Decerebrate Control of Reflexes to Primary Afferents

Self Cite

136

SUMMARY1. The effect of electrical stimulation of the brain stem on interneurones in the dorsal horn and intermediary region has been investigated in decerebrate cats after partial transection of the spinal cord.2. Stimuli that effectively depress reflex transmission without giving a primary afferent depolarization inhibit the discharge evoked from the flexor reflex afferents in interneurones.3. Brain stem stimulation did not give post-synaptic potentials in the great majority of interneurones but effectively depressed the excitatory post-synaptic potentials (EPSPs) and inhibitory post-synaptic potentials (IPSPs) evoked from the flexor reflex afferents in these interneurones.4. IPSPs were, however, evoked in five of seventy-eight intracellularly recorded interneurones. These five interneurones were monosynaptically activated from primary afferents.5. It is tentatively postulated that a dorsal reticulospinal system inhibits reflex transmission by giving post-synaptic inhibition in first order interneurones. The results are also discussed in relation to effects on interneurones from other descending pathways.

mentioning

confidence: 57%

Reticulospinal inhibition of interneurones

Engberg¹,

Lundberg²,

Ryall³

1968

Self Cite

136

“…Furthermore, it is known that the spinal mechanisms controlling primary afferent polarization are affected by supraspinal as well as peripheral afferent systems. For example, DRPs generated by peripheral nerve stimulation are smaller in decerebrate as compared to spinalized preparations (Carpenter, Engberg, Funkenstein & Lundberg, 1963;Lundberg, 1964).…”

Section: Dorsal Root Potentials Produced By Heat Pulsesmentioning

confidence: 99%

Primary afferent depolarization and flexion reflexes produced by radiant heat stimulation of the skin

Burke¹,

Rudomín²,

Vyklicky³

et al. 1971

SUMMARY1. The reflex effects of pulses of intense radiant heat applied to the skin of the central plantar pad have been studied in unanaesthetized (decerebrate) spinal cats.2. Pad heat pulses produced flexion of the ipsilateral hind limb and increased ipsilateral flexor monosynaptic reflexes, due to post-synaptic excitation of flexor alpha motoneurones. These effects were accompanied by reduction of extensor monosynaptic reflexes and post-synaptic inhibition of extensor motoneurones.3. Ipsilateral (and contralateral) pad heat pulses consistently evoked negative dorsal root potentials (DRPs) as well as increased excitability of both cutaneous and group Ib muscle afferent terminals. The excitability of group Ia afferents was sometimes also increased during pad heat pulses, but to a lesser extent.4. Pad heat pulses produced negative DRPs in preparations in which positive DRP components could be demonstrated following electrical stimulation of both skin and muscle nerves.5. The motor and primary afferent effects of heat pulses always accompanied one another, beginning after the pad surface temperature had reached rather high levels (usually 48-55°C).6. Negative DRPs increased excitability of cutaneous and group Ib afferents, and motoneurone activation produced by pad heat pulses was essentially unmodified when conduction in large myelinated afferents from

“…Also, it must be kept in mind that inhibition of the antagonist monosynaptic test reflex may be evoked not only post-synaptically but also presynaptically by depolarization of the Ia terminals conveying the test reflex. Transmission in the pathway mediating primary afferent depolarization to Ia afferent terminals is not tonically inhibited in the decerebrate cat (Carpenter et al 1963) and volleys in group I afferents from the knee extensors do indeed give presynaptic inhibition of transmission from posterior biceps and semitendinosus Ia afferents (Eccles et al 1962b). Accordingly, it was not unexpected to find significant presynaptic inhibition of the posterior biceps and 362 T.-C. FU, H. HULTBORN, R. LARSSON AND A. LUNDBERG semitendinosus test reflex during the stretch-evoked contraction in quadriceps and in order to study the role of post-synaptic reciprocal Ia inhibition it was necessary to measure and subtract the monosynaptic test reflex depression contributed by presynaptic inhibition.…”

Section: Discussionmentioning

confidence: 99%

“…Such results are seemingly contrary to our hypothesis of a balance between Ia excitation and recurrent inhibition at the level of the Ia inhibitory interneurones. It must, however, be recalled that transmission in group I pathways mediating presynaptic inhibition is not depressed in the decerebrate preparation (Carpenter, Engberg, Funkenstein & Lundberg, 1963) in contrast to lb and flexor reflex pathways to motoneurones. It is therefore conceivable that muscle stretch will cause a presynaptic inhibition at the terminals of the Ia afferents from the antagonist flexor muscle which then would contribute to the decreased amplitudes of the monosynaptic test reflex.…”

Section: Section 1 Reciprocal Inhibition During Maintained Graded Exmentioning

confidence: 99%

Reciprocal inhibition during the tonic stretch reflex in the decerebrate cat.

Fu¹,

Hultborn²,

Larsson³

et al. 1978

SUMMARY1. The aim of this study was to investigate post-synaptic reciprocal Ia inhibition during the stretch reflex; particularly the extent to which an increased Ia excitation of the Ia inhibitory interneurones will be counteracted by recurrent inhibition from motor axon collaterals. For this purpose we investigated depression of monosynaptic test reflexes to antagonist flexors (reciprocal inhibition) during static stretch of quadriceps or triceps surae in unanaesthetized decerebrate cats.2. With increasing stretch of the extensor muscle there was first a linear augmentation of reciprocal inhibition, but along with the stretch reflex in the extensor a plateau appeared in the inhibition of the flexors, although the extensor stretch reflex (judged by the e.m.g.) increased with further stretching. Within the range of stretching of triceps surae which gave increased stretch reflexes the plateau in the reciprocal inhibition was usually maintained, while during stretching of quadriceps a second phase of augmenting reciprocal inhibition often appeared. Stretch beyond the level which increased the stretch reflex activity gave augmenting reciprocal inhibition both in case of quadriceps and triceps surae.3. Excitability measurements from central terminals of Ia afferents revealed that the increasing reciprocal inhibition during increasing stretch reflex activity in quadriceps was associated with a primary afferent depolarization in knee flexor Ia afferents; there was no corresponding effect in ankle flexor Ia afferents during stretch reflexes in triceps surae.4. The primary afferent depolarization evoked in knee flexor Ia afferents by electrical nerve stimulation was then compared with the presynaptic inhibition of knee flexor monosynaptic test reflexes produced by the same stimuli. The results suggest that the second phase of increasing reciprocal inhibition in knee flexors is due to presynaptic inhibition and accordingly that the depth of post-synaptic reciprocal inhibition remains constant at different degrees of stretch reflex activity in both knee and ankle extensors. 5. It is postulated that during increasing stretch reflex activity the increment in Ia excitation and recurrent inhibition on to the Ia inhibitory interneurones almost exactly balance each other. It is suggested that recurrent inhibition of Ia inhibitory * Present address: