scholarly journals Permanent central synaptic disconnection of proprioceptors after nerve injury and regeneration. II. Loss of functional connectivity with motoneurons

2011 ◽  
Vol 106 (5) ◽  
pp. 2471-2485 ◽  
Author(s):  
Katie L. Bullinger ◽  
Paul Nardelli ◽  
Martin J. Pinter ◽  
Francisco J. Alvarez ◽  
Timothy C. Cope
Keyword(s):  
Functional Connectivity ◽  
Action Potentials ◽  
Companion Paper ◽  
Muscle Afferents ◽  
Adult Rats ◽  
Ia Afferent ◽  
Synaptic Excitation ◽  
Spike Triggered Averaging ◽  
Paired Recording ◽  
Muscle Nerve

Regeneration of a cut muscle nerve fails to restore the stretch reflex, and the companion paper to this article [Alvarez FJ, Titus-Mitchell HE, Bullinger KL, Kraszpulski M, Nardelli P, Cope TC. J Neurophysiol (August 10, 2011). doi:10.1152/jn.01095.2010] suggests an important central contribution from substantial and persistent disassembly of synapses between regenerated primary afferents and motoneurons. In the present study we tested for physiological correlates of synaptic disruption. Anesthetized adult rats were studied 6 mo or more after a muscle nerve was severed and surgically rejoined. We recorded action potentials (spikes) from individual muscle afferents classified as IA like (*IA) by several criteria and tested for their capacity to produce excitatory postsynaptic potentials (EPSPs) in homonymous motoneurons, using spike-triggered averaging (STA). Nearly every paired recording from a *IA afferent and homonymous motoneuron (93%) produced a STA EPSP in normal rats, but that percentage was only 17% in rats with regenerated nerves. In addition, the number of motoneurons that produced aggregate excitatory stretch synaptic potentials (eSSPs) in response to stretch of the reinnervated muscle was reduced from 100% normally to 60% after nerve regeneration. The decline in functional connectivity was not attributable to synaptic depression, which returned to its normally low level after regeneration. From these findings and those in the companion paper, we put forward a model in which synaptic excitation of motoneurons by muscle stretch is reduced not only by misguided axon regeneration that reconnects afferents to the wrong receptor type but also by retraction of synapses with motoneurons by spindle afferents that successfully reconnect with spindle receptors in the periphery.

Rescue of motoneuron and muscle afferent function in cats by regeneration into skin. II. Ia-motoneuron synapse

1995 ◽  
Vol 73 (2) ◽  
pp. 662-673 ◽  
Author(s):  
L. M. Mendell ◽  
J. S. Taylor ◽  
R. D. Johnson ◽  
J. B. Munson
Keyword(s):  
High Frequency ◽  
Muscle Afferents ◽  
Medial Gastrocnemius ◽  
High Frequency Stimulation ◽  
Lateral Gastrocnemius ◽  
Essentially Normal ◽  
Muscle Afferent ◽  
Muscle Nerve ◽  
Frequency Stimulation

1. In this study we describe application of high-frequency stimulation to the group Ia afferent-to-motoneuron synapse of cats to determine the extent to which regeneration of axotomized muscle afferents and motoneurons into skin or into muscle rescues their ability to generate excitatory postsynaptic potentials (EPSPs). 2. The medial gastrocnemius (MG) muscle nerve was transected and 1) left chronically axotomized, 2) cross-united to the caudal cutaneous sural (CCS) nerve, or 3) self-united. The ability of the operated MG muscle afferents to generate EPSPs in normal lateral gastrocnemius-soleus (LGS) motoneurons and of normal LGS muscle afferents to generate EPSPs in the operated MG motoneurons was tested 5 wk-30 mo later. 3. EPSPs were generated by bursts of 32 shocks at 167 Hz and averaged in register. In normal cats, EPSP amplitude decreased (negative modulation) during these bursts in type S motoneurons and could increase or decrease in type F motoneurons (positive or negative modulation). 4. After axotomy, EPSPs generated both in axotomized motoneurons and by axotomized afferents showed only negative modulation during the burst, and the negative modulation was much greater than in normal animals. Regeneration of the muscle nerve into skin significantly decreased the negative modulation relative to axotomy. Regeneration of the muscle nerve into muscle restored the EPSP modulation behaviors even more, to essentially normal values. 5. We conclude that the ability of muscle afferents to generate EPSPs in motoneurons in response to high-frequency stimulation, and the ability of motoneurons to express those EPSPs, are both influenced by the target innervated by those neurons. Synaptic efficacy is severely reduced by target deprivation (axotomy), partially rescued by cross-regeneration into skin, and rescued virtually completely by regeneration into the native muscle. We speculate on the role of target-derived neurotrophins in these effects.

