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At least 469 records · Page 26Linked to original sources
PubMed1989

Cholinergic neuromodulation by endothelin in guinea pig ileum.

The effect of endothelin on cholinergic neuroeffector transmission in guinea pig ileum was investigated. Endothelin was shown to inhibit the nerve-induced contractions and concomitantly to increase the basal muscle tone. Furthermore, endothelin inhibited the nerve-induced release of [3H]acetylcholine whereas the contractile response to exogenous acetylcholine was enhanced. In conclusion, our findings suggest that endothelin is a modulator of cholinergic neuroeffector transmission in guinea pig ileum with possible action via both inhibitory prejunctional and stimulatory postjunctional mechanisms.

Acetylcholine↗
PubMed1995

Nitric oxide is a neuromodulator in cat pancreatic ganglia: histochemical and electrophysiological study.

This study examined the distribution of NADPH-diaphorase (NADPH-d) activity in cat pancreatic ganglia and the electrophysiological effects of nitric oxide (NO) donors, NO and the effect of endogenously released NO. The majority (64%) of pancreatic ganglion neurons stained positive for NADPH-d. Large nerve trunks contained numerous non-varicose NADPH-d positive fibers. NADPH-d positive nerve fibers within individual ganglia were varicosed. L-Arginine, sodium nitroprusside and NO, applied in the vicinity of the impaled neuron, evoked a hyperpolarizing response and initiated fast excitatory postsynaptic potentials (EPSPs) in the majority of neurons tested. The hyperpolarizing response was not affected by low Ca2+ (0.1 mM), high Mg2+ (15 mM). Pretreatment with nitro-L-arginine increased the amplitude of slow EPSPs in about 50% of neurons tested. These results support the hypothesis that NO plays a role in ganglionic transmission in the cat pancreas.

Animals↗
PubMed1996

Neuromodulation of frontal and temporal cortex by intravenous d-fenfluramine: an [15O]H2O PET study in humans.

This study assessed the modulatory effect of a serotonergic agonist, d-fenfluramine, on localized neuronal firing as indexed by changes in regional cerebral blood flow (rCBF). Previously, we reported the effect of oral d, l-fenfluramine on neuronal activity as measured by change in [18F]fluorodeoxyglucose uptake. Improvements in the current study include: a more specific serotonin agonist, d-fenfluramine; a more reliable administration route, intravenous; and a one session paradigm made possible with the radiotracer [15O]H2O. Changes in relative rCBF (P < 0.001) were observed: increases within the frontal cortex bilaterally and decreases within the temporal cortex bilaterally, and left thalamus. Other significant findings were elevated cortisol and growth hormone; increased euphoria and panic symptoms and decreased tiredness. These results support further investigation with intravenous d-fenfluramine to study the net functional effects of serotonergic stimulation in health and illness.

Adult↗
PubMed1994

Neuromodulation in molluscan smooth muscle: the action of 5-HT, FMRFamide and purine compounds.

1. The RR, OR, RS and RP muscles of Buccinum did not respond directly to 5-HT, but this monoamine converted their normally tonic ACh responses to fast twitch contractions with lowered tonic force. This action was not accompanied by significant membrane potential changes. 2. Pre-treatment with dibutyryl cAMP potentiated ACh responses and enhanced 5-HT modification of the responses. 3. All muscles responded strongly to FMRFamide with twitch contractions but this was not accompanied by significant membrane potential changes. 4. FMRFamide enhanced ACh contracture force and converted the responses into fast twitch activity. FMRFamide responses were dramatically inhibited by 5-HT with loss of all tonic force and fast twitch activity. 5. While dibutyryl cAMP did not affect FMRFamide responses, the IP3 inhibitor lithium, at very high concentrations, caused a significant diminution of FMRFamide responses. 6. All four muscles were unresponsive to adenosine and ATP but all except the RP responded in a dose-dependent manner to GTP and GTP-gamma-S over the 10(-7) - 10(-4) mol l-1 range. The responses showed moderate fast twitch activity which was unaccompanied by action potential discharges. Guanosine was without effect, except at very high concentrations where it inhibited FMRFamide responses. 7. ACh and GTP acted additively to increase muscle force and to enhance ACh-induced depolarization. Similarly both GTP and GTP-gamma-S acted additively, considerably enhancing FMRFamide responses. 8. It is proposed that 5-HT, FMRFamide and GTP may, via their separate receptors or by possible interaction with ion channels, activate secondary messenger systems to modify the calcium released by ACh-induced depolarization to modulate excitation-contraction coupling and force generation in these muscles.

Acetylcholine↗
PubMed1988

Neuromodulation of hematopoiesis: a hypothesis.

