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PubMed1979

Neuropharmacology of sedatives and anxiolytics.

Sedative drugs are intended to cause various degrees of drowsiness. Animal experiments indicate that barbiturates induce these effects primarily by depression of the reticular activating system in the rostral brainstem. This in turn potentiates the thalamic recruiting system, thereby inducing 'barbiturate bursts' in the EEG. Anxiolytic drugs are intended to reduce anxiety or tension at doses which do not cause sedation or sleep. Propanediols may depress deactivating centers in the caudal brainstem, thereby releasing the activating centers in the rostral brainstem and depressing the thalamic recruiting response. These drugs may also act on the amygdala. Benzodiazepines have depressant effects on the amydala or hippocampus. These effects may release the reticular formation from inhibition. Enhanced activity of the activating and deactivating centers, to a different extent in different animals, would produce restlessness in some animals and sedation in others, accompanied by a mixture of fast and slow waves in the EEG. Sedative and anxiolytic agents also have central relaxant effects. The barbiturates act directly on the spinal cord, depressing both monosynaptic and polysynaptic reflexes. Propanediols and benzodiazepines act primarily on the descending facilitatory influence of the brainstem. Reduction of this influence depresses spinal polysynaptic but not monosynaptic reflexes. Biochemical studies suggest that barbiturates may act by antagonizing synaptic excitation induced by glutamate. Benzodiazepines may act by enhancing presynaptic inhibition mediated by GABA. The mechanism of action of propanediols is unknown.

Animals↗
PubMed2001

[Reevaluation of physiological mechanisms generating the stretch reflex: new hypotheses on the physiopathology of spasticity].

INTRODUCTION: Spasticity has been defined as tendon reflex exaggeration and increased muscle reflex contraction in response to its stretch (Lance, 1980). It has been generally admitted that stretch reflex exaggeration was due to myotatic reflex hyperexcitability (Ia fibre-motoneurone synapses). This interpretation has been recently revisited taking into account neurophysiological data obtained in cat and recent data obtained in spastic patients. PROBLEMATICS: Myotatic reflex has been described in decerebrate cat in 1924 by Liddel and Sherrington. In 1943, Lloyd demonstrated that myotatic reflex was due to monosynaptic Ia fibre motoneurone alpha synapses. Almost all the following studies of stretch reflexes were devoted to monosynaptic reflexes both in animal and humans. In fact, the existence of group II fibres coming also from spindles and some restricted experiments performed in man have led to discuss the role of group II fibres in the static component of the stretch reflexes. RESULTS: Recent studies performed in humans have shown that group II fibres play an important role in the development of stretch reflexes in leg muscles and that in spastic hemiplegic patients group II fibres facilitatory effects was deeply increased. DISCUSSION: Results obtained both in humans and animals suggest that group II fibres play also a role in a stretch reflex and led to consider that the pathophysiological modifications of group II effects could contribute to spasticity. CONCLUSION: Modifications of network fed by group II fibres and modifications of muscular fibres intrinsic properties are likely to play a role in the developments of spasticity in humans.

Animals↗
PubMed1997

The synapse between LE sensory neurons and gill motoneurons makes only a small contribution to the Aplysia gill-withdrawal reflex.

The monosynaptic connection between the mechano-sensory neurons in the LE cluster and gill motoneurons has been extensively studied and used as a model for the gill-withdrawal reflex and its behavioural plasticity. In an attempt to evaluate the contribution of this synapse to the behaviour, we used voltage-sensitive dye recording to determine the number of activated LE neurons and the number of spikes made by each neuron in response to a light touch. In five preparations, light touch activated a median of five sensory cells with a median of 1.6 spikes per cell. From a comparison of the sizes of the motoneuron synaptic potentials elicited by LE spikes and elicited by a light siphon touch, we estimate that the LE sensory neurons contribute approximately 5% of the motoneuron synaptic potential in response to this touch. This result casts doubt on the validity of using this synaptic connection as a model for gill-withdrawal behaviour. Siphon nerve recordings reveal the existence of short-latency, low-threshold neurons that may provide much of the sensory input in response to a light touch.

Animals↗
PubMed1975

Amygdala and masseteric reflex. I. Facilitation, inhibition and diphasic modifications of the reflex, induced by localized amygdaloid stimulation.