Effects of NH4+ on reflexes in cat spinal cord

1990 ◽  
Vol 64 (2) ◽  
pp. 565-574 ◽  
Author(s):  
W. Raabe
Keyword(s):  
Spinal Cord ◽  
Synaptic Transmission ◽  
Nerve Stimulation ◽  
Action Potentials ◽  
Presynaptic Inhibition ◽  
Excitatory Synaptic Transmission ◽  
P Wave ◽  
Postsynaptic Inhibition ◽  
Presynaptic Terminals ◽  
Muscle Nerve

1. In deeply barbiturate-anesthetized animals. NH4+ decreases spinal excitatory synaptic transmission by neuronal depolarization and subsequent block of conduction of action potentials into presynaptic terminals of low-threshold (presumably Ia-) afferents. Because barbiturates by themselves depress excitatory synaptic transmission and may have modified the effects of NH4+, this study examines the effect of NH4+ on excitatory synaptic transmission in the unanesthetized animal. 2. The effects of NH4+ on monosynaptic and polysynaptic excitatory reflexes as well as di- and polysynaptic inhibition were investigated in the spinal cord of the decerebrate and unanesthetized cat in vivo. 3. The monosynaptic excitatory reflex (MSR) elicited by muscle nerve stimulation and polysynaptic excitatory reflexes elicited by muscle (MSR-PSR) or cutaneous nerve stimulation (Cut-PSR) were recorded from the ventral roots L7 or S1. The P-wave was recorded from the cord dorsum. Di- and polysynaptic inhibition was elicited by muscle nerve stimulation and measured as decrease of the MSR. 4. Intravenous infusion of ammonium acetate (AA) decreased MSR and the monosynaptic motoneuron pool excitatory postsynaptic potential (EPSP) recorded from the ventral root (VR-EPSP). Decrease of MSR and VR-EPSP was accompanied by an increase of the intraspinal conduction time in presynaptic terminals. The maximal decrease of the MSR was preceded by a period of transient increase of the MSR and reflex discharges from previously subthreshold VR-EPSPs. 5. The effects of NH4+ on MSR and VR-EPSP are consistent with those in barbiturate-anesthetized animals and suggest that NH4+ also decreases monosynaptic excitation in unanesthetized animals by depolarization and subsequent conduction block for action potentials in presynaptic terminals. 6. Decrease of the MSR was accompanied by a decrease of the P-wave, indicating that NH4+ simultaneously decreases mono- and oligosynaptic excitatory synaptic transmission as well as presynaptic inhibition. 7. Decrease of the MSR was accompanied by increases of MSR-PSR and Cut-PSR and decreases of di- and polysynaptic postsynaptic inhibition. 8. The neuronal circuits underlying MSR-PSR and Cut-PSR include presynaptic inhibition of group I and II afferents as well as postsynaptic inhibition of motoneurons. It is suggested that increases of MSR-PSR and Cut-PSR are contributed to by decreases of pre- and postsynaptic inhibition and neuronal depolarization by NH4+. These effects increase afferent input to motoneurons, permit uncontrolled discharge of motoneurons, and initiate reflex discharges by previously subthreshold excitatory postsynaptic potentials.

scholarly journals Effects of tetrodotoxin and anaesthetics on brain metabolism and transport during anoxia

1972 ◽  
Vol 126 (4) ◽  
pp. 851-867 ◽  
Author(s):  
R. Shankar ◽  
J. H. Quastel
Keyword(s):  
Action Potentials ◽  
Brain Cortex ◽  
Aerobic Glycolysis ◽  
Rat Kidney ◽  
Brain Slices ◽  
Anaerobic Glycolysis ◽  
High Concentration ◽  
Adult Rats ◽  
Brain Cortex Slices ◽  
Cortex Slices

1. Tetrodotoxin, at concentrations at which it abolishes generation of action potentials in the nervous system, enhances by about 300% the rate of anaerobic glycolysis of brain-cortex slices from adult rats, or from adult and infant guinea pigs. This occurs to a greater extent in Ca2+-deficient incubation media than in Ca2+-rich media. Tetrodotoxin has no accelerative effect on cerebral aerobic glycolysis. 2. Tetrodotoxin does not affect the rate of anaerobic glycolysis of 2-day-old rat brain-cortex slices, nor that of adult rat kidney medulla, nor that of an extract of an acetone-dried powder of brain. 3. Tetrodotoxin does not affect the rate of penetration of glucose into brain slices. 4. Its effect is not apparent if it is added 10min or later after the onset of anoxia. 5. Its effect diminishes as the concentration of K+ in the incubation medium is increased while that of Na+ is decreased. 6. Its salient effect, at the onset of anoxia, is to diminish influx of Na+ into, and efflux of K+ from, the brain slices. 7. Substances that promote cerebral influx of Na+, e.g. protoveratrine, sodium l-glutamate, diminish the accelerative action of tetrodotoxin. 8. It is concluded that tetrodotoxin exerts its effect on anaerobic glycolysis by suppressing, at the onset of anoxia, the generation of action potentials and thereby the accompanying influx of Na+ and efflux of K+. It is suggested that glycolytic stimulation occurs because a rate-limiting step, e.g. operation of pyruvate kinase, is stimulated by K+ and depressed by Na+. 9. Local anaesthetics behave in a manner similar to that of tetrodotoxin in enhancing cerebral anaerobic glycolysis. 10. Sodium Amytal has a marked effect at relatively high concentration. 11. Tetrodotoxin diminishes efflux of amino acids, particularly glutamate and aspartate, at the onset of anoxia.

