Capillary electrophoresis combined with microdialysis in the human spinal cord: A new tool for monitoring rapid peroperative changes in amino acid neurotransmitters within the dorsal horn

2004 ◽  
Vol 25 (1011) ◽  
pp. 1511-1517 ◽  
Author(s):  
Sandrine Parrot ◽  
Valérie Sauvinet ◽  
Jean-Michel Xavier ◽  
Delphine Chavagnac ◽  
Laurence Mouly-Badina ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Capillary Electrophoresis ◽  
Amino Acid ◽  
Dorsal Horn ◽  
Amino Acid Neurotransmitters ◽  
Human Spinal Cord

scholarly journals Dorsal horn interneuron-derived Netrin-4 contributes to spinal sensitization in chronic pain via Unc5B

2016 ◽  
Vol 213 (13) ◽  
pp. 2949-2966 ◽  
Author(s):  
Yasufumi Hayano ◽  
Keiko Takasu ◽  
Yoshihisa Koyama ◽  
Moe Yamada ◽  
Koichi Ogawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Chronic Pain ◽  
Dorsal Horn ◽  
Molecular Mechanisms ◽  
Tyrosine Phosphatase ◽  
Intrathecal Administration ◽  
Human Spinal Cord ◽  
Similar Expression Pattern ◽  
Subsequent Activation ◽  
Spinal Sensitization

Because of the incomplete understanding of the molecular mechanisms that underlie chronic pain, the currently available treatments for this type of pain remain inefficient. In this study, we show that Netrin-4, a member of the axon guidance molecule family, was expressed in dorsal horn inner lamina II excitatory interneurons in the rat spinal cord. A similar expression pattern for Netrin-4 was also observed in human spinal cord. Behavioral analysis revealed that tactile and heat hyperalgesia after peripheral nerve injury or inflammation were abolished in Netrin-4–mutant rats. Transient suppression of Netrin-4 or its receptor Unc5B after injury could also prevent allodynia. Conversely, intrathecal administration of Netrin-4 protein to naive rats enhanced excitatory synaptic transmission in the dorsal horn and induced allodynia, suggesting that Netrin-4 is involved in spinal sensitization. Furthermore, the Unc5B receptor and subsequent activation of the tyrosine phosphatase SHP2 mediated Netrin-4–induced pain signaling in the spinal cord. These results identify Netrin-4 as a novel protein regulating spinal sensitization leading to chronic pain. Our findings provide evidence for the function of Netrin in the adult nervous system, as well as a previously unknown function in inducing pain signals from dorsal horn interneurons.

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)

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