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Results for “Reflex, Monosynaptic”

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PubMed1990

Actions of intrathecal chloroprocaine and sodium bisulfite on rat spinal reflex function utilizing a noninvasive technique.

An in situ electrophysiologic technique was developed to study the effects of intrathecal chloroprocaine and sodium bisulfite on spinal reflex activity in the anesthetized rat. By not surgically invading the subarachnoid space, this procedure allows drugs to be administered remotely through an indwelling catheter while monitoring drug effects on the spinal monosynaptic reflex with noninvasive electrophysiologic methods. In this way the normal pharmacokinetic factors are left intact so that time-action relations can be monitored under conditions that may resemble spinal anesthesia in conscious animals. Using this technique it was established that chloroprocaine with and without 0.2% sodium bisulfite blocks the monosynaptic reflex in a fully reversible manner. The reflex block of a higher concentration of bisulfite (0.6%) was poorly reversible in some preparations. These results correlate well with a previous in vivo behavioral study on the motor and sensory blocking actions of intrathecal chloroprocaine and bisulfite in the same animal species. The authors feel this technique can be used to study the temporal changes in reflex activity caused by other drugs administered via the intrathecal route.

Action Potentials↗

PubMed1996

Control of transmission in muscle group IA afferents during fictive locomotion in the cat.

1. Primary afferent depolarization (PAD) can be evoked by sensory volleys, supraspinal commands, or the activity of spinal locomotor networks (locomotor-related PAD). In this study we investigated the effect of locomotor-related PAD and of sensory-evoked PAD on the monosynaptic transmission between the group IA muscle afferents and motoneurons in the lumbosacral spinal cord. 2. Six pairs of group IA afferents and motoneurons [4 tibialis anterior (TA), 1 medial gastrocnemius (MG), 1 lateral gastrocnemius-soleus (LGS)] were successfully recorded intracellularly during spontaneous fictive locomotion in the decerebrate cat. The membrane potentials of TA axons and motoneurons were maximally depolarized during the flexor phase of the locomotor cycle. In MG and LGS pairs, the maximum depolarization in IA axons occurred during the flexor phase and, in motoneurons, during the extensor phase. There were no antidromic discharges in the recorded axons. The effects of locomotor-related PAD on IA transmission were evaluated by comparing the unitary excitatory postsynaptic potentials (EPSPs) in the motoneuron evoked by the spontaneous orthodromic firing of the group IA axon during the flexor and extensor phases, respectively. In TA pairs, the maximum amplitude of unitary EPSPs occurred during the flexor phase when the motoneuron and the axon were maximally depolarized. In the MG and LGS pairs, the maximal amplitude of unitary EPSPs occurred during the extensor phase when the motoneuron was maximally depolarized and when the axon was the least depolarized. Overall, the amplitude of unitary EPSPs was clearly modulated during the fictive step cycle and always reached a maximum during the depolarized phase of the motoneuron, whether the group IA axon was maximally depolarized or not during that phase. 3. The effect of sensory-evoked PAD on synaptic transmission was also studied in nonlocomoting preparations. One TA pair was successfully recorded and PADs were evoked by the stimulation of a peripheral nerve. The amplitude of unitary EPSPs in the motoneuron was greatly depressed during the PADs. This result is a direct demonstration of the presynaptic inhibition associated with the sensory-evoked PAD in the monosynaptic reflex pathway of the cat. 4. We conclude from these results that the locomotor-related PAD did not contribute significantly to the modulation of transmission in the monosynaptic reflex pathway of the cat during fictive locomotion. On the other hand, the results confirmed that PAD evoked by sensory input decreases group IA afferent transmission efficiently most probably by presynaptic inhibition. The results suggest therefore that, during real locomotion, sensory feedback induced by the moving limbs or perturbations will evoke an important presynaptic inhibition of the release from group IA primary afferent terminals.

Afferent Pathways↗

PubMedDate not supplied

[Effect of stimulation of the spinal cord on phasic and tonic reflexes in patients with central motor neuron damage].