The possibility that Hematopoiesis is under CNS control has been discussed in the literature; but never been conclusively proved at the molecular level. Evidence in the form of antigenic similarity between murine brain and the Stem Cell, and the decline in the number of Stem Cells following the lesioning of the Locus Coeruleus Nucleus exists. The recent establishment of the CNS control of the Immune System which had been previously proposed on similar evidence is discussed. It is suggested that the advances in the study of Colony Stimulating Factors (CSFs) provide an opportunity to test the role of Neurotransmitters on the proliferation/differentiation of Stem Cells. A series of experiments using CSF-dependent and CSF-independent cell lines and the biochemical basis of CSF activity to detect neurological influences are proposed. A model of a CNS regulatory mechanism is proposed, and used to explain many unexplained features of the in vivo activity of the CSFs.

Animals↗
PubMed1993

Insulin resistance syndrome: defective GABA neuromodulation as a possible hereditary pathogenetic factor (the 'GABA hypothesis').

The origin of the insulin resistance syndrome which, mostly through its cardiovascular implications, is characterized by a high incidence of death, is still practically unknown. Energy and glucose homeostasis are under the control of CNS centers and the neurotransmitter GABA modulates the activity of these centers. Alteration of the biochemical structure of GABA receptors is suggested as an interpretation of the origin of the syndrome.

Animals↗
PubMed1990

Neuromodulation of acute-phase responses to interleukin-6 in guinea pigs.

It is now generally recognized that interleukin-6 (IL6) is one of the cytokines that mediate the various nonspecific host defense responses to infectious pathogens. Among its now well-demonstrated effects on systemic administration are fever and acute-phase proteinemia. These effects are also activated by the cytokine, IL1, and it has been shown that they are modulated in the preoptic-anterior hypothalamus (POA). This study was undertaken to determine whether this brain region similarly drives the febrile and proteinemic responses to IL6. We compared, therefore, these responses of conscious guinea pigs to human recombinant (hr)IL6 administered intravenously (IV) and into the POA. hrIL6 given IV was not pyrogenic at 1 microgram/kg, caused low-grade, dose-independent fevers (0.4 +/- 0.1 degree C) at 5-20 micrograms/kg, and dose-related fevers at 50 and 100 micrograms/kg (0.6 +/- 0.0 and 0.9 +/- 0.1 degree C, respectively). However, all doses of hrIL6 induced elevations in the plasma levels of ceruloplasmin (as an indicator of acute-phase proteins), albeit not in a dose-dependent manner. Indomethacin (10 mg/kg, injected intramuscularly 20 min before hrIL6) abolished the febrile response, but did not prevent the rise in plasma ceruloplasmin levels. Fever and ceruloplasminemia were also evoked by 50 and 100 ng of hrIL6 injected into the POA (1 microliter bilaterally), but not by 25 ng. These results indicate that the inductions of fever and plasma ceruloplasmin by IL6 are, like those of IL1, modulated in the POA, albeit the effective doses are much higher than those of IL1.

Acute-Phase Reaction↗
PubMed1991

Neuromodulation of fever: apparent involvement of opioids.

It was recently reported that the opiate antagonist, naloxone (Nal), blocks the changes induced by the endogenous pyrogen, interferon-alpha 2 (IFN), in the electrical activity of hypothalamic thermosensitive neurons in rat brain slice preparations. This study was undertaken to determine whether the pyrogenic response to this cytokine might, therefore, be modulated through Nal-reversible opiate receptors. To examine this possibility, conscious guinea pigs were injected IV with recombinant human (rh) IFN (10 MU/animal), or, for comparison, with S. enteritidis endotoxin (lipopolysaccharide, LPS; 2 micrograms/kg), rh tumor necrosis factor-alpha (TNF; 20 micrograms/kg), or rh interleukin-6 (IL6; 50 micrograms/kg); Nal (10 mg/kg, SC) was administered immediately before the pyrogens. And also for comparison, in separate experiments, indomethacin (Indo; 10 mg/kg, IM) was injected 20 min before the pyrogens. Both Nal and Indo abolished the febrile rises evoked by IFN, TNF, and IL6. Nal reduced the first and suppressed the second of the characteristically bimodal febrile response to LPS; Indo depressed both peaks. Neither blocker had any significant thermal effect by itself. These results suggest that two processes may mediate the pyrogenic effects of these substances, viz., an endogenous opioid- and a PGE-dependent mechanism.

Animals↗
PubMed1992

Neuromodulation of vertebrate motor neuron membrane properties.

The short-term function of motor neurons is to integrate synaptic inputs converging onto the somato-dendritic membrane and to transform the net synaptic drive into spike trains. A set of voltage-gated ion channels determines the electro-responsiveness and thereby the motor neuron's input-output function. In addition, several of the decisive ion channels are transmitter controlled, which results in a flexible control of the input-output relationship.