The changes in amplitude of the monosynaptic masseteric reflex (MR), induced by stimulation of the amygdaloid area for the defence reaction (N. basalis, pars magnocellularis) and in other subdivisions of the amygdaloid complex, were studied in cats with spinal section maintained under Flaxedil. Simultaneously, the the effects of stimulation on the tonic activity of the masseteric nerve were observed. A maintained facilitation of the MR was elicited by stimulation of the lateral nucleus, the parvocellular portion of the basal nucleus and the cortical nucleus, while the reflex was inhibited during stimulation of the medial-most portion of the posterior amygdala. Diphasic changes of the MR amplitude (initial facilitation followed by delayed inhibition) were regularly observed when stimulating the magnocellular portion of the basal nucleus. These diphasic changes were closely correlated with the previously described diphasic resporatory and cardiac responses elicited from the same are (Bonvallet and Gary Bobo 1972). The initial facilitation probably corresponds to the "alerting" stage of the defence reaction and the delayed inhibition, associated with cortical, respiratory and cardiac activation, to the "defensive" stage of the reaction. Stimulation of the same area also provokes tonic or rhythmical discharges of the masseteric motoneurons which frequently occur during the delayed inhibition of the MR. The main efferent pathway mediating these motor effects is probably the ansa lenticularis.

Amygdala↗
PubMed1997

Desensitization of spinal 5-HT1A receptors to 8-OH-DPAT: an in vivo spinal reflex study.

Serotonergic influence on spinal monosynaptic transmission and the desensitization of spinal 5-HT1A receptors following a single pretreatment with a 5-HT1A ligand were examined in vivo in acutely spinalized adult rats. Administration of a selective 5-HT1A agonist, 8-OH-DPAT (0.1 mg kg-1) significantly depressed the monosynaptic mass reflex (MMR) amplitude, which was prevented effectively by S(-)-propranolol, a 5-HT1A antagonist. The inhibitory effect of 8-OH-DPAT on MMR amplitude was significantly attenuated with a single dose of 8-OH-DPAT (1 mg kg-1, s.c.) administered 24 h before the experiments, indicating a marked desensitization of spinal 5-HT1A receptors. Desensitization of 5-HT1A receptors could be reversed by treatment of spiperone (1 mg kg-1, i.p.) 3 h before 8-OH-DPAT pretreatment. These results demonstrate that 5-HT1A receptor functionally modulates the spinal motor output and confirms the ability of 8-OH-DPAT to desensitize presynaptic 5-HT1A receptors as observed for the first time in rat spinal cord.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1960

The action of local anaesthetics on the spinal cord of the cat.

The effects of intravenously injected lignocaine, procaine and amethocaine on the monosynaptic and polysynaptic reflexes and the cord dorsum potentials elicited by selective electrical stimulation of appropriate afferent fibres have been investigated in decerebrate cats before and after strychnine. The three drugs depress the amplitude of the reflex responses in the basal preparation for 40 to 50 min. Smaller doses eliminate the reflex augmentation produced by strychnine for comparable periods. Very small doses selectively abolish the augmentation of the P component of the cord dorsum response induced by strychnine. The drugs have no effect on post-tetanic potentiation of the monosynaptic reflex response evoked from the gastrocnemius muscle in the cat. Their activity on the spinal cord is roughly proportional to their local anaesthetic potency. The ratios of the doses which produce the same central activity are amethocaine 3: lignocaine 10: procaine 20.

Anesthesia, Local↗
PubMedDate not supplied

Nitrergic proprioceptive afferents originating from quadriceps femoris muscle are related to monosynaptic Ia-motoneuron stretch reflex circuit in the dog.