Spinal cord stimulation (SCS) is a method enabling the control of increased muscle tonus to be achieved in various spinal cord injuries. Polyelectromyographic (PEMG) methods were used for neurophysiological assessment of the degree of cord damage and persistent spinal reflexes as well as supramedullary influences. The analysed material comprised 40 PEMG records in 19 patients with spastic paraparesis or paraplegia after cord injury, cord tumour or multiple sclerosis. In 15 cases tentative epidural cord stimulation was done and 11 patients received implantation of a system for long-term stimulation. In most cases the epidural electrodes were implanted below the damaged segment, usually in the thoracic part of the cord. Before and after SCS beginning PEMG was done with a 16-channel Mingograph Siemens Elema with simultaneous recording of the responses from the symmetric muscles: quadriceps, semitendinous, adductor femoris, anterior tibialis and triceps surae. The effect of SCS was analysed on exteroceptive and proprioceptive reactions during testing of knee and ankle reflexes, and on the response of the muscles to vibration. In most patients a reduction was observed of the intensity of tendon reflexes, particularly the spread of the reflex to the contralateral extremity was no longer seen. The vibration reflex had a tonic character persisting in 48% of the studied muscles, even in patients with clinically complete transsection of the cord. The change of the character of monosynaptic reflexes and the presence of the vibration reflex suggest that SCS modifies the proprioceptive segmental spinal reactions.

Adult↗

PubMed1995

Can the alpha 2-adrenoceptor agonist-mediated suppression of nocifensive reflex responses be due to action on motoneurons or peripheral nociceptors?

To exclude the possibility that the suppression of nocifensive reflex responses induced by alpha 2-adrenergic agents is due to action on alpha-motoneurons or peripheral nociceptors, we studied the effect of medetomidine, an alpha 2-adrenoceptor agonist, on the monosynaptic reflex and on the primary afferent nociceptor-mediated antidromic vasodilator response in rats. Additionally, the effect on the dorsal root potential, an index of a transient excitability change in the central terminals of primary afferent fibers, was determined. Medetomidine was applied systemically at doses (100 and 300 micrograms/kg) which have proven strongly antinociceptive in previous studies. The amplitudes of a submaximal monosynaptic reflex volley or a submaximal dorsal root potential were not changed by medetomidine. Medetomidine induced a decrease of cutaneous blood flow but did not abolish the vasodilatatory response to antidromic stimulation of the sciatic nerve at C-fiber intensity as determined by the laser Doppler flow method. The results indicate that the alpha 2-adrenoceptor-mediated suppression of nocifensive reflex responses is not caused by a decreased excitability of motoneurons or peripheral nociceptors. An alpha 2-adrenoceptor agonist does not modulate the transient stimulus-evoked change in the excitability of central terminals of primary afferent fibers.

Adrenergic alpha-2 Receptor Agonists↗

PubMed2006

John Eccles' studies of spinal cord presynaptic inhibition.

Presynaptic inhibition is one of many areas of neurophysiology in which Sir John Eccles did pioneering work. Frank and Fuortes first described presynaptic inhibition in 1957. Subsequently, Eccles and his colleagues characterized the process more fully and showed its relationship to primary afferent depolarization. Eccles' studies emphasized presynaptic inhibition of the group Ia monosynaptic reflex pathway but also included group Ib, II and cutaneous afferent pathways, and the dorsal column nuclei. Presynaptic inhibition of the group Ia afferent pathway was demonstrated by depression of monosynaptic excitatory postsynaptic potentials and inhibition of monosynaptic reflex discharges. Primary afferent depolarization was investigated by recordings of dorsal root potentials, dorsal root reflexes, cord dorsum and spinal cord field potentials, and tests of the excitability of primary afferent terminals. Primary afferent depolarization was proposed to result in presynaptic inhibition by reducing the amplitude of the action potential as it invades presynaptic terminals. This resulted in less calcium influx and, therefore, less transmitter release. Presynaptic inhibition and primary afferent depolarization could be blocked by antagonists of GABA(A) receptors, implying a role of interneurons that release gamma aminobutyric acid in the inhibitory circuit. The reason why afferent terminals were depolarized was later explained by a high intracellular concentration of Cl(-) ions in primary sensory neurons. Activation of GABA(A) receptors opens Cl(-) channels, and Cl(-) efflux results in depolarization. Another proposed mechanism of depolarization was an increase in extracellular concentration of K(+) following neural activity. Eccles' work on presynaptic inhibition has since been extended in a variety of ways.