Animals↗
PubMed1993

Aromatase: neuromodulator in the control of behavior.

Estrogens are required for both the organization of the brain in early development and adult behavior. Two approaches have been used in our laboratory to study the behavioral role of brain aromatase. First, brain metabolism of testosterone (T) has been related to behavior in the same individual using a well established neuroendocrine model, the ring dove, in which estradiol-17 beta (E2) has specific effects on brain mechanisms of male behavior. Aromatase in preoptic area (POA) (a) has a high activity (Vmax) and strong substrate binding affinity (Km < 5 nM), (b) is regulated by both androgens and estrogens, and the type of regulation differs according to brain area, (c) is influenced by products of an endogenous inactivating pathway, 5 beta-reduction; 5 beta-dihydrotestosterone and other 5 beta-reduced metabolites appear to be non-genomic regulators of the brain aromatase. Preoptic aromatase activity is also influenced by photoperiod and socio-sexual stimuli. The codistribution of regulated aromatase activity and estrogen receptor cells is found to be T-dependent. Our second approach has been to relate the aromatase system to developmental sex differences in brain structure and behavior of the Mongolian gerbil. Neonatal gerbil aromatase is relatively active in the POA, but has a weaker T substrate-binding affinity (Km = 30 nM) than the dove. T acting via its metabolite, E2, masculinizes the sexually dimorphic area of the hypothalamus; the differentiating effect is asymmetric. We suggest that the regulation of the brain aromatase system may be lateralized during steroid-sensitive periods of development.

Animals↗
PubMed2004

Topiramate-induced neuromodulation of cortico-mesolimbic dopamine function: a new vista for the treatment of comorbid alcohol and nicotine dependence?

Alcohol and nicotine dependence are commonly occurring disorders that together represent the most important preventable causes of morbidity and mortality in the United States. While there have been differences of opinion as to which disorder to treat first when they occur, there is growing evidence that a management strategy addressing both conditions contemporaneously would be optimal. Advances in the neurosciences have demonstrated not only that the reinforcing effects of both alcohol and nicotine are mediated by similar mechanisms resulting in enhanced activity of the cortico-mesolimbic dopamine system, but that their neurochemical interactions can lead to an aggregation of these effects. Despite this striking neurobiological overlap between alcohol and nicotine consumption, few studies have sought to take advantage of this commonality by devising a pharmacological approach that serves to treat both disorders. The results of our proof-of-concept study showed that topiramate is a promising medication for the treatment of both alcohol and nicotine dependence, presumably by its ability to modulate cortico-mesolimbic dopamine function profoundly; however, other mechanisms might also contribute to this effect. Further studies are ongoing to establish and extend topiramate's efficacy in the treatment of each and both disorders.

Alcoholism↗
PubMed2005

Neurotransmission and neuromodulation in the chemosensory carotid body.

The mammalian carotid body is a small chemosensory organ that helps maintain the chemical composition of arterial blood via reflex control of ventilation. Thus, in response to decreased PO2 (hypoxia), increased PCO2 (hypercapnia), or decreased pH (acidity), chemoreceptor glomus or type I cells become stimulated and release neuroactive agents that excite apposed sensory terminals of the carotid sinus nerve. The resulting increase in afferent discharge ultimately leads to corrective changes in ventilation so as to maintain blood gas and pH homeostasis. Recent evidence that the organ can also sense low glucose further emphasizes its role as a polymodal sensor of blood-borne stimuli. The chemoreceptors occur in organized cell clusters that receive sensory innervation from petrosal afferents and are intimately associated with the blood supply. Additionally, synaptic specializations between neighboring receptor cells allow for autocrine and paracrine regulation of the sensory output. Though not without controversy, significant progress has been made in elucidating the various chemotransductive pathways, as well as the neurotransmitter and neuromodulatory mechanisms that translate the receptor potential into an afferent sensory discharge. Progress in the latter has been hampered by the presence of a wide variety of endogenous ligands, and an even broader spectrum of receptor subtypes, that apparently help shape the chemoreceptor output and afferent discharge. This review will highlight recent advances in understanding the role of these neuroactive ligands in carotid body function.

Animals↗
PubMed2006

Afferent pathway and neuromodulation of superficial and deeper thoracic spinal neurons receiving noxious pulmonary inputs in rats.

