High-threshold Cells Research Articles

Electrophysiological characteristics of lumbar spinal cord neurons backfired from lateral reticular nucleus in the rat.

Spinal neurons antidromically activated from either the lateral reticular nucleus (LRN) or immediately adjacent areas were identified in the rat lumbar spinal cord. In agreement with previous anatomical work (60), these neurons were widely distributed in both the dorsal and ventral horns of the spinal cord and could be subdivided into three main groups according to their location: a) deep ventromedial (DVM) cells, which project more substantially to the LRN than to other supraspinal targets; b) cells of the median portion of the neck of the dorsal horn (mNDH), which project exclusively to the LRN; c) cells lying in other parts of the dorsal horn (superficial layers, nucleus proprius, reticular extension of the neck), by their location, they are indistinguishable from cells projecting to other supraspinal targets. The probability is high that the DVM and mNDH cells contribute exclusively, or at least preferentially, to the lateral component of the spinoreticular tract (lSRT), defined as the direct spinal pathway to the LRN. Although electrophysiological properties of cells were clearly related to their spinal location, several subpopulations could be recognized in each of the three main groups. The majority of DVM neurons were in lamina VII, with some in laminae VI, VIII, and X. With the exception of a few lamina X cells, the DVM neurons had high conduction velocities. Four subpopulations of these neurons were recognized. a) Innocuous proprioceptive cells responded to small changes in joint position, some showing convergence of nonnoxious cutaneous inputs. b) High-threshold cells (approximately 50% of DVM cells). Seventy-five percent of these cells were excited from bilateral receptive fields (mostly symmetric) with noxious cutaneous pinching that extended to subcutaneous tissues. Their evoked responses had long-lasting postdischarges that continued up to several minutes after cessation of the stimulus. c) Inhibited cells had no demonstrable excitatory receptive fields and a high ongoing activity that was tonically depressed by pressure or pinch; poststimulus effects of long duration were observed. d) Cells with no resting discharge and demonstrable excitatory peripheral receptive fields. mNDH cells had recording sites at the medial border of the internal portion of the reticular area of the neck of the dorsal horn.(ABSTRACT TRUNCATED AT 400 WORDS)

Inhibition of primate spinothalamic tract neurons by stimulation in periaqueductal gray or adjacent midbrain reticular formation.

Recordings were made from spinothalamic tract (STT) cells in the lumbosacral enlargement of anesthetized monkeys. The cells were identified by antidromic activation from the contralateral ventral posterior lateral nucleus of the thalamus. Electrical stimulation at sites within the periaqueductal gray, the adjacent midbrain reticular formation, or the deep layers of the tectum were found to inhibit the activity of STT cells. In general, midbrain stimulation inhibited the background discharges and the responses of wide dynamic range cells evoked by innocuous and noxious cutaneous stimulation (29 of 37 cases). However, for six cells, midbrain stimulation preferentially inhibited the responses to noxious stimulation. The evoked responses of all 10 high-threshold cells were inhibited. In only two cases was midbrain stimulation ineffective, and no excitatory effects were observed. The mean latency to onset of inhibition resulting from midbrain stimulation was 24.9 +/- 7.2 ms (n = 35). The amount of inhibition produced by midbrain stimulation was graded with stimulus intensity. For example, trains of stimuli (333 Hz) at 50 microA produced a mean inhibition to 81.7 +/- 16.6% of control, while 200 microA resulted in a mean inhibition to 36.3 +/- 21.7%. Not only was the inhibition increased by the use of stronger current intensities, but the duration of inhibition was prolonged. Midbrain stimulation inhibited the responses of STT cells to volleys in both the A-fibers and the C-fibers of the sural nerve. However, there was a selective action in that the responses to C-fiber volleys were more strongly inhibited than were the responses to A-fiber volleys. Lesions placed in the white matter of the upper cervical spinal cord reduced the inhibition produced by stimulation in either the midbrain or the nucleus raphe magnus. The extent to which the inhibition was reduced was proportional to the extent of the cord lesions. However, even when there was an interruption of the entire lateral funiculus on the side of an STT cell and of the dorsal quadrant of the contralateral side, there was still substantial inhibition following stimulation in either brain stem site. It is concluded that while part of the inhibition is mediated by pathways descending in the dorsal lateral funiculus (DLF), at least some depends on pathways coursing through the ventral spinal cord. Inhibition of STT cells may contribute to the neuronal mechanism of the analgesia that results from stimulation in the periaqueductal gray matter in awake, behaving animals.

A further examination of effects of cortical stimulation on primate spinothalamic tract cells

1. Stimulation of the sensorimotor cortex was found to excite and/or inhibit nociceptive spinothalamic tract cells. Thirteen wide dynamic range cells were inhibited by cortical stimulation, 6 were excited and 14 were both excited and inhibited. Four of six high-threshold cells were excited and one was inhibited. 2. Intermediate (200 ms) or long (2 s) duration conditioning trains were effective in reducing responses of spinothalamic cells evoked by noxious mechanical or thermal stimuli and by A- and C-fiber volleys in the sural nerve. Preferential inhibition of low-threshold responses with little or no effect on high-threshold discharges was observed in some cases. 3. Inhibitory actions were obtained primarily from stimulation of the SI sensory cortex and area 5, while excitation or excitation followed by inhibition was the dominant effect from motor cortex (area 4). Spinothalamic cells were also excited by stimulation of the medullary pyramid. 4. In eight animals extensive mapping of the sensorimotor cortex showed that for a given cell, stimulation of the sensory cortex produced inhibition while stimulation of motor cortex resulted in excitation. 5. The average latency of inhibition from sensory cortex was 29.8 +/- 10 ms, while the average latency of excitation from motor cortex was significantly shorter, 13.5 +/- 9 ms. The shortest latencies for excitation from pyramidal stimulation in the cases evaluated ranged from 2 to 9 ms. 6. Spinal cord lesions were made in five animals to determine the descending pathway(s) mediating corticofugal effects. Cortical and pyramidal effects were eliminated or considerably reduced by lesions involving the dorsal part of the lateral funiculus. This observation combined with latency data suggest that the corticospinal tract may be involved in the mediation of cortical excitation, while both pyramidal and extrapyramidal pathways are likely to be involved in cortical inhibition.

Effects of cardiac administration of bradykinin on thoracic spinal neurons in the cat

Extracellular action potentials were recorded from single cells located in gray matter of the T2 to T4 spinal segments in chloralose-anesthetized cats. Bradykinin either was injected indirectly into the coronary circulation and the heart via a cannula placed in the left atrium or was applied directly to the epicardium. Bradykinin excited 26 of 56 cells after a latency of 11 ± 1 s and inhibited two cells. Ten of eighteen cells demonstrated tachyphylaxis to repeated injections of bradykinin; the other eight cells were excited similarly to successive injections. All cells in this study received visceral and somatic inputs and were found in laminae I through VIII with a majority located in laminae V and VII. A noxious pinch applied to the somatic receptive fields was required to excite 94% of the cells (high-threshold cells), and hair movement and touch as well as pinch excited the other 6% of the cells (wide dynamic range cells). The results demonstrated that bradykinin excited cardiac receptors whose afferent fibers influenced the activity of spinal neurons. Because convergence of visceral and somatic inputs onto the same neurons provides a basis for referred pain and bradykinin is an algesic substance, these cells could potentially be involved in pain sensation and cardiovascular adjustments associated with angina pectoris.