Afferent Pathways↗

PubMed1979

The effects of cold-induced muscle spindle secondary activity on monosynaptic and stretch reflexes in the decerebrate cat.

The effects of muscle spindle secondary ending activity on the stretch reflex were studied in unanesthetized decerebrate cats. Activation of secondary endings was accomplished by reducing the muscle temperature. This has been shown to cause a sustained asynchronous discharge from secondary endings. Cooling of the medial gastrocnemius or lateral gastrocnemius-soleus muscles caused an increase in the phasic and tonic components of their stretch reflexes. Cooling of the relaxed medial gastrocnemius muscle caused similar increases in the components of the stretch reflex of the synergistic lateral gastrocnemius-soleus muscle and an increase in its monosynaptic reflex. It was concluded that the facilitatory autogenetic and synergistic effects of muscle cooling on the stretch and monosynaptic reflexes were brought about by activity in group II afferents from muscle spindle secondary endings and could not be ascribed to any other type of muscle receptor. These results support the concept of an excitatory role for the secondary endings of the muscle spindle in the stretch reflex of the decerebrate cat.

Animals↗

PubMed1993

Significance of monosynaptic and polysynaptic reflexes in neonatal rat spinal cord in vitro.

Stimulation of a dorsal root in an isolated spinal cord, elicited a monosynaptic reflex (MSR) in the corresponding ventral root at a latency of 3-5 msec and a dorsal root reflex (DRR) in an adjacent dorsal root 2-3 times the latency of MSR. The magnitude of DRR was 10 times smaller than the MSR. These reflexes could be decreased by the agents which suppress synaptic transmission e.g. either by decreasing the [Ca2+]0 or by increasing [Mg2+]0. In the absence of magnesium ([Mg2+]0) in the perfusing medium, the MSR was 15-20% greater in its magnitude and the segmental polysynaptic reflex (PSR) was distinctly seen at 8-10 msec latency. Segmental PSR disappeared when [Mg2+]0 ions are added to perfusing medium probably indicating the involvement of N-methyl-D-aspartate receptors. Further, in this preparation homosynaptic inhibition and pre- or post-synaptic inhibitions could be elicited. This preparation, thus serves as useful model for the study of central synaptic transmission to study the pharmacological or neurotoxic agents.

Animals↗

PubMed1973

Effect of baclofen upon monosynaptic and tonic vibration reflexes in patients with spasticity.

Measurements of monosynaptic reflex activity were made in 10 patients with spasticity before and during treatment with baclofen. There was evidence of both central sensory facilitation and increased fusimotor drive in untreated patients compared with controls. During treatment with baclofen, the central facilitation was reduced but there was no evidence of a reduction in fusimotor drive. The torque developed by vibration of the belly of the biceps and triceps muscles was not significantly different in 14 patients with spasticity compared with controls, and was not altered by treatment with baclofen despite clinical improvement in 12 of the patients. It is suggested that baclofen reduces the excitability of the monosynaptic reflex arc from dynamic spindles but does not affect the mechanisms responsible for the tonic vibration reflex.

Aminobutyrates↗

PubMed1955

Mono-synaptic reflex responses of individual motoneurons.

