Classification of dorsal horn neurons based on somatic receptive fields in cats with intact and transected spinal cords: neural plasticity.

Classification of dorsal horn neurons based on cell activity responses to somatic receptive fields stimulation, was compared between anesthetized cats with transected or intact cords. Results showed a significant (P < or = 0.001) difference. In animals with transected cords, dorsal horn neurons responded with less specificity to noxious and innocuous stimulation. The results are consistent with the proposition that loss of supraspinal influences plays a significant role in determining response characteristics of dorsal horn neurons.

Effects of transcutaneous electrical nerve stimulation (TENS) on spontaneous and noxiously evoked dorsal horn cell activity in cats with transected spinal cords.

Effects of transcutaneous electrical nerve stimulation (TENS) on spontaneous and noxiously evoked dorsal horn neurons were studied in alpha-chloralose anesthetized cats after spinal cords had been transected at the T12 segment. Previous work in cats with intact cords showed that TENS applications to somatic receptive fields could significantly reduce and maintain decreased dorsal horn cell activity. The purpose of this study was to determine if supraspinal mechanisms were involved with the initial reduction of dorsal horn cell activity during TENS applications. Extracellular action potentials of dorsal horn neurons were recorded in the absence of supraspinal influences. The results demonstrated that spontaneously and noxiously evoked cell activities were reduced significantly during TENS and no significant difference was found between pre-TENS control activity and post-TENS application cell activity. This information implies that initial gating (reduction cell activity), which occurs during TENS applications, is due to a segmental effect.

A mechanism of cardiac pain suppression by spinal cord stimulation: implications for patients with angina pectoris.

Clinical reports show that electrical stimulation of the spinal cord reduces symptoms of angina pectoris, but so far have not provided evidence on the mechanisms involved. The hypothesis for this study was that inhibition of spinothalamic tract transmission may account for this result. Extracellular potentials of 28 spinothalamic tract neurons were recorded in anaesthetized monkeys, and the effects of dorsal column stimulation were determined on activity evoked by cardiac and somatic stimuli. Dorsal column stimulation reduced the number of cell potentials evoked by electrical stimulation of cardiopulmonary sympathetic afferent fibres in 11 spinothalamic tract cells tested. Activity evoked by intracardiac injection of bradykinin was decreased by dorsal column stimulation in six of seven neurons that responded to chemical stimulation of afferents. Differential effects of dorsal column stimulation were correlated to the cell responses to somatic field stimulation. Dorsal column stimulation inhibited activity in 12 of 12 neurons which were excited only by noxious pinch of somatic fields, whereas eight of 16 neurons which were excited by innocuous brushing of somatic fields were unaffected or excited. Transection of the dorsal column showed that the pathway transmitting inhibitory impulses descended from the stimulation site to the spinothalamic tract neurons examined. Results of this study are consistent with the concept that spinal cord stimulation reduces pain by decreasing the firing of spinothalamic tract cells which are activated by small fibre afferents. The paresthesias associated with nerve stimulation techniques may result from activation of spinothalamic tract cells which are excited by large fibre afferents. The clinical decision to employ spinal cord stimulation in patients with angina should balance the obvious benefit of pain relief against the risk of depriving the patient of an important warning signal while active myocardial ischaemia is in progress.

Effects of intracardiac bradykinin and capsaicin on spinal and spinoreticular neurons.

The responses of thoracic spinal and spinoreticular tract (SRT) neurons to activation of cardiac spinal afferents by injections of bradykinin (BK) and capsaicin (CAP) into the left atrium or pericardial sac were determined in vagotomized cats anesthetized with alpha-chloralose. Activities of spinal and SRT neurons in the T1-T5 spinal cord were recorded extracellularly. All neurons received excitatory somatic and cardiopulmonary sympathetic afferent input. Application of BK and CAP to the heart excited most SRT neurons and many spinal neurons but also inhibited some spinal neurons. The two drugs often affected spinal but not SRT neurons differently. Capsaicin excited high threshold and high threshold inhibitory neurons but not wide-dynamic range spinal neurons. In contrast, BK excited all three categories of spinal and SRT neurons. The differential responses of spinal neurons to intracardiac BK and CAP suggested that these compounds can stimulate functionally different populations of cardiac sympathetic afferents.

