal model for poliomyelitis. We detected poliovirus antigens in axons of the sciatic nerve. All of the Tg21 mice, which had been inoculated into the calves with 1 x 10(6) pfu of the Mahoney strain of type 1 poliovirus, showed symptoms of paralysis in the inoculated limbs (initial paralysis) within 48 h after the inoculation. The appearance of this initial paralysis was observed in mice whose sciatic nerves were transected at various times after virus inoculation. The results were indicators of the velocity of poliovirus transportation through the sciatic nerves under analysis. Poliovirus-related materials recovered from the sciatic nerve were mainly composed of intact 160S virion particles. The amount of 160S particle recovered was greatly reduced by coinjection with anti-PVR monoclonal antibody. These results suggest that one of the fast retrograde axonal transport systems is involved in poliovirus dissemination through the sciatic nerve and that IM-inoculated poliovirus is incorporated into the sciatic nerve as intact particles in a PVR-dependent manner, as it is in humans.

Animals↗

PubMed2002

Reflex mechanisms for motor impairment in spinal cord injury.

Spasticity is common feature of human spinal cord injury. It contributes to motor impairment and it also promotes joint deformity in patients who have sustained such injury. The classical definition of spasticity highlights the increased resistance of a joint to externally imposed motion. This resistance is attributable largely to changes in stretch reflex excitability, and it is manifested primarily in those muscles being stretched by the motion. Under this definition, there would be little activity in muscles crossing other joints. In spinal cord injury, however, muscles innervated from distal spinal segments often exhibit little hypertonia, yet patients report the occurrence of disabling spasms. These spasms appear as coordinated patterns of muscle activation throughout the limb, involving either limb flexors or extensors. These patterns are therefore quite different from those of classical spasticity. The receptor origins and neural pathways responsible for the spasms in spinal cord injury will be addressed.

Electric Stimulation↗

PubMed2000

Pharmacology of appetite suppression.

Despite a rising worldwide epidemic of obesity there is currently only a very small number of anti-obesity drugs available to manage the problem. Large numbers of differing pharmacological agents reliably produce a reduction in food intake when administered acutely to animals, and when administered chronically they result in a significant decrease in body mass. Behavioural analysis of drug-induced anorexia in animals demonstrates that various compounds profoundly effect feeding behaviour in differing ways. This indicates the variety of mechanisms by which pharmacological agents can induce changes in food intake, body weight and eventually body composition. Some of the same drugs produce decreases in food intake and weight loss in humans. Some of these drugs do so by modifying the functioning of the appetite system as measured by subjective changes in feelings of hunger and fullness (indices of satiety). Such drugs can be considered as "appetite suppressants" with clinical potential as anti-obesity agents. Other drugs induce changes in food intake and body weight through various physiological mechanisms inducing feelings of nausea or even by side effect related malaise. Of the drugs considered suitable candidates for appetite suppressants are agents which act via peripherally satiety peptide systems (such as CCK, Bombesin/GRP, Enterostatin and GLP-1), or alter the CNS levels of various hypothalamic neuropeptides (NPY, Galanin, Orexin and Melanocortins) or levels of the key CNS appetite monoamine neurotransmitters such as serotonin (5-HT) and noradrenaline (NA). Recently, the hormone leptin has been regarded as a hormonal signal linking adipose tissue status with a number of key central nervous system circuits. The peptide itself stimulates leptin receptors and it links with POMC and MC-4 receptors. These receptors may also provide drug targets for the control of appetite. Any changes induced by a potential appetite suppressant should be considered in terms of the (i) psychological experience and behavioural expression of appetite, (ii) metabolism and peripheral physiology, and (iii) functioning of CNS neural pathways. In humans, modulation of appetite may involve changes in total caloric consumption, subjective changes in feelings of hunger and fullness, preferences for specific food items, and general macronutrient preferences. These may be expressed behaviourally as changes in meal patterns, snacking behaviour and food choice. Within the next 20 years it is certain that clinicians will have a new range of anti-obesity compounds available to choose from. Such novel compounds may act on a single component of the appetite system or target a combination of these components detailed in this review. Such compounds used in combination with lifestyle changes and dietary intervention may be useful in dealing with the rising world epidemic of obesity.

Animals↗

PubMed2004

Motor evoked potential monitoring for spinal cord and brain stem surgery.

