K+ changes in the extracellular space of the spinal cord and their physiological role

1981 ◽  
Vol 95 (1) ◽  
pp. 93-109
Author(s):  
E. Sykova
Keyword(s):  
Spinal Cord ◽  
Neuronal Activity ◽  
Tactile Stimulation ◽  
Current Flow ◽  
Physiological Role ◽  
Primary Afferent Depolarization ◽  
Flow Through ◽  
K Concentration ◽  
Dorsal Root Potentials ◽  
Stimulation Of

K+ accumulates in the intercellular space as a result of neuronal activity. The changes in extracellular K+ concentration, delta[K]e (estimated by K+-selective microelectrodes), depends on neuronal activity, on the density of discharging neurones and the removal of the accumulated K+ by diffusion, active transport and current flow through cells. In the mammalian as well as the amphibian spinal cord a single volley in a peripheral nerve increases [K]e by 0.2-0.5 mmol. 1-1, while tetanic stimulation (100 Hz) by 7-8 m-mol. 1-1, with a maximum in the lower dorsal horn. Increased [K]e was also found in lumbar segments when the somatosensory cortex of the cat and medulla of the frog were stimulated. In the frog spinal cord, the tactile stimulation of the hindlimb evoked delta[K]e by about 0.1 mumol. 1-1, nociceptive stimulation by 0.2-1.0 mmol. 1-1. Spontaneous delta[K]e and dorsal root potentials (DRPs) were observed at various intervals after stimulation, associated with the decay phase of delta[K]e. It was shown that primary afferent depolarization (PAD) consists of two components: the ‘early’ component (mediated by GABA and depressed by picrotoxin or bicuculline) and the ‘late’ K+ component (potentiated by picrotoxin and bicuculline). Even when increased [K]e produces PAD, this does not mean that it also results in presynaptic inhibition. It was found that the delta[K]e produced depolarization of motoneurones and neuroglia and there is every reason to believe that this also applies to the interneurones. Evidence is available that an increase of [K]e up to 6 mmol. 1-1 facilitates impulse transmission in the spinal cord while higher levels result in its inhibition.

Intracellular recording from visually identified motoneurons in rat spinal cord slices

1978 ◽  
Vol 202 (1148) ◽  
pp. 417-421 ◽  
Keyword(s):  
Spinal Cord ◽  
Neuronal Activity ◽  
Intracellular Recording ◽  
Action Potentials ◽  
Intracellular Recordings ◽  
Rat Spinal Cord ◽  
Local Sensitivity ◽  
New Born ◽  
Intracellular Stimulation ◽  
Stimulation Of

Motoneurons were directly visualized with Nomarski optics in slices prepared from new born rat spinal cord. Intracellular recordings from these neurons showed spontaneous potentials, probably triggered by inter-neuronal activity. Action potentials could also be evoked by direct intracellular stimulation of the motoneurons. Iontophoretically applied L-glutamate caused a fast depolarization of the motoneuronal membrane. Considerable differences in local sensitivity to L-glutamate were found on the surface of the motoneuron.

scholarly journals Neuronal Activity Stimulated by Liquid Substrates Injection at Zusanli (ST36) Acupoint: The Possible Mechanism ofAquapuncture

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Chun-Yen Chen ◽  
Chao-Nan Lin ◽  
Rey-Shyong Chern ◽  
Yu-Chuan Tsai ◽  
Yung-Hsien Chang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuronal Activity ◽  
Spatial Configuration ◽  
The Other ◽  
Bee Venom ◽  
Neuronal Signaling ◽  
Fos Protein ◽  
Configuration Changes ◽  
Acupoint Stimulation ◽  
Stimulation Of

Aquapunctureis a modified acupuncture technique and it is generally accepted that it has a greater therapeutic effect than acupuncture because of the combination of the acupoint stimulation and the pharmacological effect of the drugs. However, to date, the mechanisms underlying the effects ofaquapunctureremain unclear. We hypothesized that both the change in the local spatial configuration and the substrate stimulation ofaquapuncturewould activate neuronal signaling. Thus, bee venom, normal saline, and vitamins B1 and B12 were injected into a Zusanli (ST36) acupoint as substrate ofaquapuncture, whereas a dry needle was inserted into ST36 as a control. Afteraquapuncture, activated neurons expressing Fos protein were mainly observed in the dorsal horn of the spinal cord in lumbar segments L3–5, with the distribution nearly identical among all groups. However, the bee venom injection induced significantly more Fos-expressing neurons than the other substrates. Based on these data, we suggest that changes in the spatial configuration of the acupoint activate neuronal signaling and that bee venom may further strengthen this neuronal activity. In conclusion, the mechanisms for the effects ofaquapunctureappear to be the spatial configuration changes occurring within the acupoint and the ability of injected substrates to stimulate neuronal activity.

