Changes in electrical activity of spinal cord neurons in adrenalectomized rats under the effects of corticosteroid hormones

1989 ◽  
Vol 21 (2) ◽  
pp. 177-181
Author(s):  
T. K. Kipriyan ◽  
V. A. Chavushyan
Keyword(s):  
Spinal Cord ◽  
Electrical Activity ◽  
Spinal Cord Neurons ◽  
Corticosteroid Hormones ◽  
Adrenalectomized Rats

Mechanism of disturbances of electrical activity of spinal cord neurons in experimental botulism

1968 ◽  
Vol 66 (5) ◽  
pp. 1201-1204 ◽  
Author(s):  
V. V. Mikhailov ◽  
V. V. Korolev
Keyword(s):  
Spinal Cord ◽  
Electrical Activity ◽  
Spinal Cord Neurons ◽  
Experimental Botulism

Role of electrical activity and trophic factors during cholinergic development in dissociated cultures

1986 ◽  
Vol 64 (3) ◽  
pp. 356-362 ◽  
Author(s):  
Douglas E. Brenneman
Keyword(s):  
Spinal Cord ◽  
Electrical Activity ◽  
Conditioned Medium ◽  
Trophic Factors ◽  
Acid Decarboxylase ◽  
Gaba Uptake ◽  
Decarboxylase Activity ◽  
Spinal Cord Neurons ◽  
Dose Dependent

The role of electrical activity in the developmental regulation of cholinergic neurons was investigated in dissociated spinal cord – dorsal root ganglion (SC-DRG) cultures. Application of tetrodotoxin (TTX) during the first 6 days after plating had no effect on choline acetyltransferase (CAT) activity. Suppression of electrical activity during the 7th day decreased CAT to 68% of control. These decreases in CAT activity were still apparent 2 weeks after removal of the TTX. GABAergic neurons, as indicated by glutamic acid decarboxylase activity and high affinity [3H]GABA uptake, were not affected by TTX treatment. Addition of 8-bromo-cAMP or conditioned medium obtained from SC-DRG cultures at certain developmental periods produced dose-dependent increases in CAT levels on TTX-treated cultures as compared with those treated with TTX alone. Similar studies with 8-bromo-cGMP revealed no significant effects on CAT activity. Vasoactive intestinal peptide (VIP) produced a dose-dependent increase in CAT activity when added to cultures between days 12 and 14. Similar studies conducted on younger cultures (days 5–7) or older cultures (days 21–23) revealed no increases in CAT activity. Addition of 0.1 nM VIP to TTX-treated cultures resulted in CAT levels which were not significantly different from those of electrically active controls. These data suggest that cyclic AMP, VIP, and trophic substances in conditioned medium may have roles in the mechanism of cholinergic toxicity produced by electrical blockade of developing spinal cord neurons.

The developmental appearance of -bungarotoxin binding sites on rodent spinal cord neurons in cell culture

1986 ◽  
Vol 390 (2) ◽  
pp. 239-247
Author(s):  
A SCHAFFNER ◽  
A OLEK
Keyword(s):  
Spinal Cord ◽  
Cell Culture ◽  
Binding Sites ◽  
Spinal Cord Neurons

scholarly journals Lipoxin A4 protects primary spinal cord neurons from Erastin‐induced ferroptosis by activating the Akt/Nrf2/HO‐1 signaling pathway

FEBS Open Bio ◽  
2021 ◽  
Author(s):  
Na Wei ◽  
Tan Lu ◽  
Libin Yang ◽  
Yonghan Dong ◽  
Xiaotan Liu
Keyword(s):  
Spinal Cord ◽  
Signaling Pathway ◽  
Lipoxin A4 ◽  
Spinal Cord Neurons

Expression of GAD mRNA in spinal cord neurons of normal and monoarthritic rats

1994 ◽  
Vol 26 (1-2) ◽  
pp. 169-176 ◽  
Author(s):  
J.M. Castro-Lopes ◽  
T.R. Tölle ◽  
B. Pan ◽  
W. Zieglgänsberger
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Neurons

Spinal cord neurons are vulnerable to rapidly triggered kainate neurotoxicity in vitro

1995 ◽  
Vol 689 (2) ◽  
pp. 265-270 ◽  
Author(s):  
Hong-zhen Yin ◽  
David D. Park ◽  
Amy D. Lindsay ◽  
John H. Weiss
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Neurons

Evidence for biological effects of exogenous LPA on rat primary afferent and spinal cord neurons

