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PubMed1992

Propofol and barbiturate depression of spinal nociceptive neurotransmission.

Barbiturates are often described as non-analgesic or even hyperalgesic agents; the newer intravenous anesthetic agent propofol is said to be non-analgesic. Both propofol and barbiturates occupy sites on the GABAA receptor. The present study was designed to compare the effects of propofol and barbiturates on nociceptive-related neurotransmission in neonatal rat spinal cord; to search for actions that might be hyperalgesic; and to determine the extent to which propofol depression of nociceptive neurotransmission is mediated by GABAA receptors. The monosynaptic reflex, a slow ventral root potential (slow VRP) and the dorsal root potential (DRP) were recorded from isolated neonatal (1-5 days old) superfused rat spinal cords in response to electrical stimulation of a lumbar dorsal root. The slow VRP and the DRP are related to nociception. Propofol (0.5-10 microM), pentobarbital (1-10 microM), and thiopental (1-10 microM) reversibly depressed the slow VRP. Dose-response curves were monophasic and linear over this range. The monosynaptic reflex was unaffected. The GABAA agonist muscimol (0.2-1 microM) also depressed the slow VRP. Propofol and barbiturate slow VRP depression was antagonized by the GABAA antagonist bicuculline (1 microM). Propofol depressed the response evoked by direct application of substance P. The DRP is a GABAA-mediated depolarization of primary afferent nerve terminals that diminishes the effectiveness of nociceptive input. Propofol and thiopental increased electrically evoked DRP amplitude and increased the DRP evoked by application of muscimol. Both propofol and barbiturates thus depressed the nociceptive-related slow VRP and enhanced the antinociceptive DRP; their effective concentrations are at or close to the general anesthetic range for these agents. No anti-analgesic or hyperalgesic effect was observed. (ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Stochastic versus deterministic variability in simple neuronal circuits: I. Monosynaptic spinal cord reflexes.

Long time series of monosynaptic Ia-afferent to alpha-motoneuron reflexes were recorded in the L7 or S1 ventral roots in the cat. Time series were collected before and after spinalization at T13 during constant amplitude stimulations of group Ia muscle afferents in the triceps surae muscle nerves. Using autocorrelation to analyze the linear correlation in the time series demonstrated oscillations in the decerebrate state (4/4) that were eliminated after spinalization (5/5). Three tests for determinism were applied to these series: 1) local flow, 2) local dispersion, and 3) nonlinear prediction. These algorithms were validated with time series generated from known deterministic equations. For each experimental and theoretical time series used, matched time-series of stochastic surrogate data were generated to serve as mathematical and statistical controls. Two of the time series collected in the decerebrate state (2/4) demonstrated evidence for deterministic structure. This structure could not be accounted for by the autocorrelation in the data, and was abolished following spinalization. None of the time series collected in the spinalized state (0/5) demonstrated evidence of determinism. Although monosynaptic reflex variability is generally stochastic in the spinalized state, this simple driven system may display deterministic behavior in the decerebrate state.

Afferent Pathways↗

PubMed2004

Aglycemia and ischemia depress monosynaptic and polysynaptic reflexes in neonatal rat spinal cord in vitro by involving different types of 5-hydroxytryptamine receptors.

Involvement of 5-hydroxytryptaminergic (5-HT) system for aglycemia- and ischemia-induced depression of the spinal reflexes was evaluated. The monosynaptic (MSR) and polysynaptic (PSR) reflex potentials were elicited in the ventral root by stimulating the corresponding dorsal root in an isolated spinal cord from neonatal rat. Superfusion of aglycemic (glucose-free) or ischemic (glucose- and O(2)-free) solution produced a time-dependent depression of the spinal reflexes and abolished them within 35 min. The time required to produce 50% depression of the reflexes (T-50) was around 19 and 13 min for aglycemia and ischemia, respectively. Spiperone (5-HT(2A) antagonist) and ketanserin, (5-HT(2A/2C) antagonist) blocked the aglycemia-induced depression of the reflexes completely while ondansetron (5-HT(3) antagonist) attenuated it partially (as abolition times were around 50 min). Ischemia-induced depression was blocked up to 50 min by ketanserin or ondansetron but not by spiperone. In the presence of ketanserin or ondansetron, the reflexes were abolished by 60 min while in spiperone the reflexes were abolished by 30 min. In 5,7-dihydroxytryptamine treated rats, aglycemia depressed the reflexes by 45 min (greater than control, P<0.05) while the time for ischemia-induced depression was not different from the control response. The results indicate that aglycemia involves mainly 5-HT(2) receptors while ischemia involves 5-HT(3) receptors.

Action Potentials↗

PubMed2003

Fatigue-related depression of the feline monosynaptic gastrocnemius-soleus reflex.