1. The aim of the present study was to examine the occurrence of the neuronal nitric oxide synthase immunoreactivity in the stretch reflex circuit pertaining to the quadriceps femoris muscle in the dog. 2. Immunohistochemical processing for neuronal nitric oxide synthase and histochemical staining for nicotinamide adenine dinucleotide phosphate diaphorase were used to demonstrate the presence of neuronal nitric oxide synthase in the proprioceptive afferents issuing in the quadriceps femoris muscle. The retrograde tracer Fluorogold injected into the quadriceps femoris muscle was used to detect the proprioceptive afferents and their entry into the L5 and L6 dorsal root ganglia. 3. A noticeable number of medium-sized intensely nitric oxide synthase immunolabelled somata (1000-2000 microm(2) square area) was found in control animals in the dorsolateral part of L5 and L6 dorsal root ganglia along with large-caliber intraganglionic nitric oxide synthase immunolabelled fibers, presumed to be Ia axons. Before entering the dorsal funiculus the large-caliber nitric oxide synthase immunolabelled fibers of the L5 and L6 dorsal roots formed a massive medial bundle, which upon entering the dorsal root entry zone reached the dorsolateral part of the dorsal funiculus and were distributed here in a funnel-shaped fashion. The largest nitric oxide synthase immunolabelled fibers, 8.0-9.2 microm in diameter, remained close to the dorsal horn, while medium-sized fibers were seen dispersed across the medial portion of the dorsal funiculus. Single, considerably tapered nitric oxide synthase immunolabelled fibers, 2.2-4.6 microm in diameter, were seen to proceed in ventrolateral direction until they reached the mediobasal portion of the dorsal horn and the medial part of lamina VII. In lamina IX, only short fragments of nitric oxide synthase immunoreactive fibers and their terminal ramifications could be seen. Nitric oxide synthase immunolabelled terminals varying greatly in size were identified in control material at the base of the dorsal horn, in the vicinity of motoneurons ventrally and ventrolaterally in L5 and L6 segments and in Clarke's column of L3 and L4 segments. Injections of the retrograde tracer Fluorogold into the quadriceps femoris muscle and cut femoral nerve, combined with nitric oxide synthase immunohistochemistry of the L5 and L6 dorsal root ganglia, confirmed the existence of a number of medium-sized nitric oxide synthase immunoreactive and Fluorogold-fluorescent somata presumed to be proprioceptive Ia neurons (1000-2000 microm(2) square area) in the dorsolateral part of both dorsal root ganglia. L5 and L6 dorsal rhizotomy caused a marked depletion of nitric oxide synthase immunoreactivity in the medial bundle of the L5 and L6 dorsal roots and in the dorsal funiculus of L5 and L6 segments. 4. The analysis of control material and the degeneration of the large- and medium-caliber nitric oxide synthase immunoreactive Ia fibers in the dorsal funiculus of L5 and L6 segments confirmed the presence of nitric oxide synthase in the afferent limb of the monosynaptic Ia-motoneuron stretch reflex circuit related to the quadriceps femoris muscle.

Animals↗
PubMed1983

Modification of the paired H reflex through the transcendental meditation and TM-Sidhi program.

The paired H reflex, considered to be the electrically evoked counterpart of the monosynaptic stretch reflex, provides a measure of motoneuron excitability under a variety of experimental and clinical conditions. This study investigated the longitudinal effects of an advanced meditation program (the TM-Sidhi program) on the paired H reflex at nine delay intervals (50, 70, 100, 150, 200, 250, 333, 500, and 1000 ms). An experimental group of 14 subjects with no mental or motor disorders was instructed in an advanced TM program known as the TM-Sidhi program and the control group (N = 8) practiced the TM technique only. The amplitude of the paired H reflex was significantly facilitated in the experimental male subjects at intervals 100 through 250 ms, whereas the experimental female subjects and controls showed no significant change. These results extend previous studies showing distinct physiologic differences between subjects practicing these two programs and are of additional interest because they show that the H reflex can be modified in normal subjects.

Adaptation, Physiological↗
PubMed1984

Academic achievement and the paired Hoffman reflex in students practicing meditation.

The paired H reflex, considered to be the electrically evoked counterpart of the monosynaptic stretch reflex, provides a measure of motoneuron excitability under a variety of experimental and clinical conditions. It also offers a potentially useful tool in examining the neurophysiologic basis of alterations in reflex response in different states of awareness. This study investigated the relationship between the paired H reflex and academic achievement in students practicing the Transcendental Meditation program. The paired H reflex correlated significantly with grade point average, but not with SAT scores or any of three IQ measurements. These results suggest that the facilitation period of the paired H-reflex recovery curve may be a useful indicator of academic achievement, perhaps as a result of its relationship to awareness or wakefulness level.

Achievement↗
PubMed1988

Origin of the specific H reflex facilitation preceding a voluntary movement in man.

