Prenatal development of somatosensory primary afferent connections in the sheep

1995 ◽  
Vol 7 (3) ◽  
pp. 427 ◽  
Author(s):  
S Rees ◽  
I Nitsos ◽  
J Rawson
Keyword(s):  
Spinal Cord ◽  
Dorsal Root Ganglion ◽  
Dorsal Horn ◽  
Dorsal Root ◽  
Muscle Spindles ◽  
Sensory Innervation ◽  
Muscle Fibres ◽  
Fetal Sheep ◽  
Primary Afferent ◽  
Dorsal Horn Neurons

A summary is presented of recently published studies on the structural and functional development of cutaneous and muscle receptors and the connections of their afferent fibres in fetal sheep (n = 26) aged between 67 and 143 days gestation (term, 146 days). In these studies it was shown that primary afferent fibres projected to, and made synaptic connections with, dorsal horn neurons in lumbosacral spinal cord by 56-61 days gestation. Sensory innervation of the skin occurred later by about 75 days gestation and, at this age, stimulation of the skin first activated cutaneous afferent fibres and evoked a discharge in dorsal root ganglion and dorsal horn neurons. Muscle stretch first activated muscle spindles and evoked a discharge in dorsal root ganglion cells by about 75 days. Prior to this (by about 67 days) primary afferent fibres had begun to innervate motoneuron pools in the spinal cord, and motor nerves had begun to innervate muscle fibres. Both muscle spindle and cutaneous innervation were relatively simple at mid gestation indicating that the structure of sensory receptors need not be complex in order to generate a response. Neural pathways necessary for reflex activity involving muscle spindles are therefore present and functional by mid gestation as are cutaneous pathways projecting from the skin to the spinal cord.

Segmental effect of spinal NK-1 receptor blockade on the pressor reflex

1998 ◽  
Vol 275 (3) ◽  
pp. H789-H796 ◽  
Author(s):  
L. Britt Wilson ◽  
Gregory A. Hand
Keyword(s):  
Skeletal Muscle ◽  
Spinal Cord ◽  
Dorsal Horn ◽  
Dorsal Root ◽  
Pressor Response ◽  
Afferent Neurons ◽  
Muscle Stretch ◽  
Primary Afferent ◽  
Static Contraction ◽  
Pressor Reflex

The physiological effects of substance P (SP) are mediated via activation of neurokinin-1 (NK-1) receptors. The purpose of this study was to test the hypothesis that blockade of NK-1 receptors in the dorsal horn, both at the site of entry for the primary afferent neurons and adjacent spinal segments, attenuates the pressor reflex evoked by static contraction and stretch of skeletal muscle. Cats were anesthetized with α-chloralose and urethan, and a laminectomy was performed. With the exception of the L7 dorsal root, the dorsal and ventral roots from L5 to S2 were sectioned on one side of the spinal cord. Thus the primary afferent fibers mediating the pressor reflex enter the spinal cord via the L7 dorsal root in these experiments. Based on dose-response data, dialysis of the NK-1 receptor antagonist CP-96,345 (5 mM for 2 h) into the L7 dorsal horn ipsilateral to the contracting muscle attenuated the pressor response to static contraction (75 ± 15 vs. 46 ± 7 mmHg; n = 5 cats) but not muscle stretch (60 ± 12 vs. 50 ± 8 mmHg). Administration of the inactive enantiomer of CP-96,345, CP-96,344 (5 mM for 2 h), into the L7 dorsal horn failed to alter the cardiovascular changes elicited by contraction (45 ± 7 vs. 43 ± 6 mmHg) and stretch (31 ± 8 vs. 32 ± 11). Dialysis of 5 mM CP-96,345 into the dorsal horn at the L6 and S1 segments for 2 h decreased the peak pressor response to static contraction (58 ± 9 vs. 31 ± 6 mmHg; n = 7) and muscle stretch (61 ± 6 vs. 44 ± 8 mmHg). These data suggest that the activation of NK-1 receptors, both at the site of entry and in regions outside of the entry site for afferent neurons, is involved in the spinal processing that produces the pressor reflex evoked by static contraction of skeletal muscle.

