Evidence for at Least Two Tachykinin Receptor Subtypes in the Mammalian Spinal Cord

1987 ◽  
pp. 328-330 ◽  
Author(s):  
M. Wienrich ◽  
I. Lues ◽  
B. E. B. Sandberg ◽  
J. Harting
Keyword(s):  
Spinal Cord ◽  
Receptor Subtypes ◽  
Tachykinin Receptor

scholarly journals Galanin-receptor ligand M40 peptide distinguishes between putative galanin-receptor subtypes

1993 ◽  
Vol 90 (23) ◽  
pp. 11287-11291 ◽  
Author(s):  
T Bartfai ◽  
U Langel ◽  
K Bedecs ◽  
S Andell ◽  
T Land ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Binding Sites ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Galanin Receptor ◽  
Flexor Reflex ◽  
Receptor Ligand ◽  
Insulinoma Cells ◽  
Galanin Receptors

The galanin-receptor ligand M40 [galanin-(1-12)-Pro3-(Ala-Leu)2-Ala amide] binds with high affinity to [mono[125I]iodo-Tyr26]galanin-binding sites in hippocampal, hypothalamic, and spinal cord membranes and in membranes from Rin m5F rat insulinoma cells (IC50 = 3-15 nM). Receptor autoradiographic studies show that M40 (1 microM) displaces [mono[125I]iodo-Tyr26]galanin from binding sites in the hippocampus, hypothalamus, and spinal cord. In the brain, M40 acts as a potent galanin-receptor antagonist: M40, in doses comparable to that of galanin, antagonizes the stimulatory effects of galanin on feeding, and it blocks the galaninergic inhibition of the scopolamine-induced acetylcholine release in the ventral hippocampus in vivo. In contrast, M40 completely fails to antagonize both the galanin-mediated inhibition of the glucose-induced insulin release in isolated mouse pancreatic islets and the inhibitory effects of galanin on the forskolin-stimulated accumulation of 3',5'-cAMP in Rin m5F cells; instead M40 is a weak agonist at the galanin receptors in these two systems. M40 acts as a weak antagonist of galanin in the spinal flexor reflex model. These results suggest that at least two subtypes of the galanin receptor may exist. Hypothalamic and hippocampal galanin receptors represent a putative central galanin-receptor subtype (GL-1-receptor) that is blocked by M40. The pancreatic galanin receptor may represent another subtype (GL-2-receptor) that recognizes M40, but as a weak agonist. The galanin receptors in the spinal cord occupy an intermediate position between these two putative subtypes.

Changes in serotonin-induced potentials during spinal cord development

1993 ◽  
Vol 69 (4) ◽  
pp. 1338-1349 ◽  
Author(s):  
L. Ziskind-Conhaim ◽  
B. S. Seebach ◽  
B. X. Gao
Keyword(s):  
Spinal Cord ◽  
Direct Action ◽  
Membrane Resistance ◽  
Ventral Horn ◽  
Repetitive Firing ◽  
Lumbar Spinal Cord ◽  
Receptor Subtypes ◽  
Gamma Aminobutyric Acid ◽  
Spinal Neurons ◽  
Lumbar Spinal

1. Motoneuron responses to serotonin (5-hydroxytryptamine, 5-HT), and the growth pattern of 5-HT projections into the ventral horn were studied in the isolated spinal cord of embryonic and neonatal rats. 2. 5-HT projections first appeared in lumbar spinal cord at days 16-17 of gestation (E16-E17) and were localized in the lateral and ventral funiculi. By E18, the projections had grown into the ventral horn, and at 1-2 days after birth they were in close apposition to motoneuron somata. 3. At E16-E17, slow-rising depolarizing potentials of 1-4 mV were recorded intracellularly in lumbar motoneurons in response to bath application of 5-HT. These potentials were not apparent after E18; at that time 5-HT generated long-lasting depolarizations with an average amplitude of 6 mV, and an increase of 11% in membrane resistance. Starting at E18, 5-HT also induced high-frequency fast-rising potentials that were blocked by antagonists of glutamate, gamma-aminobutyric acid, and glycine. 4. Motoneuron responses to 5-HT increased significantly after birth, when 5-HT produced an average depolarization of 19 mV and repetitive firing of action potentials. 5. Tetrodotoxin and high Mg2+ did not reduce the amplitude of the long-lasting depolarizations, which suggested that they were produced by direct action of 5-HT on motoneuron membrane. 6. At all developmental ages, 5-HT reduced the amplitude of dorsal root-evoked potentials. The suppressed responses were neither due to 5-HT-induced depolarization nor the result of a decrease in motoneuron excitability. 7. The pharmacological profile of 5-HT-induced potentials was studied with the use of various agonists and antagonists of 5-HT. The findings indicated that the actions of 5-HT on spinal neurons were mediated via multiple 5-HT receptor subtypes. 8. Our results suggested that 5-HT excited spinal neurons before 5-HT projections grew into the ventral horn. The characteristics of 5-HT-induced potentials changed, however, at the time when the density of 5-HT projections increased in the motor nuclei.

