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At least 631 records · Page 35Linked to original sources
PubMed1989

Neuromodulation of intestinal transport in the suckling mouse.

The influence of enteric nerves on intestinal ion and sugar transport was investigated in 3- to 4-wk-old suckling mice. Whole thickness segments of jejunum were mounted as flat sheets in flux chambers equipped to electrically stimulate nerves in the intestinal wall. Tetrodotoxin significantly reduced basal short-circuit current in a subset of tissues containing 3-O-methylglucose in the mucosal bath. Electrical field stimulation of intrinsic nerves evoked an increase in short-circuit current of 86 +/- 15 microA/cm2 that was due to an increase in active chloride secretion with no significant change in the net movement of other ions. The secretory response to neural stimulation was abolished by tetrodotoxin and reduced by the muscarinic antagonist, atropine. Mucosal-to-serosal fluxes of 3-O-methylglucose were not altered by the cholinergic agonist carbachol. These results show that ion transport in the suckling mouse jejunum is regulated by the enteric nervous system. Neural stimulation evokes a chloride secretory response that is mediated by acetylcholine and other noncholinergic transmitters. Sugar transport in the murine small intestine does not appear to be influenced by muscarinic cholinergic agonists.

3-O-Methylglucose↗
PubMed1987

Cholinergic neuromodulation by prostaglandin D2 in canine airway smooth muscle.

To determine whether prostaglandin D2 (PGD2) modulates cholinergic neurotransmission in airway smooth muscle and, if so, what the mechanism of action is, we studied bronchial segments from dogs under isometric conditions in vitro. PGD2 (10(-8)-10(-5) M) elicited dose-dependent muscle contraction, which was reduced after blockade of muscarinic receptors, so that 50% effective dose (ED50) increased from 1.3 +/- 0.3 X 10(-6) to 3.9 +/- 1.0 X 10(-6) M by atropine (10(-6) M) (mean +/- SE, P less than 0.05). Physostigmine, at a concentration insufficient to alter base-line tension (10(-8) M), enhanced the PGD2-induced contraction and decreased ED50 to 6.4 +/- 0.5 X 10(-7) M (P less than 0.05). When added at the highest doses that did not cause spontaneous contraction (1.9 +/- 0.5 X 10(-7) M), PGD2 increased the contractile response to electrical field stimulation (1-50 Hz) by 21.9 +/- 6.6% (P less than 0.001). In contrast to this effect, the response to administered acetylcholine was not affected by PGD2. On the other hand, PGD2-induced augmentation of the response to electrical field stimulation (5 Hz) was further increased from 23.6 +/- 3.0 to 70.4 +/- 8.8% in the presence of physostigmine (10(-8) M) and was abolished by atropine but not affected by the alpha-adrenergic antagonist phentolamine or the histamine H1-blocker pyrilamine. These results suggest that the contraction of airway smooth muscle induced by PGD2 is in in part mediated by a cholinergic action and that PGD2 prejunctionally augments the parasympathetic contractile response, likely involving the accelerated release of acetylcholine at the neuromuscular junction.

Animals↗
PubMed2003

Episodic bouts of activity accompany recovery of rhythmic output by a neuromodulator- and activity-deprived adult neural network.

The pyloric rhythm of the stomatogastric ganglion of the crab, Cancer borealis, slows or stops when descending modulatory inputs are acutely removed. However, the rhythm spontaneously resumes after one or more days in the absence of neuromodulatory input. We recorded continuously for days to characterize quantitatively this recovery process. Activity bouts lasting 40-900 s began several hours after removal of neuromodulatory input and were followed by stable rhythm recovery after 1-4 days. Bout duration was not related to the intervals (0.3-800 min) between bouts. During an individual bout, the frequency rapidly increased and then decreased more slowly. Photoablation of back-filled neuromodulatory terminals in the stomatogastric ganglion (STG) neuropil had no effect on activity bouts or recovery, suggesting that these processes are intrinsic to the STG neuronal network. After removal of neuromodulatory input, the phase relationships of the components of the triphasic pyloric rhythm were altered, and then over time the phase relationships moved toward their control values. Although at low pyloric rhythm frequency the phase relationships among pyloric network neurons depended on frequency, the changes in frequency during recovery did not completely account for the change in phase seen after rhythm recovery. We suggest that activity bouts represent underlying mechanisms controlling the restructuring of the pyloric network to allow resumption of an appropriate output after removal of neuromodulatory input.