scholarly journals Effects of Acetazolamide on Transient K+ Currents and Action Potentials in Nodose Ganglion Neurons of Adult Rats

2011 ◽  
Vol 17 (1) ◽  
pp. 66-79 ◽  
Author(s):  
Shigeji Matsumoto ◽  
Shinki Yoshida ◽  
Mizuho Ikeda ◽  
Jun Kadoi ◽  
Masayuki Takahashi ◽  
...  
Keyword(s):  
Action Potentials ◽  
Nodose Ganglion ◽  
Adult Rats ◽  
Nodose Ganglion Neurons ◽  
Ganglion Neurons ◽  
K Currents

Ammonium decreases excitatory synaptic transmission in cat spinal cord in vivo

1989 ◽  
Vol 62 (6) ◽  
pp. 1461-1473 ◽  
Author(s):  
W. Raabe
Keyword(s):  
Spinal Cord ◽  
Synaptic Transmission ◽  
Action Potentials ◽  
Conduction Block ◽  
Excitatory Synaptic Transmission ◽  
Excitatory Postsynaptic Potential ◽  
Presynaptic Terminals ◽  
Ia Afferent ◽  
Afferent Fibers ◽  
Low Threshold

1. Glutamine is thought to be a precursor of the pool of glutamate that is used as synaptic transmitter. NH4+ inhibits glutaminase, the enzyme presumed to cleave glutamine into glutamate in synaptic terminals. Therefore a decrease by NH4+ of excitatory synaptic transmission in hippocampus was suggested to be due to the inability to utilize glutamine as a precursor for glutamate and subsequent transmitter depletion. This study reexamines the effects of NH4+ on excitatory synaptic transmission. 2. The effects of NH4+ on excitatory synaptic transmission from low-threshold afferent fibers, presumably Ia-afferent fibers, to motoneurons was investigated in the spinal cord of anesthetized cats in vivo. 3. Action potentials of low-threshold afferent fibers were recorded at the entry of the dorsal roots into the spinal cord. An extracellular electrode within a motoneuron nucleus recorded the action potential of low-threshold afferent fibers and the extracellular monosynaptic excitatory postsynaptic potential, i.e., the focal synaptic potential (FSP). This extracellular electrode also recorded the antidromic field potential (AFP) in response to ventral root stimulation. Electrodes on the ventral roots recorded the monosynaptic reflex (MSR) and the monosynaptic excitatory postsynaptic potential in motoneurons electrotonically conducted into the ventral roots (VR-EPSP). 4. Intravenous infusion of ammonium acetate (AA) reversibly decreased MSR, VR-EPSP, and FSP, i.e., decreased excitatory synaptic transmission. 5. The decrease of VR-EPSP and FSP was accompanied initially by a decrease of conduction and, eventually, a conduction block in presynaptic terminals of low-threshold afferent fibers. 6. The decreases of VR-EPSP and FSP were also accompanied by the transient appearance of a reflex discharge, triggered by VR-EPSPs of decreased amplitude, and changes of the AFP indicating increased invasion of motoneuron somata by antidromic action potentials. 7. It is suggested that NH4+ depolarizes intraspinal Ia-afferent fibers and motoneurons. This depolarization initially decreases and then blocks conduction of action potentials into the presynaptic terminals of Ia-afferent fibers. The conduction block prevents the release of excitatory transmitter and decreases excitatory synaptic transmission. 8. The suggested depolarizing action of NH4+ may be due to K+-like ionic properties of NH4+ and/or an inhibition of K+-uptake into astrocytes. 9. The conduction block in presynaptic terminals of low-threshold afferent fibers can fully explain the decrease of excitatory synaptic transmission by NH4+. Because of the conduction block in presynaptic terminals, this study does not permit a conclusion as to an inhibition by NH4+ fo the utilization of glutamine as a precursor for glutamate used as synaptic transmitter.