1. In a reaction time situation, the monosynaptic spinal reflex (H reflex) is facilitated before the onset of an electromyographic (EMG) response. The aim of the present investigation was to test if the facilitation can be attributed either to a subliminal depolarization of motoneurones or to an increase of the excitatory effect of the afferent volley reaching the motoneurones. 2. At the onset of an acoustic warning signal, human subjects were required to concentrate on a reaction time task and, in addition, to initiate a steady isometric plantar flexion of medium intensity in both feet. In response to a following visual stimulus, they carried out a ballistic plantar flexion randomly with the right or left foot. At different times after the visual reaction signal, H reflexes were elicited bilaterally. 3. The facilitation of the H reflex was similar in the presence and absence of a steady activation. In addition, the facilitations were similar in absolute amplitude and duration when the stimuli evoking the H reflexes were at threshold intensities, or at an intensity which produced control H reflexes of 60% maximum amplitude. 4. In a second series of experiments, no H reflexes were elicited but the strength of the steady plantar flexion was varied. Premotor time, i.e. the interval between the onset of the visual stimulus and the EMG response, and reaction time, i.e. the interval between the onset of the visual stimulus and the mechanical response, were computed. Neither parameter depended significantly on the intensity of steady flexion and they were the same with steady flexion as without. 5. The rectified EMG records and the torque records were aligned by the end of premotor time. Three-dimensional displays of average activity as a function of time and steady activation level were computed. No activation before premotor and reaction time was detected which could have been related to the H reflex facilitation. 6. The present results suggest that all motoneurones, in particular those being activated during the voluntary contraction, can contribute to the H reflex facilitation before movement onset and that the basis of this facilitation is an enhanced excitatory effect of the afferent volley elicited by the H reflex stimulus. Mechanisms leading to the facilitation could be removal of presynaptic inhibition at I a terminals or facilitation of interneurones intercalated in polysynaptic components of the reflex pathways.

Adult↗
PubMed1995

N-methyl-D-aspartate and alpha 2-adrenergic mechanisms are involved in the depressant action of flupirtine on spinal reflexes in rats.

In urethane-chloralose anesthetised rats the muscle relaxant activity of flupirtine was investigated on the monosynaptic Hoffmann reflex recorded from plantar foot muscles and on the polysynaptic flexor reflex recorded from tibialis muscle. Intraperitoneal (i.p.; 2.5-25 mumol/kg) and intrathecal (i.t.; 33-330 nmol) administration of flupirtine depressed the polysynaptic flexor reflex in anesthetised rats in a dose-dependent manner without affecting the monosynaptic Hoffmann reflex. Flupirtine produced a similar pattern on spinal reflexes as NMDA receptor antagonists, such as (-)-2-amino-7-phosphonoheptanoic acid (500 nmol i.t.) and memantine (125 mumol/kg i.p.), the benzodiazepines diazepam (18 mumol/kg i.p.) and midazolam (80 nmol i.t.), and the alpha 2-adrenoceptor agonist tizanidine (2 mumol/kg). In contrast, the GABAA receptor agonist muscimol (21 mumol/kg i.p.; 20 nmol i.t.) and the GABAB receptor agonist baclofen (47 mumol/kg i.p.; 2 nmol i.t.) reduced the magnitude of both the flexor and the Hoffmann reflex, whereas the non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX; 10 nmol i.t.) depressed the Hoffmann reflex without affecting the flexor reflex. The effect of i.t. injection of flupirtine was prevented by coadministration of the mixed alpha 1/alpha 2-adrenoceptor antagonist yohimbine (10 nmol) and the excitatory amino acid N-methyl-D-aspartate (NMDA; 0.1 nmol), but neither by coadministration of the alpha 1-adrenoceptor antagonist prazosine (10 nmol), the GABAA receptor antagonist bicuculline (1 nmol), the GABAB receptor antagonist phaclofen (100 nmol), the non-NMDA receptor agonist alpha-amino-3-hydroxy-5-tertbutyl-4-isoxazolepropionic acid (ATPA; 0.1 pmol) nor by pre-treatment with the benzodiazepine receptor antagonist flumazenil (16 mumol/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-2 Receptor Agonists↗
PubMed1980

Descriptive studies of H-reflex recovery curves in psychiatric patients.

The rate of recovery of the H-reflex, an electrical evoked monosynaptic spinal cord reflex, was abnormally high (fast) in over 20% of unmedicated psychotic patients of all major diagnostic classes. A few patients had significantly lower H-reflex recovery curves. Chronic neuroleptic treatment produced relatively lower recovery curves, whereas fluoxetine, a specific serotonin uptake blocker, produced relatively higher curves.

Adolescent↗
PubMed1984

Relation between the specific H reflex facilitation preceding a voluntary movement and movement parameters in man.