2004 ◽  
Vol 1022 (1-2) ◽  
pp. 205-213 ◽  
Author(s):  
Steven J.R. Elmes ◽  
Paul J. Millns ◽  
Darren Smart ◽  
David A. Kendall ◽  
Victoria Chapman
Keyword(s):  
Spinal Cord ◽  
Biological Effects ◽  
Primary Afferent ◽  
Spinal Cord Neurons

Effects of N- and L-type calcium channel antagonists on the responses of nociceptive spinal cord neurons to mechanical stimulation of the normal and the inflamed knee joint

1996 ◽  
Vol 76 (6) ◽  
pp. 3740-3749 ◽  
Author(s):  
V. Neugebauer ◽  
H. Vanegas ◽  
J. Nebe ◽  
P. Rumenapp ◽  
H. G. Schaible
Keyword(s):  
Spinal Cord ◽  
Knee Joint ◽  
Calcium Channels ◽  
Mechanical Stimulation ◽  
Topical Administration ◽  
Knee Joints ◽  
Spinal Cord Neurons ◽  
Inflammatory Conditions ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

1. The present study addresses the involvement of voltage-dependent calcium channels of the N and L type in the spinal processing of innocuous and noxious input from the knee joint, both under normal conditions and under inflammatory conditions in which spinal cord neurons become hyperexcitable. In 30 anesthetized rats, extracellular recordings were performed from single dorsal horn neurons in segments 1–4 of the lumbar spinal cord. All neurons had receptive fields in the ipsilateral knee joint. In 22 rats, an inflammation was induced in the ipsilateral knee joint by kaolin and carrageenan 4–16 h before the recordings. The antagonist at N-type calcium channels, omega-conotoxin GVIA (omega-CTx GVIA), was administered topically in solution to the dorsal surface of the spinal cord at the appropriate spinal segments in 6 rats with normal joints and in 12 rats with inflamed knee joints. The antagonist at L-type channels, nimodipine, was administered topically in 5 rats with normal joints and in 11 rats with inflamed knee joints. In another five rats with inflamed joints, antagonists at L-type calcium channels (diltiazem and nimodipine) and omega-CTx GVIA were administered ionophoretically with multibarrel electrodes close to the neurons recorded. 2. The topical administration of omega-CTx GVIA to the spinal cord reduced the responses to both innocuous and noxious pressure applied to the knee joint in a sample of 11 neurons with input from the normal joint and in a sample of 16 neurons with input from the inflamed joint (hyperexcitable neurons). The responses were decreased to approximately 65% of the predrug values within administration times of 30 min. A similar reduction of the responses to innocuous and noxious pressure was observed when omega-CTx GVIA was administered ionophoretically to nine hyperexcitable neurons. In neurons with input from the normal or the inflamed knee joint, the administration of omega-CTx GVIA led also to a reduction of the responses to innocuous and noxious pressure applied to the noninflamed ankle joint. 3. The topical administration of nimodipine decreased the responses to innocuous and noxious pressure applied to the knee in a sample of 9 neurons with input from the normal joint and in a sample of 16 neurons with input from the inflamed knee joint (hyperexcitable neurons). Within administration times of 30 min, the responses were reduced to approximately 70% of the predrug values. In hyperexcitable neurons, the responses to innocuous and noxious pressure applied to the knee were also decreased during ionophoretic administration of nimodipine (6 neurons) and diltiazem (9 neurons). When the noninflamed ankle was stimulated, the responses to innocuous pressure were reduced neither in neurons with input from the normal knee nor in neurons with input from the inflamed knee, but the responses of hyperexcitable neurons to noxious pressure onto the ankle were reduced. The ionophoretic administration of the agonist at the L-type calcium channel, S(-)-Bay K 8644, enhanced the responses to mechanical stimulation of the knee joint in all 14 hyperexcitable neurons tested. The effect of S(-)-Bay K 8644 was counteracted by both diltiazem (in 6 of 6 neurons) and nimodipine (in 5 of 5 neurons). 4. These data show that antagonists at both the N- and the L-type voltage-dependent calcium channels influence the spinal processing of input from the knee joint. The data suggest, therefore, that voltage-dependent calcium calcium channels of both the N and the L type are important for the sensory functions of the spinal cord. They are involved in the spinal processing of nonnociceptive as well as nociceptive mechanosensory input from the joint, both under normal and inflammatory conditions. The present results show in particular that N- and L-type channels are likely to be involved in the generation of pain evoked by noxious mechanical stimulation in normal tissue as well as in the mechanical hyperalgesia that is usually pres

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