Adenosine as an Endogenous Regulator of Central Excitability

Emotions ◽  
2015 ◽  
pp. 429-440
Author(s):  
J. W. Phillis ◽  
R. A. Barraco ◽  
R. E. Delong
2014 ◽  
Vol 20 (16) ◽  
pp. 2621-2630 ◽  
Author(s):  
Bedoor Qabazard ◽  
Ling Li ◽  
Jan Gruber ◽  
Meng Teng Peh ◽  
Li Fang Ng ◽  
...  

2006 ◽  
Vol 100 (6) ◽  
pp. 1757-1764 ◽  
Author(s):  
J. M. Kalmar ◽  
E. Cafarelli

After fatigue, motor evoked potentials (MEP) elicited by transcranial magnetic stimulation and cervicomedullary evoked potentials elicited by stimulation of the corticospinal tract are depressed. These reductions in corticomotor excitability and corticospinal transmission are accompanied by voluntary activation failure, but this may not reflect a causal relationship. Our purpose was to determine whether a decline in central excitability contributes to central fatigue. We hypothesized that, if central excitability limits voluntary activation, then a caffeine-induced increase in central excitability should offset voluntary activation failure. In this repeated-measures study, eight men each attended two sessions. Baseline measures of knee extension torque, maximal voluntary activation, peripheral transmission, contractile properties, and central excitability were made before administration of caffeine (6 mg/kg) or placebo. The amplitude of vastus lateralis MEPs elicited during minimal muscle activation provided a measure of central excitability. After a 1-h rest, baseline measures were repeated before, during, and after a fatigue protocol that ended when maximal voluntary torque declined by 35% (Tlim). Increased prefatigue MEP amplitude ( P = 0.055) and cortically evoked twitch ( P < 0.05) in the caffeine trial indicate that the drug increased central excitability. In the caffeine trial, increased MEP amplitude was correlated with time to task failure ( r = 0.74, P < 0.05). Caffeine potentiated the MEP early in the fatigue protocol ( P < 0.05) and offset the 40% decline in placebo MEP ( P < 0.05) at Tlim. However, this was not associated with enhanced maximal voluntary activation during fatigue or recovery, demonstrating that voluntary activation is not limited by central excitability.


2021 ◽  
Author(s):  
Oren Even‐Chen ◽  
Leonie Herburg ◽  
Ekaterini Kefalakes ◽  
Nataly Urshansky ◽  
Claudia Grothe ◽  
...  
Keyword(s):  

1978 ◽  
Vol 73 (1) ◽  
pp. 47-63 ◽  
Author(s):  
B. M. Bush ◽  
J. P. Vedel ◽  
F. Clarac

In the walking legs of decapod crustaceans, intersegmental reflex actions originate from various joint proprioceptors. The activity of the ‘accessory flexor’ (AF) muscle, which with the myochordotonal organ (MCO) constitutes a muscle proprioceptor for the mero-carpopodite (M-C) joint, is modulated by the sensory discharge of a joint receptor (CB chordotonal organ) for the more proximal, coxo-basal (C-B) joint. Selective mechanical stimulation of the CB organ also reflexly modifies the motor activities of the main M-C flexor and extensor muscles (recorded as EMGs). 1. Dynamic CB stretch (as would occur during a dorso-ventral C-B movement - i.e. ‘depression’ of the limb) stimulates motor discharge to the M-C extensor muscle, while dynamic release of CB (as during a ventrodorsal C-B movement - or leg ‘elevation’) excites the accessory flexor as well as the main flexor muscle. 2. Successive M-C muscle responses to repetitive sinusoidal changes of CB length differ quantitatively according to the direction (stretch or release) of the first CB movement, in some cases increasing but more commonly ‘adapting’ with repetition. 3. Reflex discharge frequencies of the extensor, flexor and accessory flexor motoneurones increase with velocity of CB movement. 4. Eye illumination, and spontaneous or other sources of increased central excitability, generally increase the CB reflex drive to the flexor and accessory flexor muscles and, in parallel, decrease the reflex action on the extensor muscle. The results are discussed in terms of the role of proprioceptive reflexes in intersegmental co-ordination of the leg joints. In particular the significance of the reflex regulation of the myochordotonal receptors, and thereby the gain of the M-C resistance reflexes, is considered in the light of the observed ‘co-activation’ of main flexor and receptor muscle motoneurones.


