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Descending amygdalar modulation of upper thoracic spinal neurons responding to inhaled ammonia in rats: role of C1‐C2 spinal neurons
Author(s) -
Farber Jay P,
Qin Chao,
Foreman Robert D
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1271-a
Subject(s) - inhibitory postsynaptic potential , spinal cord , ibotenic acid , neuroscience , excitatory postsynaptic potential , amygdala , premovement neuronal activity , chemistry , stimulation , central nervous system , neuron , medicine , noxious stimulus , anesthesia , nociception , biology , receptor
The aim of this study was to examine whether the amygdala influenced activity of thoracic spinal neurons with noxious pulmonary input via C1‐C2 spinal neurons. Extracellular potentials of single thoracic (T3) spinal neurons were recorded in pentobarbital anesthetized, paralyzed, and ventilated male rats. Lower airways and lungs were irritated by injecting ammonia vapor into the inspiratory line of the ventilator. Electrical stimulation of amygdala (ESA) at 10, 30, 60, 90 μA (50 Hz, 0.2 ms) was performed to activate neurons in central nucleus. A pledget with ibotenic acid (0.3 mg/ml, >15 min) was placed on the surface of C1‐C2 spinal cord to inactivate underlying neurons. ESA changed activity of 31/41 (76%) T3 spinal neurons responding to inhaled ammonia (IA). Of these, ESA increased activity of 6 neurons excited by and 2 neurons inhibited by IA. ESA decreased activity of 19 neurons excited by and 4 neurons inhibited by IA. Ibotenic acid on C1‐C2 abolished inhibitory responses to ESA in 7 neurons and excitatory responses to ESA in 2 neurons. Rostral C1 spinal transection eliminated inhibitory responses to ESA in 4 neurons unaffected by inactivation of C1‐C2 neurons. These results showed that activation of central amygdala modulated activity of thoracic spinal neurons with noxious pulmonary inputs and this descending modulation was in part mediated by upper cervical spinal neurons. (NS‐035471, HL‐075524)