Action Potentials↗
PubMed2004

Neuromodulation by a cytokine: interferon-beta differentially augments neocortical neuronal activity and excitability.

The immunomodulatory cytokine interferon-beta (IFN-beta) is used in the treatment of autoimmune diseases such as multiple sclerosis. However, the effect of IFN-beta on neuronal functions is currently unknown. Intracellular recordings were conducted on somatosensory neurons of neocortical layers 2/3 and 5 exposed to IFN-beta. The excitability of neurons was increased by IFN-beta (10-10,000 U/ml) in two kinetically distinct, putatively independent manners. First IFN-beta reversibly influenced the subthreshold membrane response by raising the membrane resistance R(M) 2.5-fold and the membrane time constant tau 1.7-fold dose-dependently. The effect required permanent exposure to IFN-beta and was reduced in magnitude if the extracellular K+ was lowered. However, the membrane response to IFN-beta in the subthreshold range was prevented by ZD7288 (a specific blocker of I(h)) but not by Ni2+, carbachol, or bicuculline, pointing to a dependence on an intact I(h). Second, IFN-beta enhanced the rate of action potential firing. This effect was observed to develop for >1 h when the cell was exposed to IFN-beta for 5 min or >5 min and showed no reversibility (< or =210 min). Current-discharge (F-I) curves revealed a shift (prevented by bicuculline) as well as an increase in slope (prevented by carbachol and Ni2+). Layer specificity was not observed with any of the described effects. In conclusion, IFN-beta influences the neuronal excitability in neocortical pyramidal neurons in vitro, especially under conditions of slightly increased extracellular K+. Our blocker experiments indicate that changes in various ionic conductances with different voltage dependencies cause different IFN-beta influences on sub- and suprathreshold behavior, suggesting a more general intracellular process induced by IFN-beta.

Action Potentials↗
PubMed1999

Neuromodulation of dendritic action potentials.

The extent to which regenerative action potentials invade hippocampal CA1 pyramidal dendrites is dependent on both recent activity and distance from the soma. Previously, we have shown that the amplitude of back-propagating dendritic action potentials can be increased by activating either protein kinase A (PKA) or protein kinase C (PKC) and a subsequent depolarizing shift in the activation curve for dendritic K+ channels. Physiologically, an increase in intracellular PKA and PKC would be expected upon activation of beta-adrenergic and muscarinic acetylcholine receptors, respectively. Accordingly, we report here that activation of either of these neurotransmitter systems results in an increase in dendritic action-potential amplitude. Activation of the dopaminergic neurotransmitter system, which is also expected to raise intracellular adenosine 3',5'-cyclic monophosphate (cAMP) and PKA levels, increased action-potential amplitude in only a subpopulation of neurons tested.

Action Potentials↗
PubMed2001

Effects of spike parameters and neuromodulators on action potential waveform-induced calcium entry into pyramidal neurons.

Neocortical pyramidal neurons express several different calcium channel types. Previous studies with square voltage steps have found modest biophysical differences between these calcium channel types as well as differences in their modulation by transmitters. We used acutely dissociated neocortical pyramidal neurons to test whether this diversity extends to different activation by physiological stimuli. We conclude that 1) peak amplitude, latency to peak, and the total charge entry for the Ca(2+) channel current is dependent on the shape of the mock action potential waveforms (APWs). 2) The percent contribution of the five high-voltage-activated currents to the whole cell current was not altered by using an APW as opposed to a voltage step to elicit the current. 3) The identity of the charge carrier affects the amplitude and decay of the whole cell current. With Ca(2+), there was a greater contribution of T-type current to the whole cell current. 4) Total Ba(2+) charge entry is linearly dependent on the number of spikes in the stimulating waveform and relatively insensitive to spike frequency. 5) Current decay was greatest with Ca(2+) as the charge carrier and with minimal internal chelation. 6) Voltage-dependent neurotransmitter-mediated modulations can be reversed by multiple spikes. The extent of the reversal is dependent on the number of spikes in the stimulating waveform. Thus the neuronal activity pattern can determine the effectiveness of voltage-dependent and -independent modulatory pathways in neocortical pyramidal neurons.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1998

Neurostimulation and neuromodulation: a guide to selecting the right urologic patient.