scholarly journals Stance-phase force on the opposite limb dictates swing-phase afferent presynaptic inhibition during locomotion

2012 ◽  
Vol 107 (11) ◽  
pp. 3168-3180 ◽  
Author(s):  
Heather Brant Hayes ◽  
Young-Hui Chang ◽  
Shawn Hochman
Keyword(s):  
Spinal Cord ◽  
Presynaptic Inhibition ◽  
Stance Phase ◽  
Swing Phase ◽  
Primary Afferent Depolarization ◽  
Environmental Perturbations ◽  
Opposite Limb ◽  
Dorsal Root Potentials ◽  
Powerful Mechanism

Presynaptic inhibition is a powerful mechanism for selectively and dynamically gating sensory inputs entering the spinal cord. We investigated how hindlimb mechanics influence presynaptic inhibition during locomotion using pioneering approaches in an in vitro spinal cord–hindlimb preparation. We recorded lumbar dorsal root potentials to measure primary afferent depolarization-mediated presynaptic inhibition and compared their dependence on hindlimb endpoint forces, motor output, and joint kinematics. We found that stance-phase force on the opposite limb, particularly at toe contact, strongly influenced the magnitude and timing of afferent presynaptic inhibition in the swinging limb. Presynaptic inhibition increased in proportion to opposite limb force, as well as locomotor frequency. This form of presynaptic inhibition binds the sensorimotor states of the two limbs, adjusting sensory inflow to the swing limb based on forces generated by the stance limb. Functionally, it may serve to adjust swing-phase sensory transmission based on locomotor task, speed, and step-to-step environmental perturbations.

Primary afferent depolarization of muscle afferents elicited by stimulation of joint afferents in cats with intact neuraxis and during reversible spinalization

1993 ◽  
Vol 70 (5) ◽  
pp. 1899-1910 ◽  
Author(s):  
J. Quevedo ◽  
J. R. Eguibar ◽  
I. Jimenez ◽  
R. F. Schmidt ◽  
P. Rudomin
Keyword(s):  
Spinal Cord ◽  
Knee Joint ◽  
High Threshold ◽  
Primary Afferent Depolarization ◽  
Delayed Response ◽  
Primary Afferent ◽  
Myelinated Fibers ◽  
Group I ◽  
Posterior Knee ◽  
Stimulation Of

1. In the anesthetized and artificially ventilated cat, stimulation of the posterior articular nerve (PAN) with low strengths (1.2-1.4 x T) produced a small negative response (N1) in the cord dorsum of the lumbosacral spinal cord with a mean onset latency of 5.2 ms. Stronger stimuli (> 1.4 x T) produced two additional components (N2 and N3) with longer latencies (mean latencies 7.5 and 15.7 ms, respectively), usually followed by a slow positivity lasting 100-150 ms. With stimulus strengths above 10 x T there was in some experiments a delayed response (N4; mean latency 32 ms). 2. Activation of posterior knee joint nerve with single pulses and intensities producing N1 responses only, usually produced no dorsal root potentials (DRPs), or these were rather small. Stimulation with strengths producing N2 and N3 responses produced distinct DRPs. Trains of pulses were clearly more effective than single pulses in producing DRPs, even in the low-intensity range. 3. Cooling the thoracic spinal cord to block impulse conduction, increased the DRPs and the N3 responses produced by PAN stimulation without significantly affecting the N2 responses. Reversible spinalization also increased the DRPs produced by stimulation of cutaneous nerves. In contrast, the DRPs produced by stimulation of group I afferents from flexors were reduced. 4. Conditioning electrical stimulation of intermediate and high-threshold myelinated fibers in the PAN depressed the DRPs produced by stimulation of group I muscle and of cutaneous nerves. 5. Analysis of the intraspinal threshold changes of single Ia and Ib fibers has provided evidence that stimulation of intermediate and high threshold myelinated fibers in the posterior knee joint nerve inhibits the primary afferent depolarization (PAD) of Ia fibers, and may either produce PAD or inhibit the PAD in Ib fibers, in the same manner as stimulation of cutaneous nerves. In 7/16 group I fibers the inhibition of the PAD was increased during reversible spinalization. 6. The results obtained suggest that intermediate and high-threshold myelinated fibers in the PAN have the same actions on Ia and Ib fibers as intermediate and high-threshold cutaneous afferents and may therefore be considered as belonging to the same functional system. They further indicate that in anesthetized preparations the pathways mediating the PAD of group I fibers, as well as the pathways mediating the inhibition of the PAD, may be subjected to a descending control that is removed by spinalization.