Individual motoneuron responses to a variety of afferent inputs have been examined. At a given input some motoneurons respond to every trial, some to no trial, and some respond to a certain percentage of trials that is characteristic for the motoneuron at that input. The performance of a motoneuron is expressed by means of a firing index that relates the number of responses to the number of trials. In a representative assemblage of individual motoneurons some 20 to 30 per cent display intermediate firing indices. This number, comprising an "intermediate zone" remains fairly constant at different levels of input although the individuals within it may be entirely different at two different levels of input. Frequency distribution of individuals with respect to firing indices is U-shaped. Intermediacy of firing indices depends upon temporal fluctuation of excitability which, in the first approximation, is normal. The individual motoneurons are approximately equally frequently distributed with respect to transmitter potentiality of their monosynaptic reflex afferent connections. The distribution of motoneurons with respect to transmitter potentiality of their monosynaptic reflex connections is considered representative of a natural pool in that the sum of their individual post-tetanic response behaviors accurately reproduces the course of post-tetanic potentiation in a natural pool.

Humans↗

PubMed2002

The influence of increased muscle spindle sensitivity on Achilles tendon jerk and H-reflex in relaxed human subjects.

Whether the fusimotor system contributes to reflex gain changes during reinforcement maneuvers is re-examined in the light of new data. Recently, from direct recordings of spindle afferent activity originating from ankle flexor muscles, we showed that mental computation increased the muscle spindle mechanical sensitivity in completely relaxed human subjects without concomitant alpha-motoneuron activation, providing evidence for selective fusimotor drive activation. In the present study, the effects of mental computation were investigated on monosynaptic reflexes elicited in non-contracting soleus muscle either by direct nerve stimulation (Hoffmann reflex, H) or by tendon tap (Tendinous reflex, T). The aim was to relate the time course of the changes in reflex size to the increase in spindle sensitivity during mental task in order to explore whether fusimotor activation can influence the size of the monosynaptic reflex. The results show changes in reflex amplitude that parallel the increase in muscle spindle sensitivity. When T-reflex is consistently facilitated during mental effort, the H-reflex is either depressed or facilitated, depending on the subjects. These findings suggest that the increased activity in muscle spindle primary endings may account for mental computation-induced changes in both tendon jerk and H-reflex. The facilitation of T-reflex is attributed to the enhanced spindle mechanical sensitivity and the inhibition of H-reflex is attributed to post-activation depression following the increased Ia ongoing discharge. This study supports the view that the fusimotor sensitization of muscle spindles is responsible for changes in both the mechanically and electrically elicited reflexes. It is concluded that the fusimotor drive contributed to adjustment of the size of tendon jerk and H-reflex during mental effort. The possibility that a mental computation task may also operate by reducing the level of presynaptic inhibition is discussed on the basis of H-reflex facilitation.

Achilles Tendon↗

PubMed1985

The role of substance P as a neurotransmitter in the reflexes of slow time courses in the neonatal rat spinal cord.

In order to reveal the spinal reflexes involving the transmitter action of substance P (SP), the effects of capsaicin and an SP antagonist on the isolated spinal cord of the neonatal rat studied. When a single shock stimulus was given to a dorsal root (L3-L5) or a sciatic nerve, depolarizing responses of various time courses were recorded extracellularly from both ipsi- and contra-lateral ventral roots of the corresponding segments. The reflex response recorded from the contralateral ventral root consisted of fast and slow components, which will be referred to as contralateral fast and slow ventral root potentials (v.r.ps). The latter contralateral slow v.r.p. had a time-to-peak of 2-5 s and lasted 10-30 s. The threshold for the contralateral slow v.r.p. was about two times higher than that for the monosynaptic reflex, and it coincided with the threshold for activating the slow-conducting afferent fibres. The contralateral slow v.r.p. was abolished after the spinal cord was treated with capsaicin (1 microM for 30 min) in vitro. The contralateral slow v.r.p. was absent in the spinal cord derived from 4-day-old rats that had received capsaicin (50 mg kg-1, s.c.) on the 2nd day of life. The contralateral fast v.r.p. and other reflexes of fast time courses remained unaltered after treatment with capsaicin in vitro or in vivo. Administration of an SP antagonist, [D-Arg1, D-Pro2, D-Trp7,9 Leu11]-SP in concentrations of 5-16 microM depressed the contralateral slow v.r.p., but did not affect the monosynaptic reflex, the dorsal root potential and the contralateral fast v.r.p. [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-SP (5 microM) markedly depressed the SP-induced depolarizing response recorded from the ventral root whereas the responses to noradrenaline, 5-hydroxytryptamine, neurotensin and thyrotrophin releasing hormone (TRH) were unaffected by the SP antagonist. The response of the ventral root to acetylcholine was slightly depressed by the antagonist. The SP antagonist at 5-10 microM did not exert any agonist action on the motoneurones. The present results in conjunction with those of previous studies support the hypothesis that SP released from certain primary afferent fibres acts as a neurotransmitter, producing in dorsal horn neurones slow excitatory postsynaptic potentials which lead to the generation of the contralateral slow v.r.p.