Sensory input has an important influence on the integrity of neural circuitry. Central nervous system circuitry is programmed and reinforced by everyday experience. Even the simplest of behaviors participate in this process. A balance between inhibition and facilitation must be maintained for the CNS to function normally. For example, the bladder stores urine because of the inhibition from a closed sphincter, and relaxation of the sphincter disinhibits the bladder to permit voiding. This synergistic 'seesaw' in reflex neural activity preserves the functional and anatomical integrity of the lower urinary tract. Dysfunction and anatomical change results when an unnatural bias develops between inhibitory and facilitatory neural activity. Neurostimulation has an inherent conditioning effect on neural excitability and can restore the neural equilibrium. Voiding diaries are very useful in documenting these changes.

Electric Stimulation Therapy↗
PubMed1994

C-type natriuretic peptide neuromodulates independently of guanylyl cyclase activation.

Of the four endogenous members of the natriuretic peptide family, only atrial natriuretic peptide has been demonstrated to have neuromodulatory effects. This study compares the neuromodulatory effects of atrial natriuretic peptide and a recently identified natriuretic peptide, C-type natriuretic peptide, in the rabbit isolated vas deferens. The ability of these peptides to alter cyclic nucleotide concentrations was assessed to determine the potential contribution of either cyclic AMP or cyclic GMP to the observed responses. The central hypothesis tested was that C-type natriuretic peptide modulates neurotransmission via an interaction with a guanylyl cyclase. C-type natriuretic peptide inhibited both purinergic and adrenergic neurotransmission in a concentration-dependent manner but failed to alter either cyclic GMP or cyclic AMP concentrations. Maximal inhibitory effects of C-type natriuretic peptide averaged 35 +/- 4% for purinergic and 49 +/- 7% for adrenergic neurotransmission. Atrial natriuretic peptide not only attenuated both purinergic and adrenergic neurotransmission but also increased cyclic GMP concentrations. C-type natriuretic peptide probably inhibited the release of the neurotransmitters because it failed to alter contractions to exogenously administered norepinephrine or ATP, the two putative neurotransmitters. These results suggest that the C-type natriuretic peptide receptor, guanylyl cyclase B, is not present in rabbit vas deferens and that C-type natriuretic peptide suppresses peripheral sympathetic neurotransmission independently of guanylyl cyclase activation.

Animals↗
PubMedDate not supplied

Flexible couplings: diffusing neuromodulators and adaptive robotics.

Recent years have seen the discovery of freely diffusing gaseous neurotransmitters, such as nitric oxide (NO), in biological nervous systems. A type of artificial neural network (ANN) inspired by such gaseous signaling, the GasNet, has previously been shown to be more evolvable than traditional ANNs when used as an artificial nervous system in an evolutionary robotics setting, where evolvability means consistent speed to very good solutions--here, appropriate sensorimotor behavior-generating systems. We present two new versions of the GasNet, which take further inspiration from the properties of neuronal gaseous signaling. The plexus model is inspired by the extraordinary NO-producing cortical plexus structure of neural fibers and the properties of the diffusing NO signal it generates. The receptor model is inspired by the mediating action of eurotransmitter receptors. Both models are shown to significantly further improve evolvability. We describe a series of analyses suggesting that the reasons for the increase in evolvability are related to the flexible loose coupling of distinct signaling mechanisms, one "chemical" and one "electrical."

Adaptation, Physiological↗
PubMed1992

Neuropeptide Y is a neuromodulator of pulsatile luteinizing hormone-releasing hormone release in the gonadectomized rhesus monkey.