Intraoperative Neurophysiology (ION) has established itself as one of the means by which modern neurosurgery can improve surgical results while minimizing morbidity. The advent of motor evoked potential (MEP) monitoring represents a landmark in this recent progress. ION consists of monitoring (the continuous "on-line" assessment of the functional integrity of neural pathways) and mapping (the functional identification and preservation of anatomically ambiguous nervous tissue) techniques. In this chapter we have attempted to critically review the evolution of MEP use during monitoring and mapping techniques for neurosurgical procedures in the brainstem and the spinal cord, providing the neurophysiological theoretical background and practical aspects of clinical applications. According to the experience from our and other groups involved in ION, we suggest the following: 1) ION is mandatory whenever neurological complications are expected as predicted by a known pathophysiological mechanism. It is therefore advisable to perform ION when dealing with brain stem and intramedullary spinal cord lesions. 2) MEP monitoring after transcranial electrical stimulation is today a feasible and reliable technique for use under general anesthesia. MEP monitoring is the most appropriate technique to assess the functional integrity of descending motor pathways in the brainstem and, foremost, in the spinal cord. 3) Mapping of the corticospinal tract at the level of the cerebral peduncle as well as mapping of the VII, IX-X and XII cranial nerve motor nuclei on the floor of the fourth ventricle is of great value with which to identify "safe entry zones" into the brainstem. 4) Other techniques, although safe and feasible, still lack rigorous validation in terms of prognostic value and correlation with the postoperative neurological outcome. These techniques include mapping of the corticospinal tract within the spinal cord and monitoring of the corticobulbar tracts. These techniques, however, are expected to open new perspectives in the near future.

Adult↗

PubMed1995

The inhibitory modulation of guinea-pig intestinal peristalsis caused by capsaicin involves calcitonin gene-related peptide and nitric oxide.

The effect of capsaicin-induced stimulation of afferent neurons on peristalsis and the possible neural mediators involved in this action were examined in the guinea-pig isolated ileum. The intraluminal pressure threshold for eliciting peristaltic waves was used to quantify facilitation (decrease in threshold) or inhibition (increase in threshold) of peristalsis. Capsaicin (0.1-1 microM) caused an initial short-lasting stimulation of peristalsis followed by a prolonged inhibition of peristaltic activity. Capsaicin (1 microM) was ineffective when the gut segments had been pretreated with 3.3 microM capsaicin, which is indicative of an afferent neuron-dependent action of the drug. In contrast, the abolition of peristalsis caused by a high concentration of capsaicin (33 microM) was fully reversible on removal and reproducible on readministration of capsaicin, a feature characteristic of a nonspecific depression of smooth muscle excitability. Baseline peristalsis and the excitatory/inhibitory effect of capsaicin (1 microM) on peristalsis remained unaltered by a combination of the tachykinin NK1 receptor antagonist (+)-(2S, 3S)-3-(2-methoxybenzylamino)-2-phenyl piperidine (CP-99,994; 0.3 microM) and the tachykinin NK2 receptor antagonist (L(-)-N-methyl-N[4-acetylamino-4-phenyl-piperidine-2-(3,4- -dichlorophenyl)butyl]-benzamide (SR-48,968; 0.1 microM). Further experiments, performed in the presence of a low concentration of atropine (10 nM) showed that the calcitonin gene-related peptide (CGRP) antagonist human alpha-calcitonin gene-related peptide (8-37) [hCGRP(8-37); 10 microM] attenuated the delayed inhibitory effect of capsaicin on peristalsis, but did not influence baseline peristaltic activity and the capsaicin-induced facilitation of peristalsis. Blockade of nitric oxide (NO) synthesis by NG-nitro-L-arginine methylester (L-NAME, 300 microM) facilitated baseline peristaltic activity and reduced the delayed inhibition of peristalsis caused by capsaicin (1 microM) without affecting the initial peristalsis-stimulating action of capsaicin. The effects of L-NAME were prevented by L-arginine (1 mM). The data of the current study indicate that capsaicin-sensitive afferent neurons do not participate in the neural pathways subserving peristalsis in the guinea-pig small intestine, but modulate peristaltic activity upon stimulation with capsaicin. The initial stimulant action of capsaicin on peristalsis is independent of tachykinins acting via NK1 or NK2 receptors, while the delayed capsaicin-induced depression of peristalsis involves CGRP and NO.