Factors determining segmental reflex action in normal and decerebrate cats

1990 ◽  
Vol 64 (5) ◽  
pp. 1625-1635 ◽  
Author(s):  
T. Sinkjaer ◽  
J. A. Hoffer
Keyword(s):  
Muscle Length ◽  
Muscle Spindles ◽  
Radiant Heat ◽  
Companion Paper ◽  
Muscle Afferents ◽  
Short Latency ◽  
Lateral Gastrocnemius ◽  
Implanted Electrodes ◽  
Extensor Muscles ◽  
Before And After

1. In the companion paper the gain of the stretch reflex in the ankle extensor muscles of normal cats was shown to increase after decerebration. The objectives of this study were 1) to identify the origin of the increased reflex and 2) to evaluate the contribution from afferents other than ankle extensor muscle afferents to the short-latency reflex. 2. Six cats were trained to stand unaided on four pedestals. Three cats were also trained to control the force exerted with the left hindlimb. The left soleus (SOL) and lateral gastrocnemius (LG) electromyogram (EMG), length, force, and temperature were recorded by chronically implanted electrodes and transducers. Measurements were taken before and after decerebration at the premammillary level. After decerebration limb temperature was returned to its normal range by the use of radiant heat. 3. Reproducible ramp-and-hold stretches and releases of the ankle extensor muscles were produced by a servo-controlled motor that rotated the left rear pedestal about the ankle joint. The length of the ankle extensor muscles changed by 2-3 mm within 30-35 ms after the onset of a ramp perturbation. Reflex responses before and after decerebration were compared at matched background values of muscle length and force. 4. In both the SOL and LG muscles, a short-latency EMG burst appeared 8-12 ms after stretch onset and lasted approximately 20 ms. After decerebration the onset of the rectified and smoothed EMG burst remained unchanged, but its area was increased by 36-89%. 5. The lateral gastrocnemius-soleus (LG-S) electroneurogram (ENG) was chronically recorded in two cats with a nerve cuff recording electrode implanted on the LG-S nerve. LG-S ENG activity started to increase soon after stretch onset and remained high during the entire ramp phase. The stretch-evoked LG-S ENG burst started approximately 8 ms earlier than the short-latency SOL and LG EMG bursts. It was interpreted to reflect mainly an increase in the activity of Group Ia and Ib muscle afferents, caused by increases in both muscle length and muscle force during the stretch. After the cats were decerebrated, for matched postural conditions, the area of the stretch-evoked LG-S ENG burst was increased by 29-35%. Because the length and force changes sensed by the muscle receptors before and after decerebration were similar, this suggests that the sensitivity of muscle spindles was increased as a consequence of altered activity in fusimotor neurons after decerebration.(ABSTRACT TRUNCATED AT 400 WORDS)

Low-Voltage-Activated Calcium Current Does Not Regulate the Firing Behavior in Paired Mechanosensory Neurons With Different Adaptation Properties

2000 ◽  
Vol 83 (2) ◽  
pp. 746-753 ◽  
Author(s):  
Shin-Ichi Sekizawa ◽  
Andrew S. French ◽  
Päivi H. Torkkeli
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Low Voltage ◽  
Firing Frequency ◽  
Oscillatory Behavior ◽  
Firing Behavior ◽  
Single Action ◽  
Synaptic Excitation ◽  
Intracellular Ca ◽  
The Difference

Low-voltage-activated Ca2+ currents (LVA- I Ca) are believed to perform several roles in neurons such as lowering the threshold for action potentials, promoting burst firing and oscillatory behavior, and enhancing synaptic excitation. They also may allow rapid increases in intracellular Ca2+ concentration. We discovered LVA- I Ca in both members of paired mechanoreceptor neurons in a spider, where one neuron adapts rapidly (Type A) and the other slowly (Type B) in response to a step stimulus. To learn if I Ca contributed to the difference in adaptation behavior, we studied the kinetics of I Ca from isolated somata under single-electrode voltage-clamp and tested its physiological function under current clamp. LVA- I Ca was large enough to fire single action potentials when all other voltage-activated currents were blocked, but we found no evidence that it regulated firing behavior. LVA- I Ca did not lower the action potential threshold or affect firing frequency. Previous experiments have failed to find Ca2+-activated K+ current ( I K(Ca)) in the somata of these neurons, so it is also unlikely that LVA- I Ca interacts with I K(Ca) to produce oscillatory behavior. We conclude that LVA-Ca2+ channels in the somata, and possible in the dendrites, of these neurons open in response to the depolarization caused by receptor current and by the voltage-activated Na+ current ( I Na) that produces action potential(s). However, the role of the increased intracellular Ca2+ concentration in neuronal function remains enigmatic.

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