Ablation of primary afferent terminals reduces nicotinic receptor expression and the nociceptive responses to nicotinic agonists in the spinal cord

2004 ◽  
Vol 33 (5) ◽  
pp. 543-556 ◽  
Author(s):  
Imran M. Khan ◽  
Michelle Wennerholm ◽  
Erin Singletary ◽  
Kimberley Polston ◽  
Limin Zhang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Nicotinic Receptor ◽  
Receptor Expression ◽  
Primary Afferent ◽  
Nicotinic Agonists ◽  
Nociceptive Responses ◽  
Afferent Terminals

Nicotinic receptor gene cluster on rat chromosome 8 in nociceptive and blood pressure hyperresponsiveness

2002 ◽  
Vol 11 (2) ◽  
pp. 65-72 ◽  
Author(s):  
Imran M. Khan ◽  
Erin Singletary ◽  
Adamu Alemayehu ◽  
Shanaka Stanislaus ◽  
Morton P. Printz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gene Cluster ◽  
Nicotinic Receptor ◽  
Receptor Gene ◽  
Repeated Administration ◽  
Chromosome 8 ◽  
Brown Norway ◽  
Spontaneously Hypertensive ◽  
Nicotinic Agonists ◽  
Nociceptive Responses

Spontaneously hypertensive rats (SHR) exhibit enhanced pressor, heart rate, and nociceptive responses to spinal nicotinic agonists. This accompanies a paradoxical decrease in spinal nicotinic receptor number in SHR compared with normotensive rats. The congenic strain, SHR-Lx, with an introgressed chromosome 8 segment from the normotensive Brown-Norway-Lx strain (BN-Lx) exhibits reduced blood pressure. This segment contains a gene cluster for three nicotinic receptor subunits expressed in the nervous system. We examined the implication of this gene cluster in the enhanced responsiveness of the SHR. Pressor and nociceptive responses to spinal cytisine, a nicotinic agonist, were diminished in SHR-Lx. Moreover, with repeated administration, these responses desensitized faster in SHR-Lx and progenitor BN-Lx than in progenitor SHR/Ola. This implicates the gene cluster in both cardiovascular and nociceptive responses to spinal nicotinic agonists. Since diminished responsiveness to agonist stimulation is greater than the basal blood pressure differences between the strains and the introgressed rat chromosome maps to a quantitative trait locus in human hypertension, polymorphisms in the three nicotinic receptor genes become candidates for altered central control of blood pressure.

Ultrastructure of Pacinian corpuscle primary afferent terminals in the cat spinal cord

1984 ◽  
Vol 302 (1) ◽  
pp. 135-150 ◽  
Author(s):  
K. Semba ◽  
P. Masarachia ◽  
S. Malamed ◽  
M. Jacquin ◽  
S. Harris ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Pacinian Corpuscle ◽  
Primary Afferent ◽  
Afferent Terminals

GABAergic terminals are presynaptic to primary afferent terminals in the substantia gelatinosa of the rat spinal cord

1978 ◽  
Vol 141 (1) ◽  
pp. 35-55 ◽  
Author(s):  
Robert P. Barber ◽  
James E. Vaughn ◽  
Kihachi Saito ◽  
Barbara J. McLaughlin ◽  
Eugene Roberts
Keyword(s):  
Spinal Cord ◽  
Substantia Gelatinosa ◽  
Rat Spinal Cord ◽  
Primary Afferent ◽  
Afferent Terminals

Primary afferent depolarization in frog spinal cord is associated with an increase in membrane conductance

1983 ◽  
Vol 61 (6) ◽  
pp. 626-631 ◽  
Author(s):  
Ante L. Padjen ◽  
Toshio Hashiguchi
Keyword(s):  
Spinal Cord ◽  
Linear Part ◽  
Membrane Conductance ◽  
Potassium Sulfate ◽  
Equilibrium Potential ◽  
Primary Afferent Depolarization ◽  
Primary Afferent ◽  
Frog Spinal Cord ◽  
Voltage Dependent ◽  
Afferent Terminals

The mechanism of primary afferent depolarization (PAD) was studied in the isolated frog spinal cord using intrafibre recording (microelectrodes filled with 0.6 M potassium sulfate) from large myelinated axons of dorsal roots. Standard current–clamp technique was used to obtain voltage–current (V–I) relationship. It was found that: (i) PAD is voltage dependent: its amplitude and rate of rise are increased with hyperpolarization; (ii) the slope of the linear part of the V–I curve obtained during PAD is decreased compared with the V–I curve at rest; (iii) the PAD equilibrium potential, estimated by extrapolation, ranged from −66 to −40 mV. These results suggest that PAD is associated with an increase in conductance of primary afferent terminals and thus seem to provide the first experimental evidence for the hypothesis that shunting of primary afferent membrane is the mechanism of presynaptic inhibition in the vertebrate nervous system.

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