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At least 343 records · Page 19Linked to original sources

[The effect of thyroid hormones on inhibition of monosynaptic extensor reflexes].

In thyreotoxic cats with intact or transected spinal cord, intensity of direct and presynaptic inhibition induced by a single volley in a flexor nerve afferent fibers was diminished and the delayed postsynaptic (polysynaptic) inhibition from the skin afferent fibers was more intense than in control cats. The mechanisms for the thyroid hormone effect on the cerebrospinal control of the extensor reflex inhibition, are discussed.

Animals↗

[Homosynaptic depression of the monosynaptic spinal reflex in healthy people and patients, suffering from a cerebral stroke].

Homosynaptic depression of H-reflex was studied in 25 healthy persons and 33 patients with hemiplegia. The mean duration of the homosynaptic depression in healthy persons was 5200 ms. After the initial relative facilitation the time course of the homosynaptic depression corresponded to a logarithmic function of the interval between the conditioning and testing stimuli. The homosynaptic depression in patients with hemiplegia decreased depending on the degree of the muscular spasticity.

Cerebrovascular Disorders↗

Transmission in fractionated monosynaptic spinal reflex systems.

A study has been made of conditions that support monosynaptic reflex transmission from afferent fibers of one part of a synergic muscle mass to motoneurons of another part. Heteronymous response so called can be brought on by prior tetanization of the afferent pathway and by asphyxiation to a critical stage. The response is facilitated by cooling and may appear in the cold preparation without need for prior tetanization. By appropriate asymmetrical subdivision of a monosynaptic reflex system an afferent inflow can be obtained that is sufficiently powerful to secure heteronymous transmission without the need for prior tetanization or cooling. Each junction between a monosynaptic afferent fiber and a motoneuron possesses some degree of potentiality for transmitting. Transmitter potentiality of an afferent fiber at its several junctions with motoneurons varies widely. Reasons are advanced for supposing the variation to be graded rather than stepwise, and quantitative rather than qualitative.

Motor Neurons↗

Method for recording spinal reflexes in mice: effects of thyrotropin-releasing hormone, DOI, tolperisone and baclofen on monosynaptic spinal reflex potentials.

Mice were used to record the spinal reflex potentials and to examine the effects of some drugs upon them. In anesthetized mice, laminectomy was performed in the lumbo-sacral region, and monosynaptic reflex potential (MSR) and polysynaptic reflex potential were recorded from the L5 ventral root after stimulation of the L5 dorsal root. Thyrotropin-releasing hormone (TRH) and 1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride (DOI) produced transient and long-lasting increases in the MSR amplitude, respectively. Tolperisone hydrochloride and baclofen produced transient and long-lasting MSR depressions, respectively. These results show that mice can be used to record spinal reflex potentials, and that it may be possible to study the spinal cord function of mutant and knockout mice using this method.

Amphetamines↗

Sensitivity of monosynaptic test reflexes to facilitation and inhibition as a function of the test reflex size: a study in man and the cat.

In parallel experiments on humans and in the cat it was investigated how the sensitivity of monosynaptic test reflexes to facilitation and inhibition varies as a function of the size of the control test reflex itself. In man the monosynaptic reflex (the Hoffmann reflex) was evoked in either the soleus muscle (by stimulation of the tibial nerve) or the quadriceps muscle (by stimulation of the femoral nerve). In the decerebrate cat monosynaptic reflexes were recorded from the nerves to soleus and medial gastrocnemius muscles; they were evoked by stimulation of the proximal ends of the sectioned L7 and S1 dorsal roots. Various excitatory and inhibitory spinal reflex pathways were used for conditioning the test reflexes (e.g. monosynaptic Ia excitation, disynaptic reciprocal inhibition, cutaneous inhibition, recurrent inhibition, presynaptic inhibition of the Ia fibres mediating the test reflex). It was shown that the additional number of motoneurones recruited in a monosynaptic test reflex by a constant excitatory conditioning stimulus was very much dependent on the size of the test reflex itself. This dependency had the same characteristic pattern whatever the conditioning stimulus. With increasing size of the test reflex the number of additionally recruited motoneurones first increased, then reached a peak (or plateau) and finally decreased. A similar relation was also seen with inhibitory conditioning stimuli. The basic physiological factors responsible for these findings are discussed. Finally, the implications for the interpretation of experiments in man with the H-reflex technique are considered.

Adolescent↗

The effect of L-Dopa on the spinal monosynaptic mass reflex.

After i.v. injection of reserpine, the monosynaptic mass reflex (MSMR) is depressed in spinalized cats. However, the complete recovery of MSMR was obtained 30 min after L-Dopa application. Pimozide, a dopamine-receptor blocking agent, blocked this action of L-Dopa. It is presumed that dopaminergic receptors are involved in the action of L-Dopa on spinal MSMR.

Animals↗

Development of the monosynaptic stretch reflex circuit.

Significant advances have been made during the past few years in our understanding of how the spinal monosynaptic reflex develops. Transcription factors in the Neurogenin, Runt, ETS, and LIM families control sequential steps of the specification of various subtypes of dorsal root ganglia sensory neurons. The initiation of muscle spindle differentiation requires neuregulin 1, derived from Ia afferent sensory neurons, and signaling through ErbB receptors in intrafusal muscle fibers. Several retrograde signals from the periphery are important for the establishment of late connectivity in the reflex circuit. Finally, neurotrophin 3 released from muscle spindles regulates the strength of sensory-motor connections within the spinal cord postnatally.

Afferent Pathways↗

Cyclobenzaprine, a centrally acting muscle relaxant, acts on descending serotonergic systems.

The centrally acting muscle relaxant cyclobenzaprine was thought to be an alpha 2-adrenoceptor agonist that reduced muscle tone by decreasing the activity of descending noradrenergic neurons. In the present study, we examined the effects of cyclobenzaprine on descending neurons by measuring the monosynaptic reflex in rats. Cyclobenzaprine reduced the monosynaptic reflex amplitude dose dependently and this effect was not inhibited by the alpha 2-adrenoceptor antagonists idazoxan and yohimbine. Cyclobenzaprine-induced monosynaptic reflex depression was not attenuated by noradrenergic neuronal lesions produced by 6-hydroxydopamine. However, cyclobenzaprine inhibited monosynaptic reflex facilitation induced by (+/-)-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane, a 5-HT2 receptor agonist, in spinalized rats markedly, and 5-HT depletion by DL-p-chlorophenylalanine inhibited the depressive effect of cyclobenzaprine on the monosynaptic reflex. These results suggest that cyclobenzaprine is a 5-HT2 receptor antagonist and that its muscle relaxant effect is due to inhibition of serotonergic, not noradrenergic, descending systems in the spinal cord.

Adrenergic alpha-2 Receptor Antagonists↗