Physiologic coupling of glial glycogen metabolism to neuronal activity in brain

1992 ◽  
Vol 70 (S1) ◽  
pp. S138-S144 ◽  
Author(s):  
Raymond A. Swanson
Keyword(s):  
Neuronal Activity ◽  
Tactile Stimulation ◽  
Glycogen Content ◽  
Brain Activity ◽  
Glycogen Metabolism ◽  
Normal Brain ◽  
Brain Glycogen ◽  
Glycogen Utilization ◽  
Glucose Supply ◽  
Stimulation Of

Brain glycogen is localized almost exclusively to glia, where it undergoes continuous utilization and resynthesis. We have shown that glycogen utilization increases during tactile stimulation of the rat face and vibrissae. Conversely, decreased neuronal activity during hibernation and anesthesia is accompanied by a marked increase in brain glycogen content. These observations support a link between neuronal activity and glial glycogen metabolism. The energetics of glycogen metabolism suggest that glial glycogen is mobilized to meet increased metabolic demands of glia rather than to serve as a substrate for neuronal activity. An advantage to the use of glycogen may be the potentially faster generation of ATP from glycogen than from glucose. Alternatively, glycogen could be utilized if glucose supply is transiently insufficient during the onset of increased metabolic activity. Brain glycogen may have a dynamic role as a buffer between the abrupt increases in focal metabolic demands that occur during normal brain activity and the compensatory changes in focal cerebral blood flow or oxidative metabolism.Key words: brain, glia, glycogen, glycolysis, hibernation.

Modulation of synaptic effectiveness of Ia and descending fibers in cat spinal cord

1975 ◽  
Vol 38 (5) ◽  
pp. 1181-1195 ◽  
Author(s):  
P. Rudomin ◽  
R. Nunez ◽  
J. Madrid
Keyword(s):  
Spinal Cord ◽  
Time Course ◽  
Peak Amplitude ◽  
Primary Afferent Depolarization ◽  
Base Line ◽  
Conditioning Stimulation ◽  
Ia Epsp ◽  
Threshold Strength ◽  
Low Threshold ◽  
Stimulation Of

1. In the unanesthetized spinal cord, conditioning stimulation of low-threshold afferents (below 1.3 times threshold strength) in the biceps semitendinosus (BST) nerve often reduced the peak amplitude of the monosynaptic Ia EPSPs evoked in gastrocnemius motoneurons without affecting the monosynaptic component of the EPSPs evoked by stimulation of the ipsilateral ventral funiculus (VF) in the thoracic cord. 2. Volleys to the BST nerve comprising higher threshold afferents (usually above 1.4 times threshold strength) reduced the peak amplitude of the monosynaptic Ia and VF EPSPs and shortened their falling phase. 3. Conditioning volleys to low-threshold cutaneous afferents often increased the Ia-EPSP peak amplitude, sometimes without affecting the monosynaptic component of the VF EPSP. 4. In most cases the Ia nd VF monosynaptic EPSPs elicited in a given motoneuron summated nonlinearly. The amount of nonlinear summation between Ia and VF monosynaptic EPSPs was often reduced by low-threshold BST conditioning volleys. These observations suggest that in many instances, both species of fibers end in "electrotonically close" synaptic loci over the motoneuron surface. Therefore, amplitude changes of monosynaptic Ia EPSPs produced by conditioning afferent volleys without concomitant changes of monosynaptic VF EPSPs do not appear to result from postsynaptic remote conductance changes and may be attributed to a presynaptic mechanism. 5. At the time of occurrence of the Ia and VF monosynaptic EPSP the variance of the motoneuron membrane potential may be increased above base-line levels with a time course approximately matching the EPSP itself. Conditioning stimulation of BST afferents usually reduced Ia EPSP variance, often without affecting or even increasing the variance of the monosynaptic VF EPSPs. These observations provide additional evidence that Ia EPSP variability is introduced, at least in part, through the segmental pathways mediating primary afferent depolarization. 6. The possibility of a differential control of the information flow transmitted through two independent channels converging on a given cell ensemble is discussed.