In decerebrate cats, changes in the monosynaptic reflex (MSR) of gastrocnemius-soleus (G-S) motoneurones were studied after fatiguing stimulation (FST) of the G-S muscles. Monosynaptic reflexes were evoked by stimulation of Ia fibres in the G-S nerve and recorded from a filament of ventral root (VR) L7. FST (intermittent 40 s(-1) stimulation for 10-12 min) was applied to the distal part of the cut VR S1. FST reduced MSR amplitudes to 0.64 +/- 0.04 (mean +/-s.e.m.) of the prefatigue values. The suppression remained stable for approximately 25 min and then MSR amplitudes gradually returned towards the normal. To test for the involvement of presynaptic and recurrent inhibition, MSRs were conditioned by stimulation of the nerve to the posterior biceps and semitendinosus (PBSt) muscles or a filament of VR L7, respectively. The intensity of presynaptic inhibition (reduction of the normalized value of MSR amplitude during conditioning) increased from 0.19 +/- 0.02 in prefatigue to 0.44 +/- 0.04 within a 5.3-18.2 min interval after FST, followed by a recovery. In contrast, the intensity of recurrent inhibition first diminished from 0.23 +/- 0.02 in prefatigue to 0.15 +/- 0.01 within 15.6-30.1 min after FST and then gradually recovered. Both primary afferent depolarization and the intensity of antidromic discharges in primary afferents increased with the presynaptic inhibition intensity. These results demonstrate a fatigue-related suppression of Ia excitation of synergistic motoneurones, probably arising from the activation of group III and IV afferents. The effects could in part be due to increased presynaptic inhibition, while recurrent inhibition plays a minor role.

Animals↗

PubMed1996

Anticipatory responses to a self-applied load in normal subjects and hemiparetic patients.

A bimanual loading task was studied in eight right-handed normal subjects and nine hemiparetic patients in order to detect anticipatory adjustments and to analyse the reflex and voluntary, responses induced by the perturbation. The left forearm (or the impaired side in patients) was flexed at approximately 90 degrees and free to rotate in a vertical sagittal plane. It was held to resist a load (2-3 kg) dropped either by an experimenter (control situation), or by the subject himself with no visual control (self-applied situation). The load was dropped from the right hand by normal subjects and from the unimpaired hand by hemiparetic patients. The initial distance the load fell was 0.05-0.35 m. The elbow movements of the limb receiving the load were recorded with a linear accelerometer at the wrist, a potentiometer at the elbow and via the EMG signals from flexor muscles. Normal subjects always made an anticipatory flexion movement prior to the impact in the self-applied situation, but not in the control situation. The anticipatory flexion of hemiparetic patients was slower and longer. The amplitude of the anticipatory flexion at the time of impact and its duration were correlated with the mass of the load and the initial distance between the two hands in both groups. The anticipatory flexion reduced the distance through which the load fell and thus its kinetic energy at impact. The impact induced a brisk extension which was always smaller in the self-applied situation for a given kinetic energy. In normal subjects, the amplitude of the monosynaptic reflex (MSR) following the impact in flexor muscles was usually greater in the self-applied situation, but its gain was either reduced or unchanged. The gain of the functional stretch reflex (FSR) was consistently reduced in the self-applied situation. Depression of the FSR gain occurred in only two hemiparetic patients who had the best recovered motor function. Anticipation always ended up minimizing the perturbation following different motor strategies. The normal subjects fell into two groups. One group adjusted the anticipatory forearm flexion to correct the extension disturbance as fast as possible; the second group relied on an accurate adjustment of the final position. Hemiparetic patients showed idiosyncratic intermediate behavior.

Adult↗

PubMed1989

Ammonium decreases excitatory synaptic transmission in cat spinal cord in vivo.

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.

Action Potentials↗

PubMed2003

The H-reflex as a tool in neurophysiology: its limitations and uses in understanding nervous system function.

The Hoffmann reflex (H-reflex) is extensively used as both a research and clinical tool. The ease with which this reflex can be elicited in several muscles throughout the body makes it an attractive tool. This review discusses some of the important limitations in using the H-reflex. In particular, the inaccurate but widely held assumptions that the H-reflex (1). represents the monosynaptic reflex of the Ia afferent onto homonymous motoneurons, and (2). can be used to measure motoneuronal excitability are addressed. The second part of this review explores the utility of the H-reflex as a neural probe in neurophysiology and motor control research. Applications ranging from the investigation of the functional organization of neural circuitry to the study of adaptive plasticity in spinal structures in health and disease suggest that the H-reflex will continue to be an extensively used tool in motor control neurophysiology.

Animals↗

PubMed1983

Glucocorticoid modification of spinal dopamine receptor activation by apomorphine.

The effects of an intensive short-term glucocorticoid (e.g. triamcinolone) regimen in cats have been studied on the actions of the dopamine (DA) receptor agonist apomorphine (APO) on spinal lumbar primary afferent excitability (dorsal root reflex or DRR) and monosynaptic reflex (MSR) transmission. Glucocorticoid dosing significantly decreased the APO-induced depression of the spinal DRR, but not the similar action of APO on the MSR. This complex effect of triamcinolone on spinal dopaminergic activation by APO may represent a differential action of glucocorticoid on two types of spinal DA receptors with one type, but not the other, undergoing partial desensitization.

Afferent Pathways↗

PubMed1969