In a reaction-time situation, the monosynaptic spinal reflex (H reflex) is facilitated before the onset of an electromyographic (e.m.g.) response. The aim of the present investigation was to study aspects of this facilitation. Human subjects were required to perform isometric plantarflexions of the foot in response to a visual stimulus. The movement was always on the same side in the simple reaction-time situation, and randomly with the right or left foot in the choice reaction-time situation. Stimuli to evoke H reflexes were applied bilaterally 40-400 ms after the onset of the visual stimulus. Pre-motor time, i.e. the interval between the onset of the visual stimulus and the e.m.g. response, and reaction time, i.e. the interval between the onset of the visual stimulus and the response on the torque recording, were computed. In both reaction-time situations, there was a significant facilitation of the ipsilateral H reflex 100-160 ms before e.m.g. onset and, in some subjects, a small facilitation of the contralateral H reflex. The specific facilitation, i.e. the difference between the facilitation on the ipsi- and contralateral side relative to the movement, was not significantly different on the right and left side. Pre-motor time was divided into the interval from the light onset until the onset of the specific facilitation, and the interval from the onset of the facilitation until the onset of the voluntary response. Both intervals increased, and the slope and the amplitude of the facilitation decreased with increasing pre-motor time and reaction time. The specificity of the H reflex facilitation in a choice reaction-time situation implies that the interval from light onset until the onset of the facilitation includes stimulus identification and response selection, and the interval from the onset of the facilitation until the e.m.g. response preparation of the motor system for the required movement. The present results suggest that the specific facilitation of the H reflex before a movement is caused by removal of presynaptic inhibition at I a terminals or by activation of interneurones intercalated in polysynaptic components of the H reflex rather than by a subthreshold activation of motoneurones.

Action Potentials↗
PubMed1979

Compensation of postural reactions to fall in the vestibular neurectomized monkey. Role of the reamining labyrinthine afferences.

The electromyographic (EMG) responses from soleus and tibialis anterior muscles and the monosynaptic H- and T-reflex responses from soleus muscles were recorded bilaterally from conscious baboon while unexpectedly dropping it with unrestricted vision. These responses were recorded either after unilateral vestibular neurectomy (U.N. Baboons) or after bilateral neurectomy performed in one stage (B.N. 1 baboons) and in two stages (B.N. 2 baboons). A positive correlation was found between modifications and development of EMG responses and reflex data. In the U.N. baboons, some differences were observed when comparing data from the H- and T-reflex methods, suggesting that recovery of normal responses to fall is achieved both by means of direct influences on alpha-motoneurons and via the gamma-loop. In the U.N. baboons postural reactions to fall developed in three distinct periods. The first or critical stage showed asymmetrical EMG and reflex responses with increased responses from contralateral soleus muscle and decreased responses from ipsilateral soleus. Opposite effects were recorded from tibialis anterior flexor muscles. The second or acute stage which began around 4 to 7 days after surgery exhibited symmetrical, but very reduced, responses when compared to the control in soleus muscles, and symmetrical, but increased, responses from tibialis anterior muscles. This stage lasted until about the end of the second postoperative week and was followed by the third or compensatory stage during which EMG as well as reflex responses developed towards the control pattern in all tested muscles. Almost normal responses were recorded on both sides 3 weeks after surgery. Only a partial recovery was found in the B.N. 1 baboons, indicating that the contralateral remaining labyrinthine afferences constitute a necessary condition for the full compensation of postural reactions to fall in the case of unilateral vestibular neurectomy. The Bechterew's compensation was obtained in the B.N. 2 baboons. These results are discussed in relation with the general organization of the vestibulospinal pathways and with those concerning development of the postoperative activity at the vestibular nuclei level. A model of vestibular compensation achieved by means of a multisensory substitution process is suggested.

Afferent Pathways↗
PubMed1989

Intrathecal fentanyl depresses nociceptive flexion reflexes in patients with chronic pain.

To investigate the selective role of intraspinal opioids on the perception and modulation of pain, seven subjects with chronic hip or back pain and one subject with C-6 quadriplegia received 25 micrograms of intrathecal fentanyl. The effect of lumbar intrathecal fentanyl on reported pain, nociceptive flexor withdrawal reflexes, a monosynaptic motor arc (H-reflex), and supraspinal effects such as miosis, nausea, respiratory depression was evaluated. In five of eight subjects the flexor withdrawal reflex was completely abolished within 15 min. In the others the reflex was significantly depressed from control values. Decreases in reported pain paralleled the decrease in the flexor reflex, H-reflexes remained unchanged, and no supraspinal side effects were observed. It is likely that these selective changes observed were from the isolated effect of fentanyl modulating nociception at the spinal cord level.

Aged↗