Animals↗

PubMed1987

Motoneuron properties during motor inhibition produced by microinjection of carbachol into the pontine reticular formation of the decerebrate cat.

It is well established that cholinergic agonists, when injected into the pontine reticular formation in cats, produce a generalized suppression of motor activity (1, 3, 6, 14, 18, 27, 33, 50). The responsible neuronal mechanisms were explored by measuring ventral root activity, the amplitude of the Ia-monosynaptic reflex, and the basic electrophysiological properties of hindlimb motoneurons before and after carbachol was microinjected into the pontine reticular formation of decerebrate cats. Intrapontine microinjections of carbachol (0.25-1.0 microliter, 16 mg/ml) resulted in the tonic suppression of ventral root activity and a decrease in the amplitude of the Ia-monosynaptic reflex. An analysis of intracellular records from lumbar motoneurons during the suppression of motor activity induced by carbachol revealed a considerable decrease in input resistance and membrane time constant as well as a reduction in motoneuron excitability, as evidenced by a nearly twofold increase in rheobase. Discrete inhibitory postsynaptic potentials were also observed following carbachol administration. The changes in motoneuron properties (rheobase, input resistance, and membrane time constant), as well as the development of discrete inhibitory postsynaptic potentials, indicate that spinal cord motoneurons were postsynaptically inhibited following the pontine administration of carbachol. In addition, the inhibitory processes that arose after carbachol administration in the decerebrate cat were remarkably similar to those that are present during active sleep in the chronic cat. These findings suggest that the microinjection of carbachol into the pontine reticular formation activates the same brain stem-spinal cord system that is responsible for the postsynaptic inhibition of alpha-motoneurons that occurs during active sleep.

Action Potentials↗

PubMed2007

Posterior root-muscle reflexes elicited by transcutaneous stimulation of the human lumbosacral cord.

Continuous epidural stimulation of lumbar posterior root afferents can modify the activity of lumbar cord networks and motoneurons, resulting in suppression of spasticity or elicitation of locomotor-like movements in spinal cord-injured people. The aim of the present study was to demonstrate that posterior root afferents can also be depolarized by transcutaneous stimulation with moderate stimulus intensities. In healthy subjects, single stimuli applied through surface electrodes placed over the T11-T12 vertebrae with a mean intensity of 28.6 V elicited simultaneous, bilateral monosynaptic reflexes in quadriceps, hamstrings, tibialis anterior, and triceps surae by depolarization of lumbosacral posterior root fibers. The nature of these posterior root-muscle reflexes was demonstrated by the duration of the refractory period, and by modifying the responses with vibration and active and passive movements. Stimulation over the L4-L5 vertebrae selectively depolarized posterior root fibers or additionally activated anterior root fibers within the cauda equina depending on stimulus intensity. Transcutaneous posterior root stimulation with single pulses allows neurophysiological studies of state- and task-dependent modulations of monosynaptic reflexes at multiple segmental levels. Continuous transcutaneous posterior root stimulation represents a novel, non-invasive, neuromodulative approach for individuals with different neurological disorders.

Adult↗

PubMed1998

Differential effects of wortmannin on the release of substance P and amino acids from the isolated spinal cord of the neonatal rat.