In a previous study, we have demonstrated that infusion of neuropeptide Y (NPY) into the stalk-median eminence (S-ME) of gonadectomized rhesus monkeys stimulated LHRH in a dose-dependent manner. This finding led us to address the following questions: 1) What are the characteristics of NPY release in vivo? 2) How does NPY release relate to LHRH release? 3) Is endogenous NPY essential to pulsatile LHRH release? To answer these questions, three experiments using push-pull perfusion were performed in adult gonadectomized rhesus monkeys. Perfusate samples from the S-ME were collected at 10-min intervals for 6 to 12-h periods, and the concentrations of LHRH and NPY in perfusates were determined by RIA. In Exp I, the release pattern of NPY and LHRH in the S-ME was independently determined in a group of 11 conscious monkeys: NPY release in the S-ME was pulsatile with an interpulse interval of 44.9 +/- 3.3 min (n = 11). This interpulse interval was similar to that seen for LHRH release (43.8 +/- 1.1 min, n = 7). Exp II was designed to determine whether NPY pulses and LHRH pulses occur synchronously and to examine whether NPY release in the S-ME is correlated with circulating LH pulses. NPY and LHRH concentrations in aliquots of the same perfusate sample from the S-ME and circulating LH levels were concurrently measured in 8 monkeys sedated with Saffan. It was found that NPY pulses were temporally correlated (P less than 0.001) with LHRH pulses, which were also temporally correlated (P less than 0.001) with LH pulses. Moreover, NPY pulses were correlated (P less than 0.05) with LH pulses. NPY peaks preceded LHRH peaks by 4.5 +/- 0.6 min, LHRH peaks preceded LH peaks by 5.5 +/- 0.6 min, and NPY peaks preceded LH peaks by 9.7 +/- 0.8 min. In Exp III, the role of endogenous NPY in LHRH release was evaluated by infusing a specific antiserum to NPY into the S-ME during push-pull perfusion in 8 conscious monkeys. Infusion of a specific antiserum to NPY into the S-ME at 1:100 and 1:1000 dilutions suppressed pulsatile LHRH release significantly (P less than 0.05). Infusion of nonimmune serum as a control was without effect. These results are summarized as follows: 1) NPY release in the S-ME is pulsatile, 2) NPY pulses occur synchronously with LHRH and LH pulses, and 3) immunoneutralization of endogenous NPY in the S-ME suppresses pulsatile LHRH release.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2001

Novel role of macrophage migration inhibitory factor in angiotensin II regulation of neuromodulation in rat brain.

Previously we determined that angiotensin II (Ang II) activates neuronal AT(1) receptors, located in the hypothalamus and the brainstem, to stimulate noradrenergic pathways. To link Ang II to the regulation of norepinephrine metabolism in neurons cultured from newborn rat hypothalamus and brainstem we have used cDNA arrays for high throughput gene expression profiling. Of several genes that were regulated, we focused on macrophage migration inhibitory factor (MIF), which has been associated with the modulation of norepinephrine metabolism. In the presence of the selective AT(2) receptor antagonist PD123,319 (10 microM), incubation of cultures with Ang II (100 nM; 1-24 h) elicited an increase in MIF gene expression. Western immunoblots further revealed that Ang II (100 nM; 1-24 h) increased neuronal MIF protein expression. This effect was inhibited by the AT(1) receptor antagonist losartan (10 microM), the PLC inhibitor U-73122 (10 or 25 microM), the PKC inhibitor chelerythrine (10 microM), and the Ca(2+) chelator 1,2-bis-[2-aminophenoxy]-ethane-N,N,N',N'-tetraacetic acid tetrakis acetoxymethyl ester (10 microM). Taken together with our observation that MIF is expressed in the terminal fields of noradrenergic neurons (hypothalamus) and that Ang II increases the expression of MIF in this region in vivo, our data may suggest a novel role of Ang II in norepinephrine metabolism.

Angiotensin II↗
PubMed2001

Gene expression profiling of rat brain neurons reveals angiotensin II-induced regulation of calmodulin and synapsin I: possible role in neuromodulation.