Dimerization of neurokin A and B COOH-terminal heptapeptide fragments enhanced the selectivity for tachykinin receptor subtypes

1988 ◽  
Vol 151 (2) ◽  
pp. 317-320 ◽  
Author(s):  
Hiroaki Kodama ◽  
Yasuyuki Shimohigashi ◽  
Kazuyasu Sakaguchi ◽  
Michinori Waki ◽  
Yukio Takano ◽  
...  
Keyword(s):  
Receptor Subtypes ◽  
Tachykinin Receptor

Endogenous Tachykinin Release Contributes to the Locomotor Activity in Lamprey

2007 ◽  
Vol 97 (5) ◽  
pp. 3331-3339 ◽  
Author(s):  
Carolina Thörn Pérez ◽  
Russell H. Hill ◽  
Sten Grillner
Keyword(s):  
Spinal Cord ◽  
Steady State ◽  
Locomotor Activity ◽  
Initial Period ◽  
Burst Frequency ◽  
Ongoing Activity ◽  
Initial Burst ◽  
Tachykinin Receptor ◽  
Spinal Network ◽  
Endogenous Release

Tachykinins are present in lamprey spinal cord. The goal of this study was to investigate whether an endogenous release of tachykinins contributes to the activity of the spinal network generating locomotor activity. The locomotor network of the isolated lamprey spinal cord was activated by bath-applied N-methyl-d-aspartate (NMDA) and the efferent activity recorded from the ventral roots. When spantide II, a tachykinin receptor antagonist, was bath-applied after reaching a steady-state burst frequency (>2 h), it significantly lowered the burst rate compared with control pieces from the same animal. In addition, the time to reach the steady-state burst frequency (>2 h) was lengthened in spantide II. These data indicate that an endogenous tachykinin release contributes to the ongoing activity of the locomotor network by modulating the glutamate–glycine neuronal network responsible for the locomotor pattern. We also explored the effects of a 10-min exogenous application of substance P (1 μM), a tachykinin, and showed that its effect on the burst rate depended on the initial NMDA induced burst frequency. At low initial burst rates (∼0.5 Hz), tachykinins caused a marked further slowing to 0.1 Hz, whereas at higher initial burst rates, it instead caused an enhanced burst rate as previously reported, and in addition, a slower modulation (0.1 Hz) of the amplitude of the motor activity. These effects occurred during an initial period of ∼1 h, whereas a modest long-lasting increase of the burst rate remained after >2 h.

Roles of adenosine receptor subtypes on the antinociceptive effect of sildenafil in rat spinal cord

2010 ◽  
Vol 480 (3) ◽  
pp. 182-185 ◽  
Author(s):  
Hyung Gon Lee ◽  
Woong Mo Kim ◽  
Jeong Il Choi ◽  
Myung Ha Yoon
Keyword(s):  
Spinal Cord ◽  
Adenosine Receptor ◽  
Antinociceptive Effect ◽  
Receptor Subtypes ◽  
Rat Spinal Cord

scholarly journals Upregulation of EphA Receptor Expression in the Injured Adult Rat Spinal Cord

2002 ◽  
Vol 11 (3) ◽  
pp. 229-239 ◽  
Author(s):  
Christopher A. Willson ◽  
Margarita Irizarry-Ramírez ◽  
Hope E. Gaskins ◽  
Lillian Cruz-Orengo ◽  
Johnny D. Figueroa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Gray Matter ◽  
Receptor Expression ◽  
Axonal Guidance ◽  
Receptor Subtypes ◽  
Rat Spinal Cord ◽  
Functional Connections ◽  
Cord Injury ◽  
Epha Receptor

After spinal cord injury (SCI), the inability of supraspinal neurons to regenerate or reform functional connections is likely due to proteins in the surrounding microenvironment restricting regeneration. EphAs are a family of receptor tyrosine kinases that are involved in axonal guidance during development. These receptors and their ligands, the Ephrins, act via repulsive mechanisms to guide growing axons towards their appropriate targets and allow for the correct developmental connections to be made. In the present study, we investigated whether EphA receptor expression changed after a thoracic contusion SCI. Our results indicate that several EphA molecules are upregulated after SCI. Using semiquantitative RT-PCR to investigate mRNA expression after SCI, we found that EphA3, A4, and A7 mRNAs were upregulated. EphA3, A4, A6, and A8 receptor immunoreactivity increased in the ventrolateral white matter (VWM) at the injury epicenter. EphA7 had the highest level of immunoreactivity in both control and injured rat spinal cord. EphA receptor expression in the white matter originated from glial cells as coexpression in both astrocytes and oligodendrocytes was observed. In contrast, gray matter expression was localized to neurons of the ventral gray matter (motor neurons) and dorsal horn. After SCI, specific EphA receptor subtypes are upregulated and these increases may create an environment that is unfavorable for neurite outgrowth and functional regeneration.

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