1. Effects of wortmannin, an inhibitor of myosin light chain kinase, on the release of substance P and amino acids, GABA and glutamate, were investigated in the isolated spinal cord preparation of the neonatal rat. 2. Wortmannin at 0.5 - 10 microM depressed the release of substance P evoked by high-K+ (90 mM) medium from the spinal cord (IC50 = 1.1 microM). Wortmannin also depressed the high-K+ (70 mM)-evoked release of substance P from cultured dorsal root ganglion neurons of neonatal rats. In contrast, the high-K+ (90 mM)-evoked release of GABA and glutamate from the spinal cord was not affected by wortmannin (0.1 - 10 microM). 3. Upon stimulation of a dorsal root, a monosynaptic reflex and a subsequent slow ventral root depolarization were evoked in the ipsilateral ventral root of the same segment in the isolated spinal cord preparation. The magnitude of the slow ventral root depolarization was depressed gradually to about 70% of the control during the course of 30 min under wortmannin (1 microM). In contrast, the monosynaptic reflex was unaffected by wortmannin. 4. Immunofluorescent staining revealed that immunoreactivities of substance P and myosin II were colocalized at presynaptic terminals in the dorsal horn of the neonatal rat spinal cord. 5. The present results suggest that myosin phosphorylation by myosin light chain kinase may play a crucial role in the release of substance P, but not in the release of GABA and glutamate in the neonatal rat spinal cord. This may reflect a difference in the exocytic mechanisms of substance P-containing large dense core vesicles and amino acid-containing small clear vesicles.

Amino Acids↗

PubMed1976

Ascending long spinal actions on forelimb motoneurons in the acute spinal cat.

Ascending long spinal reflex system were investigated by means of monosynaptic reflex testing in the acutely spinalized unanesthetized cat. 1. Hindlimb nerve stimulation gave bilateral facilitatory effects on the motoneuron pools of pectoralis major and physiological flexors of the forelimb such as biceps brachii, extensor carpi radialis, extensor digitorum communis, but elicited depressive effects on the physiological extensors such as triceps brachii, flexor carpi radialis, flexor digitorum profundus. 2. In the latissimus dorsi, which is the antagonist of pectoralis major, a depressive effect was elicited by the stimulation of ipsilateral hindlimb nerves, and a facilitatory effect by contralateral stimulation. 3. These effects were evoked mainly from group II afferent fibers in muscle as well as cutaneous nerves. 4. Intracellular recordings from motoneurons of extensor carpi radialis revealed EPSPs following stimulation of hindlimb nerves with time courses corresponding to those of the facilitatory effects. We failed to detect any potential changes in the motoneurons of flexor carpi radialis following stimulation of hindlimb nerves.

Afferent Pathways↗

PubMed1993

Depression of primary afferent-evoked responses by GR71251 in the isolated spinal cord of the neonatal rat.