Serotonin Increases the Incidence of Primary Afferent-Evoked Long-Term Depression in Rat Deep Dorsal Horn Neurons

2001 ◽  
Vol 85 (5) ◽  
pp. 1864-1872 ◽  
Author(s):  
Sandra M. Garraway ◽  
Shawn Hochman
Keyword(s):  
Spinal Cord ◽  
Dorsal Horn ◽  
Long Term Potentiation ◽  
Neonatal Rat ◽  
Long Term Depression ◽  
Primary Afferent ◽  
Dorsal Horn Neurons ◽  
Sensory Evoked ◽  
Synaptic Responses

5-hydroxytryptamine (5-HT) is released in spinal cord by descending systems that modulate somatosensory transmission and can potently depress primary afferent-evoked synaptic responses in dorsal horn neurons. Since primary afferent activity-induced long-term potentiation (LTP) may contribute to central sensitization of nociception, we studied the effects of 5-HT on the expression of sensory-evoked LTP and long-term depression (LTD) in deep dorsal horn (DDH) neurons. Whole cell, predominantly current clamp, recordings were obtained from DDH neurons in transverse slices of neonatal rat lumbar spinal cord. The effect of 5-HT on dorsal-root stimulation-evoked synaptic responses was tested before, during, or after high-frequency conditioning stimulation (CS). In most cells (80%), 5-HT caused a depression of the naı̈ve synaptic response. Even though 5-HT depressed evoked responses, CS in the presence of 5-HT was not only still capable of inducing LTD but also increased its incidence from 54% in controls to 88% ( P < 0.001). Activation of ligands selective for 5-HT1A/1B and 5-HT1B, but not 5-HT2A/2C or 5-HT3receptors, best reproduced these actions. 5-HT also potently depressed postconditioning synaptic responses regardless of whether the induced plasticity was LTP or LTD. Our results demonstrate that in addition to depressing the amplitude of evoked sensory input, 5-HT can also control the direction of its long-term modifiability, favoring the expression of LTD. These findings demonstrate cellular mechanisms that may contribute to the descending serotonergic control of nociception.

scholarly journals Mechanism of dorsal root ganglion stimulation for pain relief in painful diabetic polyneuropathy is not dependent on GABA release in the dorsal horn of the spinal cord

2019 ◽  
Vol 26 (1) ◽  
pp. 136-143 ◽  
Author(s):  
Eva Koetsier ◽  
Glenn Franken ◽  
Jacques Debets ◽  
Lonne Heijmans ◽  
Sander M.J. Kuijk ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Pain Relief ◽  
Dorsal Root Ganglion ◽  
Dorsal Horn ◽  
Dorsal Root ◽  
Diabetic Polyneuropathy ◽  
Gaba Release

Selective cephalic upregulation of p-ERK, CamKII and p-CREB in response to glyceryl trinitrate infusion

Cephalalgia ◽  
2017 ◽  
Vol 38 (6) ◽  
pp. 1057-1070 ◽  
Author(s):  
Roshni Ramachandran ◽  
Sara Hougaard Pedersen ◽  
Dipak Vasantrao Amrutkar ◽  
Steffen Petersen ◽  
Julie Mie Jacobsen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Dorsal Root Ganglion ◽  
Dorsal Horn ◽  
Trigeminal Ganglion ◽  
Dura Mater ◽  
Dorsal Root ◽  
Spinal Cord Dorsal Horn ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Extracellular Signal

Background A common characteristic of migraine-inducing substances is that they cause headache and no pain in other areas of the body. Few studies have compared pain mechanisms in the trigeminal and spinal systems and, so far, no major differences have been noted. We compared signalling molecules in the trigeminal and spinothalamic system after infusion of the migraine-provoking substance glyceryltrinitrate. Method A catheter was placed in the femoral vein of rats and one week later glyceryltrinitrate 4 µg/kg/min was infused for 20 min. Protein expression in the dura mater, trigeminal ganglion, nucleus caudalis, dorsal root ganglion and the dorsal horn of the thoracic spinal cord was analysed at different time points using western blotting and immunohistochemistry. Results Glyceryltrinitrate caused a threefold increase in expression of phosphorylated extracellular signal-regulated kinases at 30 min in the dura mater and nucleus caudalis ( P < 0.05) and at 2 h in the trigeminal ganglion with very few expressions in the dorsal root ganglion. In the nucleus caudalis, expression of phosphorylated extracellular signal-regulated kinases and Cam KII increased 2.6-fold and 3.2-fold, respectively, at 2 h after glycerytrinitrate infusion ( P < 0.01). p-CREB/ATF-1 upregulation was observed only at 30 min ( P < 0.05) in the nucleus caudalis. None of these markers showed increased expression in the regions of thoracic spinal cord dorsal horn. Conclusion The dura, trigeminal ganglion and nucleus caudalis are activated shortly after glycerytrinitrate infusion with long-lasting expression of phosphorylated extracellular signal-regulated kinases observed in the nucleus caudalis. These activations were not observed at the spinal level.