Angiotensin (Ang II) activates neuronal AT(1) receptors located in the hypothalamus and the brainstem and stimulates noradrenergic neurons that are involved in the control of blood pressure and fluid intake. In this study we used complementary DNA microarrays for high throughput gene expression profiling to reveal unique genes that are linked to the neuromodulatory actions of Ang II in neuronal cultures from newborn rat hypothalamus and brainstem. Of several genes that were regulated, we focused on calmodulin and synapsin I. Ang II (100 nM; 1-24 h) elicited respective increases and decreases in the levels of calmodulin and synapsin I messenger RNAs, effects mediated by AT(1) receptors. This was associated with similar changes in calmodulin and synapsin protein expression. The actions of Ang II on calmodulin expression involve an intracellular pathway that includes activation of phospholipase C, increased intracellular calcium, and stimulation of protein kinase C. Taken together with studies that link calmodulin and synapsin I to axonal transport and exocytotic processes, the data suggest that Ang II regulates these two proteins via a Ca(2+)-dependent pathway, and that this may contribute to longer term or slower neuromodulatory actions of this peptide.

Angiotensin II↗
PubMed2006

Neuromodulation of the locust frontal ganglion during the moult: a novel role for insect ecdysis peptides.

In insects, continuous growth requires the periodic replacement of the exoskeleton during the moult. A moulting insect displays a stereotypical set of behaviours that culminate in the shedding of the old cuticle at ecdysis. Moulting is an intricate process requiring tightly regulated physiological changes and behaviours to allow integration of environmental cues and to ensure the proper timing and sequence of its components. This is under complex hormonal regulation, and is an important point of interaction between endocrine and neural control. Here, we focus on the locust frontal ganglion (FG), an important player in moulting behaviour, as a previously unexplored target for ecdysis peptides. We show that application of 10(-7) mol l(-1) ecdysis-triggering hormone (ETH) or 10(-7) mol l(-1) and 10(-6) mol l(-1) Pre-ecdysis-triggering hormone (PETH) to an isolated FG preparation caused an increase in bursting frequency in the FG, whereas application of 10(-6) mol l(-1) eclosion hormone (EH) caused an instantaneous, though temporary, total inhibition of all FG rhythmic activity. Crustacean cardioactive peptide (CCAP), an important peptide believed to turn on ecdysis behaviour, caused a dose-dependent increase of FG burst frequency. Our results imply a novel role for this peptide in generating air-swallowing behaviour during the early stages of ecdysis. Furthermore, we show that the modulatory effects of CCAP on the FG motor circuits are dependent on behavioural state and physiological context. Thus, we report that pre-treatment with ETH caused CCAP-induced effects similar to those induced by CCAP alone during pre-ecdysis. Thus, the action of CCAP seems to depend on pre-exposure to ETH, which is thought to be released before CCAP in vivo.

Animals↗
PubMed1995

Matrix of neuromodulators in neurosecretory structures of the crab Cancer borealis.

The crustacean stomatogastric ganglion, which is situated in the ophthalmic artery, can be modulated by both intrinsically released molecules and hormones. In the crab Cancer borealis, over a dozen neuroactive compounds have been identified in the input axons that project into the stomatogastric neuropil. However, little is known about the modulator content of the two major neurohemal organs, the sinus glands and the pericardial organs, in this crab. We now report the results of a series of immunocytochemical experiments designed to identify putative neurohormones in these tissues. We find that the majority of modulators present in the input axons of the stomatogastric ganglion are also present in at least one of the neurohemal organs. Specifically, allatostatin-like, buccalin-like, cholecystokinin-like, FLRFamide-like, GABA-like, locustatachykinin-like, myomodulin-like, proctolin-like, red pigment concentrating hormone-like and serotonin-like immunoreactivities are all present in both the stomatogastric neuropil and at least one of the neurohemal organs. Thus, these substances are likely to serve a dual role as both local and hormonal modulators of the stomatogastric network. Two other substances, beta-pigment dispersing hormone and crustacean cardioactive peptide, are not present in the stomatogastric neuropil, but beta-pigment dispersing hormone immunoreactivity is present in the sinus glands and crustacean cardioactive peptide immunoreactivity is present in the pericardial organs. It is likely that crustacean cardioactive peptide exerts its influence on the stomatogastric neural circuit via hormonal pathways. Double-labeling experiments show that the patterns of modulator co-localization present in the stomatogastric neuropil are different from those in the neurosecretory organs, suggesting that few rules of colocalization hold across these tissues.

Animals↗