Animals↗

PubMed1994

Synergistic role of muscarinic acetylcholine and tachykinin NK-2 receptors in intestinal peristalsis.

It is known that tachykinins (substance P, neurokinin A) participate in the excitatory neural pathways subserving peristaltic motor activity in the intestine. The aim of the present study was to elucidate the types of tachykinin receptor (NK-1 or NK-2) involved in peristalsis by the use of receptor subtype-selective antagonists. Peristaltic motility in isolated segments of the guinea-pig ileum was induced by pumping fluid into the oral end of the intestinal segment. By way of the intraluminal pressure the compliance of the intestinal wall during the preparatory phase and the pressure threshold to trigger the emptying phase of peristalsis were recorded. The tachykinin antagonists were used at concentrations that were at least 30 times in excess of the equilibrium dissociation constants which had previously been evaluated with receptor subtype-selective agonists on the guinea-pig ileum circular muscle. The NK-1 selective antagonist CP-96,345 (0.3 microM) had a slight stimulant influence on peristalsis, whereas the NK-2 selective antagonists MEN-10,376 (10 microM), GR-94,800 (0.3 microM) and SR-48,968 (0.1 microM) led to a small inhibition of motor activity. However, when given after exposure of the ileum to a threshold concentration of atropine (5-20 nM) causing little depression of peristalsis, the tachykinin NK-2 receptor antagonists invariably abolished peristalsis. This synergistic interaction was not seen when SR-48,968 was administered after the ileal segments had been exposed to concentrations of hexamethonium, isoproterenol or calcitonin gene-related peptide that by themselves caused a slight inhibition of peristalsis only.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Human auditory-evoked potentials before and after magnetic resonance imaging.

The effect of magnetic fields on auditory brainstem responses (ABRs) was examined under two conditions. The first involved recording ABRs before and immediately after magnetic resonance imaging (MRI). ABRs were then recorded as the static magnetic field was increased stepwise to 2T. No significant changes in ABR latencies were noted under either condition. These results indicate that MRI has no measurable effect on the transmission latencies of auditory brainstem neural pathways.

Adult↗

PubMed1994

Sound production evoked by electrical stimulation of the forebrain in the oyster toadfish.

In mammals, birds and amphibians the neural pathways controlling sound production descend from higher centers in the forebrain, whereas in fishes only brainstem and spinal centers have been explicitly implicated in sound production. We now report that electrical stimulation of the forebrain of the oyster toadfish (Opsanus tau) readily evokes both the agonistic grunt and the courtship boatwhistle. Boatwhistles are more realistic than ones previously evoked from lower centers. Positive stimulation sites are localized in the preoptic area (nucleus preopticus parvocellularis anterior) and the supra-commissural nucleus of the ventral telencephalon, a likely homologue of the amygdala. Both sites contain gonadal steroid-concentrating neurons and play a central role in fish courtship behavior. Evoked sounds form a continuum from knock grunts, burst grunts, transition boatwhistles to complete boatwhistles; sound pressure level (SPL), fundamental frequency and duration increase consistently within the continuum. For all sound types, SPLs exhibit the smallest variation (coefficients of variation of 2.7 to 5.7%), fundamental frequency is intermediate (5 to 13%) and durations vary most widely (18 to 60%). Boatwhistles, with the smallest variation and greatest amplitude, are likely generated by a maximal output of the CNS and sonic muscles. Grunt SPLs however, vary over a range of 26 dB for all fish and by as much as 18 dB in an individual; suggesting recruitment of variable numbers of motor units despite electrical coupling within the sonic motor nucleus.

Animals↗

PubMed1995

A single pair of interneurons controls motor neuron activity during pre-ecdysis compression behavior in larval Manduca sexta.

Manduca sexta molts several times as a larva (caterpillar) before becoming a pupa and then an adult moth. Each molt culminates in ecdysis behavior, during which the old cuticle is shed. Prior to each larval ecdysis, the old cuticle is loosened by pre-ecdysis behavior, which includes rhythmic, synchronous compressions of the abdomen. A previous study indicated that motor neuron activity during pre-ecdysis compression behavior is driven by an ascending neural pathway from the terminal abdominal ganglion. The present study describes a pair of interneurons, designated IN-402, that are located in the terminal ganglion and belong to the ascending pathway. Each IN-402 is synchronously active with pre-ecdysis compression motor bursts, and bilaterally excites compression motor neurons throughout the abdominal nerve cord via apparently monosynaptic connections. The pair of IN-402s appears to be the sole source of rhythmic synaptic drive to the motor neurons during the pre-ecdysis compression motor pattern. These interneurons play a key role in the production of larval pre-ecdysis behavior, and are candidates for contributing to the developmental weakening of pre-ecdysis behavior at pupation.