1974 ◽  
Vol 61 (3) ◽  
pp. 655-666
Author(s):  
D. A. DORSETT ◽  
A. O. D. WILLOWS

The seven neurones that command the three stages of branchial tuft withdrawal interact by electrotonic and chemically mediated polysynaptic pathways. The pleural tuft retractors, L and R Pl 6, make electrotonic synapses with the ipsilateral neuronesPd2, which cause retraction of the tips of the tufts. The chemically transmitting pathways, between these and other retractor neurones, are mostly reciprocal and can be classified as weak or strong. The former are small in amplitude, with long latencies (1-3 sec) and are labile to repeated activation; the latter are of large amplitude and shorter latency (0·5-0·8 sec), but may still show decrement with repeated use. Frequently the p.s.p. shows indications of 1:1 correlation with the spike pattern in the driven neurone, but the long latencies require the presence of at least one interneurone in the pathway. The progressive spread of the behavioural response (withdrawal of the tips, complete unilateral withdrawal, complete bilateral withdrawal of all tufts), which occurs with increasing stimulus intensity, is not dependent on a central hierarchy in the activation of the tuft retractor neurones. Reciprocal feedback leads to a general increase in central excitability, the threshold for more extensive responses being probably determined largely by the sensory input to individual neurones. The unique pleural cell R Pl 5 is exceptional, both in the variety of motor activity it commands and in the absence of reciprocal connexions from other retractor neurones.


1986 ◽  
Vol 55 (4) ◽  
pp. 689-695 ◽  
Author(s):  
P. Skorupski ◽  
K. T. Sillar

Both negative feedback, resistance reflexes and positive feedback, assistance reflexes are mediated by the thoracocoxal muscle receptor organ (TCMRO) in the crayfish, depending on the central excitability of the preparation. In this paper we present evidence that the velocity-sensitive afferent T fiber of the TCMRO may elicit either resistance or assistance reflexes in different preparations. In preparations displaying assistance reflexes, the S and T fibers of the TCMRO exert reciprocal effects on leg motor neurons (MNs). The S fiber excites promotor MNs (negative feedback) and inhibits remotor MNs, the T fiber excites remotor MNs (positive feedback) and inhibits promotor MNs. During reciprocal motor output of promotor and remotor MNs, reflexes mediated by the TCMRO are modulated in a phase-dependent manner. The TCMRO excites promotor MNs during their active phases (negative feedback) but inhibits them during their reciprocal phases. Remotor MNs are excited by the TCMRO during their active phases (positive feedback). It is proposed that depolarizing central inputs that occur in the S and T fibers at opposite phases of the motor output cycle (21) facilitate the output effects of each afferent in alternation, effectively mediating a phase-dependent shift between the effects of one afferent and the other. The implications of central modulation of reflex pathways and the possible functions of positive and negative feedback reflexes during locomotion are discussed.


Peptides ◽  
2006 ◽  
Vol 27 (5) ◽  
pp. 1099-1103 ◽  
Author(s):  
Willis K. Samson ◽  
Meghan M. Taylor

1984 ◽  
Vol 246 (3) ◽  
pp. C301-C307 ◽  
Author(s):  
R. J. Schimmel ◽  
L. McCarthy

The action of endogeneous adenosine on isolated hamster brown adipocytes was examined. Adenosine production from brown adipocytes was measured after labeling of the intracellular nucleotide pool with [3H]adenine. Accumulation of [3H]adenosine in the incubation medium was maximum after 5 min of incubation and was still present after 20 min. When adenosine accumulation was prevented by addition of adenosine deaminase, the stimulatory effects of isoproterenol on oxygen uptake, lipolysis, and adenosine 3',5'-cyclic monophosphate (cAMP) generation were enhanced. However, basal rates of lipolysis and oxygen consumption and levels of cAMP were not affected on addition of adenosine deaminase. A similar potentiation of isoproterenol responses was produced by the adenosine receptor antagonist, 3-isobutyl-1-methylxanthine, present at a concentration (10 microM) which did not change basal levels of respiration or lipolysis. Addition of the adenosine analogue 2-chloroadenosine antagonized isoproterenol-stimulated respiration and lipolysis and prevented potentiation of isoproterenol responses with 3-isobutyl-1-methylxanthine. To localize the site of adenosine action, activity of adenylate cyclase in membrane preparations from brown adipocytes was measured. Isoproterenol-stimulated adenylate cyclase activity was partially inhibited by 2-chloroadenosine in a GTP-dependent manner. Addition of Na+ enhanced the inhibitory effect of 2-chloroadenosine, and 3-isobutyl-1-methylxanthine blocked it. The calculated 50% effective dose for 2-chloroadenosine inhibition was between 10 and 15 nM. These data suggest that adenosine produced by brown adipocytes is an endogenous regulator of respiration in these cells acting at the level of the adenylate cyclase enzyme.


2004 ◽  
Vol 559 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Richardson N. Leao ◽  
Amy Berntson ◽  
Ian D. Forsythe ◽  
Bruce Walmsley

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