Lamina-specific effects of morphine and naloxone in dorsal horn of rat spinal cord in vitro

1991 ◽  
Vol 66 (6) ◽  
pp. 1941-1950 ◽  
Author(s):  
D. S. Magnuson ◽  
A. H. Dickenson
Keyword(s):  
Spinal Cord ◽  
Amino Acid ◽  
Dorsal Horn ◽  
Dorsal Root ◽  
Excitatory Amino Acid ◽  
Substantia Gelatinosa ◽  
Rat Spinal Cord ◽  
Spinal Cord Neurons ◽  
Dorsal Horn Neurons ◽  
Electrical Stimuli

1. Extracellular recordings were made from 95 dorsal horn neurons in a sagittal slice preparation of rat spinal cord. Neurons were synaptically activated by electrical stimulation of the dorsal root entry zone (n = 72) or driven by pressure ejection of L-glutamate into the substantia gelatinosa (SG; n = 23). For the majority of neurons low-intensity electrical stimuli evoked a burst of spikes with short latency (early firing). An increase in the stimulus intensity evoked the early firing followed by a characteristic prolonged period of activity (late firing). 2. The patterns of synaptically induced activity observed from neurons located in the SG (n = 45) and in deeper laminae (n = 27) were similar. Early and late firing of both SG and deep neurons was reduced by the nonspecific excitatory amino acid antagonist kynurenate. Raising [Mg2+] in the superfusate to 5 from 2.0 mM selectively reduced the late firing of both SG and deep neurons. These findings suggest that fibers present in the dorsal root zone make excitatory amino acid-mediated synapses with dorsal horn neurons. 3. The majority of deep neurons showed reduced responses to electrical stimuli in the presence of morphine, mimicking the findings reported in vivo. Naloxone reversed morphine inhibitions or, when applied to morphine-naive slices, caused modest increases in the responses of some deep neurons. 4. Most neurons located in the SG had their responses enhanced by morphine (late firing: 86.5 +/- 19.6%, mean +/- SE) and were inhibited by naloxone (-78.3 +/- 22.7%). Morphine-induced enhancements often persisted long after the morphine had washed out of the bath. Inhibitions by naloxone, whether pre- or postmorphine, were short lived; and responses generally returned to either control or morphine-enhanced levels on washout of the naloxone. 5. The gamma-aminobutyric acid (GABA) antagonist bicuculline, applied to GABA-naive slices, caused an increase in response of SG neurons while slightly depressing activity of deep neurons. A tonic release or presence of endogenous GABA, affecting neurons that are inhibited by exogenously applied GABA, may be responsible for the observed action of bicuculline. 6. Intracellular recordings were made from a further 32 dorsal horn neurons located in the translucent band of the spinal cord slices. Of 11 neurons examined, 5 showed increased input resistance (Rin) and were depolarized in response to morphine applied in the superfusate. One neuron showed no change in Rin or potential with morphine, whereas 5 of the 11 were hyperpolarized with decreased Rin.(ABSTRACT TRUNCATED AT 400 WORDS)

Local Anesthetic Inhibition of Voltage-activated Potassium Currents in Rat Dorsal Root Ganglion Neurons

2001 ◽  
Vol 94 (6) ◽  
pp. 1089-1095 ◽  
Author(s):  
Hirochika Komai ◽  
Thomas S. McDowell
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Horn ◽  
Local Anesthetic ◽  
Local Anesthetics ◽  
Dorsal Root ◽  
Drg Neurons ◽  
Dorsal Horn Neurons ◽  
K Currents

Background Local anesthetic actions on the K+ channels of dorsal root ganglion (DRG) and dorsal horn neurons may modulate sensory blockade during neuraxial anesthesia. In dorsal horn neurons, local anesthetics are known to inhibit transient but not sustained K+ currents. The authors characterized the effects of local anesthetics on K+ currents of isolated DRG neurons. Methods The effects of lidocaine, bupivacaine, and tetracaine on K+ currents in isolated rat DRG neurons were measured with use of a whole cell patch clamp method. The currents measured were fast-inactivating transient current (I(Af)), slow-inactivating transient current (I(As)), and noninactivating sustained current (I(Kn)). Results One group of cells (type 1) expressed I(Af) and I(Kn). The other group (type 2) expressed I(As) and I(Kn). The diameter of type 2 cells was smaller than that of type 1 cells. Lidocaine and bupivacaine inhibited all three K+ currents. Tetracaine inhibited I(As) and I(Kn) but not I(Af) For bupivacaine, the concentration for half-maximal inhibition (IC50) of I(Kn) in type 2 cells was lower than that for I(Kn) in type 1 cells (57 vs. 121 microM). Similar results were obtained for tetracaine (0.6 vs. 1.9 mM) and for lidocaine (2.2 vs. 5.1 mM). Conclusions Local anesthetics inhibited both transient and sustained K+ currents in DRG neurons. Because K+ current inhibition is known to potentiate local anesthetic-induced impulse inhibition, the lower IC50 for I(Kn) of small type 2 cells may reflect preferential inhibition of impulses in nociceptive neurons. The overall modulatory actions of local anesthetics probably are determined by their differential effects on presynaptic (DRG) and postsynaptic (dorsal horn neurons) K+ currents.

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