Modulation of spinal cord transmission by changes in extracellular K+ activity and extracellular volume

1987 ◽  
Vol 65 (5) ◽  
pp. 1058-1066 ◽  
Author(s):  
Eva Syková
Keyword(s):  
Spinal Cord ◽  
Neuronal Activity ◽  
Time Course ◽  
Extracellular Volume ◽  
Limiting Factor ◽  
Dorsal Horns ◽  
Low Threshold ◽  
Repetitive Electrical Stimulation ◽  
Stimulation Of ◽  
K Activity

The neuronal activity in spinal cord in response to electrical or adequate stimulation of afferent fibres increases extracellular K+ activity. The increase during a stimulation can reach 9–10 mM (so-called ceiling level) and persists for some time even when a stimulation is discontinued. The activation of a neuronal Na–K pump is a limiting factor in stimulation-evoked increase in extracellular K+ activity and in the time course of its recovery to the resting level. Drugs that affect either the neuronal activity (picrotoxin, strychnine, GABA, 5-HT) or activity of Na–K ATPase (oubain, naloxone, morphine, enkephalins) substantially change the K+ transience. Repetitive electrical stimulation of low threshold cutaneous afferents at frequency 1–100 Hz induced transient shrinkage of extracellular space in spinal dorsal horns by 5–75%. The increase in extracellular K+ activity depolarizes the membranes of neurones, glial cells, and primary afferent fibres and may eventually lead to either facilitation or inhibition of synaptic transmission. It is also suggested that the transient poststimulation changes in extracellular volume may alter synaptic potency in spinal cord.

PAD and PAH response patterns of group Ia- and Ib-fibers to cutaneous and descending inputs in the cat spinal cord

1986 ◽  
Vol 56 (4) ◽  
pp. 987-1006 ◽  
Author(s):  
P. Rudomin ◽  
M. Solodkin ◽  
I. Jimenez
Keyword(s):  
Spinal Cord ◽  
Type A ◽  
Nerve Fibers ◽  
Primary Afferent Depolarization ◽  
Type B ◽  
Group I ◽  
Afferent Fibers ◽  
Conduction Velocities ◽  
Type C ◽  
Stimulation Of

The characteristics of the primary afferent depolarization (PAD) of Ia- and Ib-fibers generated by segmental and descending inputs have been analyzed in the spinal cord of anesthetized cats. The PAD was inferred from the changes produced by conditioning inputs on the intraspinal stimulus current required to produce a constant antidromic firing of single group I afferent fibers from the gastrocnemius (GS) or posterior biceps and semitendinosus (PBSt) nerves. Group I GS and PBSt fibers ending in the intermediate nucleus could be classified in three different types according to their PAD patterns in response to stimulation of cutaneous nerves and of descending fibers. In one set of group I fibers stimulation of cutaneous nerves and of the ipsilateral brain stem reticular formation, or the contralateral red nucleus, produced no PAD, but was able to inhibit the PAD generated by stimulation of group I fibers from flexors (type A PAD pattern). PBSt nerve fibers with this PAD pattern had peripheral thresholds and conduction velocities between 1.01 and 1.56 times threshold and 76.3 to 118 m/s, respectively. A second set of group I fibers was found to be depolarized by cutaneous nerves as well as by stimulation of rubrospinal and reticulospinal fibers (type B PAD pattern). The peripheral thresholds and conduction velocities of PBSt afferent fibers with a type B PAD pattern were of 1.66-2.03 times threshold and 71-83 m/s, respectively. We found a third set of group I fibers that were also depolarized by reticulospinal and rubrospinal inputs, but not by cutaneous nerves that instead inhibited the PAD elicited by group I volleys in flexor nerves (type C PAD pattern). All PBSt afferent fibers with a type C PAD pattern, with the exception of two, had peripheral thresholds and velocities between 1.46 and 2.16 times threshold and between 72 and 89 m/s, respectively. Stimulation of the Deiter's nucleus was found to depolarize the intraspinal terminals of a small fraction of group I GS fibers with a type A PAD pattern and of all group I GS and PBSt fibers with type B and C PAD patterns. The PAD produced by vestibulospinal stimulation in fibers with type A and C PAD patterns could be inhibited by conditioning volleys applied to cutaneous nerves. It is suggested that group I afferent fibers from flexors and extensors with a type A PAD pattern are group Ia, and that most fibers with type B and type C PAD patterns are group Ib.(ABSTRACT TRUNCATED AT 400 WORDS)

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