The occurrence of vagally mediated afferent signaling by lung irritants is well known. However, spinal visceral afferent pathways also might be relevant to pulmonary irritation. In the present study, responses and modulation of superficial and deep T3 spinal neurons were examined using inhaled ammonia, and the peripheral afferent fibers were also characterized in part. Extracellular potentials of single thoracic (T3) spinal neurons were recorded in pentobarbital anesthetized, paralyzed, and ventilated male rats. Ammonia vapor (0.5, 1.0, 2.0 ml) was injected into the inspiratory line of the ventilator for 20 s. Inhaled ammonia (IA, 1.0 ml) excited 5/6 neurons and inhibited one spinal neuron recorded in superficial laminae, whereas deeper neurons responded with excitatory (E, n = 20), inhibitory (I, n = 4) or biphasic patterns (6 E-I, 3 I-E). Electrical and chemical stimulation of C1-C2 spinal neurons primarily suppressed T3 neuronal responses to IA. Resiniferatoxin (2 microg/kg, i.v.), which desensitizes afferent fibers containing transient receptor potential vanilloid receptor-1 (TRPV-1), abolished excitatory responses of 8/8 neurons to IA. Bilateral cervical vagotomy did not affect IA responses in 5 superficial neurons while 7 deeper neurons showed variable responses. 82% (32/39) of the spinal neurons responding to IA also received convergent noxious inputs from somatic fields in the chest and back areas. These results suggested that superficial and deeper spinal neuronal activation by inhaled ammonia mainly depended upon pulmonary sympathetic afferent fibers expressing TRPV-1. Additionally, C1-C2 spinal neurons, supraspinal sites and vagal afferents modulated the thoracic spinal neuronal responses to lower airway irritation.

Action Potentials↗
PubMed2004

Nitric oxide and angiotensin II: neuromodulation of thermoregulation during combined heat and hypohydration stress.

We investigated the central role of nitric oxide and AngII on thermoregulation in rats (Rattus norvegicus, Sabra strain,) undergoing heat-stress in euhydration or hypohydration (water deprivation, -10% b.wgt). Experimental rats received AngII (100 pm), 7-nitroindazole-an antagonist of neuronal nitric oxide synthase (7NI-100 nm), or AngII+7NI in a 5-microl bolus intracerebroventricularly (i.c.v.) under light chloroform anesthesia; untreated control rats received saline or DMSO (5%). We used three experimental paradigms: (1) heat defense responses [salivation (STsh), vasodilatation (VTsh) temperature thresholds and heat-endurance] in conscious, heat-stressed (39 degrees C) rats; (2) Western immunoblotting to detect AngII AT(1) and AT(2) receptors and nNOS protein expression; (3) real-time PCR to measure gene transcripts. In the in vivo experiment, 7NI decreased thermoregulatory thresholds, namely, NO had a reciprocal effect that was more pronounced during hypohydration (e.g. euhydration: STsh: -0.7+/-0.01 degrees C, hypohydration: -0.9+/-0.18 degrees C, p<0.05). AngII decreased STsh by 0.9+/-0.18 degrees C (p<0.05) upon euhydration but increased it in hypohydration (+1.7+/-0.28 degrees C, p<0.05). A novel finding was the involvement of AT(2) receptors in thermoregulation, which was more pronounced upon hypohydration. The response to NO was mediated via AT(1) and AT(2) receptors signaling, as well as independently. A synthesis of the results from all experimental paradigms suggests (1) a dominant influence (decrease) of NO on AT(1) receptors, thereby changing AT(1)/AT(2) receptor ratio and their signaling pathway; primarily upon hypohydration; (2) an influence of AngII (increase) on receptor density, more pronounced during hypohydration, at both gene transcription and translation levels; and (3) an effect of AngII on nNOS protein levels, implying a mutual effect of AngII and NO.

Analysis of Variance↗
PubMed2006

Long term results of neuromodulation by sacral nerve stimulation for lower urinary tract symptoms: a retrospective single center study.

OBJECTIVE: To analyse the influence of technical improvements of Sacral Nerve Stimulation (SNS) on the incidence of surgical interventions and subjective long-term results of SNS. METHODS: Retrospective, transversal study analyzing records of implanted patients at our department of Urology. RESULTS: Of 149 patients analyzed, 107 had overactive bladder symptoms and 42 had urinary retention. Mean follow-up was 64,2 (sd = 38,5) months. In the whole group 194 adverse events occurred. 6 Patients had infection in their implanted system, one was explanted for infection. Most events could be solved by giving advice or by reprogramming the stimulator. 129 reoperations have been performed and 21 patients had their system explanted. Analysis of the data shows a striking difference in the incidence of reoperations, but small differences in subjective results in the groups of patients implanted before or after 1996, suggesting that a proactive approach towards adverse events is worthwhile. CONCLUSIONS: SNS gives lasting benefit in patients with refractory symptoms of overactive bladder and non-obstructive urinary retention. The differences in outcomes and incidence of reoperation can be attributed to the learning curve and technical and surgical improvements in the application of SNS.

Adult↗