Animals↗

PubMed1987

Do conditioned taste aversions result from activation of emetic mechanisms?

The conditioned taste aversion (CTA) literature is extensive, yet little is known about the mechanisms by which treatments induce CTA. This paper describes and evaluates Garcia's hypothesis (e.g., Garcia et al. 1985) that treatments produce taste aversions by activating the receptors and neural pathways proposed by Borison and Wang (1953) to underlie emesis. Research on the mechanisms by which various treatments induce emesis is reviewed and compared with similar research on CTA. Emetic mechanisms appear to be involved appear to be involved in the formation of CTAs produced by some treatments, but there is contrary evidence for other treatments. This suggests that some CTAs are mediated by emetic mechanisms and others are not, so that Garcia's hypothesis is not generally correct. However, methodological and theoretical ambiguities make it premature to draw this conclusion.

Animals↗

PubMed1980

Photoperiod-dependent neural control of the activity of the neurosecretory canopy cell in the lateral lobes of the cerebral ganglia of the freshwater pulmonate Lymnaea stagnalis (L.).

In the lateral lobes of the cerebral ganglia of the pulmonate freshwater snail Lymnaea stagnalis (L.) one large neurosecretory canopy cell (CC) and two droplet cells (DC) are present. With the ganglion-transplantation technique and with quantitative electron microscopy it is shown that photoperiodic stimuli control the neurosecretory activity of the CC via a stimulatory extrinsic neural pathway. The eyes do not play an important role in this regulatory process. The neurosecretory activity of the DC is not affected by differences in photoperiod. The significance of the photoperiodic control of CC activity is discussed in relation to the pathway for the endocrine control of reproduction which is known to be photoperiod-dependent.

Animals↗

PubMed1987

Prolonged electrical stimulation of the nipples evokes intermittent milk ejection in the anaesthetised lactating rat.

Intermittent and continuous electrical stimulation of the nipples elicited milk-ejection responses in the lactating rat. The responses occurred intermittently, with similar amplitudes and periodicity as those seen in suckled rats. The responses were always associated with synchronization of the electroencephalogram (EEG), but some rats with synchronized EEG activity did not milk eject during stimulation. Since continuous stimulation also resulted in intermittent milk ejection it seems unlikely that the periodicity of the reflex in suckled rats depends upon changes in the intensity of sensory stimulation. The techniques of nipple stimulation may be a useful method with which to study neural pathways and other phenomena such as gating involved in oxytocin release and milk ejection. The success of the technique depends on a variety of factors such as parameters of the stimulation and state of anaesthesia.

Anesthesia↗

PubMed1982

ACTH and corticosterone secretion following insulin in intact and in variously hypothalamic deafferented male rats.

Adult male rats, intact (N) or with posterior (PHD), anterior (AHD) or complete (CHD) hypothalamic deafferentations, were injected with either 0.04 or 0.2 mu/100 g b.wt. of insulin. Forty-five minutes later they were decapitated and trunk blood was collected for serum glucose, adrenocorticotropic hormone (ACTH) and corticosterone (CS) determinations. The high insulin dose reduced serum glucose by approximately 50% and elicited a marked increase in serum ACTH and CS levels in all groups of animals as compared to the vehicle-treated group. In contrast, the low insulin dose which reduced serum glucose approximately 30% elicited a significant adrenocortical response only in the intact or PHD groups but failed to stimulate this response in animals with CHD or AHD. These results demonstrate that (1) CNS sites, outside the medial basal hypothalamus (MBH), mediate the adrenocortical response during the initial stages of hypoglycemia by a neural pathway impinging upon the CRF neurons from the rostral direction, and (2) the adrenocortical response during the more enhanced hypoglycemia stages is mediated by a systemic mechanism which acts directly on the MBH.

Adrenocorticotropic Hormone↗