1. The pharmacological profile of GR71251, a new tachykinin receptor antagonist, and its effect on the responses evoked by stimulation of primary afferent fibres were studied in isolated spinal cord preparations of neonatal rats. Potential changes were recorded extracellularly from a lumbar ventral root (L3-L5). 2. Bath-application of substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) at 0.01-3 microM to the spinal cord induced depolarization of the ventral root in normal artificial cerebrospinal fluid (CSF). The NK1 agonist, acetyl-Arg6-septide, and the NK3 agonist, senktide, at 0.01-3 microM, also had potent depolarizing actions whereas two NK2 agonists, beta-Ala8NKA4-10 and Nle10NKA4-10, showed little depolarizing effects at 1 microM. 3. GR71251 (0.3-3 microM) caused a rightward shift of the concentration-response curves for SP, acetyl-Arg6-septide and NKA with pA2 values of 6.14, 6.75 or 6.70, respectively. The effects of GR71251 were readily reversible within 15-30 min after its removal. By contrast, GR71251 (1-5 microM) had little effect on the depolarizing responses to NKB and senktide. 4. GR71251 (1-3 microM) did not depress the depolarizing responses to bombesin, neuromedin B and gastrin-releasing peptide in normal artificial CSF. 5. Application of capsaicin to the spinal cord induced a depolarizing response, which was partially depressed by GR71251 (3-10 microM). 6. In the isolated spinal cord preparation, intense electrical stimulation of a dorsal root evoked a slow depolarizing response of the contralateral ventral root of the same segment. A similar slow ventral root depolarization was evoked by electrical stimulation of the ipsilateral saphenous nerve in an isolated spinal cord-saphenous nerve preparation. GR71251 (0.3-10 microM) dose-dependently depressed these slow ventral root potentials.7. In the spinal cord-peripheral nerve preparation, conditioning stimulation of the saphenous nerve evoked an inhibition of the muscle nerve-evoked monosynaptic reflex lasting about 20 s. The late part of the inhibition was markedly depressed by GR71251 (1-3 microM).8. The present results indicate that GR71251 is a potent and specific antagonist for tachykinin receptors in the spinal cord. The present study further provides evidence for the involvement of SP and NKA in the slow ventral root depolarization and the prolonged inhibition of monosynaptic reflex that are evoked by primary afferent stimulation.

Analgesics↗

PubMedDate not supplied

Effects of radiographic contrast agents on spinal cord physiology.

Segmental reflexes in the spinal cords of cats anesthetized with chloralose were used to evaluate the neurophysiologic effects of radiographic contrast agents. The exposed lumbar spinal cord was bathed with concentrations of ionic and nonionic agents including saline, sodium meglumine diatrizoate, meglumine iothalamate, meglumine iocarmate, and metrizamide. The following responses were evaluated: flexor and extensor monosynaptic reflex; polysynaptic flexion reflexes; spontaneous ventral root activity. Hypertonic solutions generally produced a transient decrease in all reflex activity for up to 1 hour. Isotonic solutions produced no significant changes in the monosynaptic responses, but an increase in amplitude of polysynaptic responses, and increased spontaneous activity. The usual facilitory effects of flexion reflex on the flexor monosynaptic reflex were unchanged, but the expected inhibitory effect of flexion reflex on the extensor monosynaptic reflex was changed to excitatory. The relative ability to produced these effects was sodium meglumine diatrizoate greater than meglumine iothalamate greater than meglumine iocarmate greater than metrizamide.

Action Potentials↗

PubMed1995

Selective effects of ketamine on amino acid-mediated pathways in neonatal rat spinal cord.

Many ion channels have been proposed as target sites for anaesthetic action; for some agents multiple receptors-ion channels may be implicated. In addition to acting as a non-competitive antagonist at glutamate NMDA receptors, ketamine also affects other ion channels. The present study was undertaken to determine if the effects of ketamine in an integrated portion of the central nervous system involve multiple actions at glutamate non-NMDA, glutamate NMDA, and GABAA receptor. The effects of ketamine 1-50 mumol litre-1 were examined on three pharmacologically distinct responses in isolated superfused neonatal rat spinal cord: the monosynaptic reflex (glutamate non-NMDA); a slow ventral root potential (VRP) with a large NMDA-mediated component; and the dorsal root potential (DRP) (GABAA). Ketamine, at concentrations relevant to anaesthesia (1-50 mumol litre-1), reversibly depressed the area under the curve of the slow VRP in a concentration-dependent fashion. The effects of ketamine were selective for the early (0-1 s) component of the slow VRP. The monosynaptic reflex was unaffected at these concentrations. The actions of ketamine resembled those of the NMDA antagonist APV. Dorsal root potentials evoked by dorsal root stimulation or by muscimol were either unaffected or reversibly depressed by ketamine 1-20 mumol litre-1. The concentrations tested include the anaesthetic range for both rats and humans. The effects of ketamine on neurotransmission in this preparation can be accounted for entirely by its action at NMDA receptors. Glutamate non-NMDA receptors were unaffected and GABAA transmission was not enhanced.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