Effects of chemical and electrical stimulation of the midbrain on feline T2-T6 spinoreticular and spinal cell activity evoked by cardiopulmonary afferent input.

Responses to electrical and chemical stimulation of the periaqueductal gray (PAG) and midbrain reticular formation (RF) were examined on extracellular activity of 28 spinoreticular tract (SRT) and 56 spinal neurons in T2-T6 segments of anesthetized cats. All cells received excitatory viscerosomatic convergent input from the left forelimb triceps region and from cardiopulmonary sympathetic afferents. Evoked activity that resulted from pinching the left triceps was reduced by PAG and midbrain RF stimulation (100 Hz, 100 microseconds, 50-500 microA). Visceral afferent input to the neurons was elicited during electrical stimulation of cardiopulmonary sympathetic afferent fibers and following injection of bradykinin into the left atrium of the heart. Electrical stimulation of the PAG and adjacent RF decreased A-delta and C-fiber activation of these neurons produced during electrical stimulation of cardiopulmonary afferents and decreased the activity of cells during excitatory responses to intracardiac bradykinin. Electrical stimulation of the PAG or midbrain RF similarly decreased spontaneous and evoked cell activity. Selective activation of cell bodies with microinjection of glutamate into the PAG reduced the activity of 6 of 8 cells whereas glutamate injections into midbrain RF reduced the activity of only 3 of 13 neurons. This difference in the effectiveness of chemically stimulating the PAG vs midbrain RF was significant (P less than 0.05). These data demonstrate that (1) neuronal activity evoked by visceral afferent input from the heart was decreased by electrical stimulation of the PAG and midbrain RF and (2) a portion of this descending inhibition may be mediated by cell bodies in the PAG.

Urinary bladder and hindlimb afferent input inhibits activity of primate T2-T5 spinothalamic tract neurons.

1. Extracellular recordings were made from 41 spinothalamic tract (STT) neurons on the left side of the T2-T5 spinal segments of 20 monkeys (Macaca fascicularis) anesthetized with alpha-chloralose. Manipulation of the left triceps-chest region and electrical stimulation of cardiopulmonary sympathetic afferent fibers excited these cells. 2. Isotonic urinary bladder distensions (UBD) to pressures between 20 and 80 cmH2O reduced the spontaneous activity in 33 of 41 cells. Cell activity was significantly reduced by UBD at 20 cmH2O. Distensions to 40, 60, and 80 cmH2O produced progressively greater reductions in spontaneous discharge. Activity was decreased throughout distension in 29 cells (tonic inhibition) and at the onset of distension in 3 neurons (phasic inhibition). In one cell, inhibition followed a brief excitation at the onset of distension (phasic excitation-tonic inhibition). Spontaneous bladder contractions also inhibited STT cell activity. 3. Inhibition by UBD was observed in STT cells characterized as wide dynamic range, high threshold, and high threshold inhibitory. No correlation existed between cell type or laminar location and inhibition by urinary bladder distension. Cells excited by cardiopulmonary sympathetic afferent A delta- and C-fibers had a significantly greater tendency to be inhibited by UBD (17 of 18) than cells activated by A delta- but not C-fibers (13 of 20). 4. Urinary bladder distension and pinch of the hindlimbs also reduced activity of STT cells excited by input from cardiopulmonary sympathetic afferents and from the proximal forelimb. 5. Urinary bladder distension to 40, 60, or 80 cmH2O produced a greater absolute but smaller relative reduction in the firing frequency of STT cells as spontaneous activity increased. Thus the magnitude of this inhibitory effect may depend on whether the inhibitory effect is measured as an absolute or relative change in cell activity. 6. Convergent inhibitory input from somatic regions also was observed. Noxious pinch of the hamstring region of the right hindlimb decreased activity in 32 of 39 cells. Left hindlimb pinch inhibited 21 of 38 cells, and 15 of 29 cells were inhibited by right triceps pinch. 7. Convergent inhibitory input from the hamstring region of the hindlimbs and from the urinary bladder to upper thoracic STT cells may be important for coding the intensity and location of noxious visceral and somatic stimuli and for organizing the appropriate sequence of motor responses when multiple noxious stimuli are present.