Primary Afferent Depolarization Evoked from the Sensorimotor Cortex

Abstract

CARPENTER: D., A. LUNDBERG and U. NORRSELL. Primary afferent depolarization evoked from the sensorimotor cortex. Acta physiol. scand. 1963. 59. 126-142. -Stimulation of the sensorimotor cortex evokes dorsal root potentials (DRP) in the lumbo-sacral cord. Primary afferent depolarization is evoked in group I b and group I1 muscle afferents and cutaneous afferents but not in Ia afferents. The effects are mediated by the pyramidal tract. There is spatial facilitation between the paths from primary afferents and cortex. It is concluded that the pyramidal tract acts on primary afferents by giving excitatory action to interneiirones of spinal reflex arcs to primary afferents. Activity in the pyramidal tract causes widespread activation of interneurones in the dorsal horn and intermediary region (LLOYD 1941, LUNDBERG, NORRSELL And VOORHOEVE 1962. A recent detailed analysis has revealcd facilitation from the pyramidal tract of interneurones transmitting actions to motorneiirones from Ia, I b and flexor reflex afferents (FRA) . Findings during this investigation gave rise to the question whether tlie pyramidal tract also had effect on primary afferents or on the spinal refkx paths to primary afferents. The reults of a systematic investigation of this problem will be presented below-. A basis for the present work has been tlie recent analysis of spinal reflex paths to primary afferents: Ia afferents are depolarized by volleys in Ia and Ib afferents mainly from flexors (ECCLES. MAGNI and WILLIS 1962 a), I b afferents are depolarized by 111 vollqs from flexor and extensor muscles (ECCLES, SCHMIDT and WILLIS I962 d j uhereas 1 Prrscnt address: Harvard Medical School, Bobton 15.I26

Up-regulation of 5-HT2 receptors is involved in the increased H-reflex amplitude after contusive spinal cord injury

“…Segmental hind limb reflexes located in the lumbar spinal cord are heavily influenced by descending and ascending pathways (Carpenter, et al, 1966, Chen, et al, 2001. When these pathways are disrupted after spinal cord injury (SCI), abnormalities of the local lower limb reflexes often develop (Hornby, et al, 2004, Thompson, et al, 1992.…”

Gating of transmission to motoneurones by stimuli applied in the locus coeruleus and raphe nuclei of the cat.

“…It is not clear at present whether monoaminergic or non-monoaminergic systems are involved in these actions (see Discussion of Riddell et al 1992). Terminals of group I a afferents are negligibly affected by such stimuli, although terminals of group I b afferents may be depolarized by stimuli applied in some of the raphe nuclei and in the neighbouring reticular formation (see Carpenter, Engberg & Lundberg, 1966;Rudomin, Jimenez, Solodkin & Duenas, 1983). It is thus possible that the presynaptic inhibition of transmission from I b afferents was responsible for producing the depression of disynaptic I b IPSPs that was sometimes observed in the present experiments following stimulation on the KF and raphe nuclei.…”

Medullary reticulospinal tract mediating the generalized motor inhibition in cats: Parallel inhibitory mechanisms acting on motoneurons and on interneuronal transmission in reflex pathways

“…9,10,15,65,66 So far as the inhibitory aspects of MRF function are concerned, MRF-induced generalized motor inhibition was associated with postsynaptic inhibition of MNs 37,41,42,64,66,68 and presynaptic inhibition of primary afferents. 8 These inhibitory effects were mediated by inhibitory interneurons. 8,37,64,66 Spike-triggered averaging studies demonstrated that a particular group of reticulospinal neurons in the nucleus reticularis gigantocellularis (NRGc), which descended in the ventrolateral funiculus, induced IPSPs in hindlimb MNs located in multiple levels of the lumbosacral segments.…”

“…8 These inhibitory effects were mediated by inhibitory interneurons. 8,37,64,66 Spike-triggered averaging studies demonstrated that a particular group of reticulospinal neurons in the nucleus reticularis gigantocellularis (NRGc), which descended in the ventrolateral funiculus, induced IPSPs in hindlimb MNs located in multiple levels of the lumbosacral segments. 64,66 Analyses of the triggered IPSPs led to the conclusion that the inhibition is mediated by interneurons located in each level of the 6 lumbosacral segments.…”