Modulation of synchronous sympathetic firing behaviors by endogenous GABA(A) and glycine receptor-mediated activities in the neonatal rat spinal cord in vitro.

Abstract:

:Delivering effective commands in the nervous systems require a temporal integration of neural activities such as synchronous firing. Although sympathetic nerve discharges are characterized by synchronous firing, its temporal structures and how it is modulated are largely unknown. This study used a collagenase-dissociated splanchnic sympathetic nerve-thoracic spinal cord preparation of neonatal rats in vitro as an experimental model. Several single-fiber activities were recorded simultaneously and verified by rigorous computational algorithms. Among 3763 fiber pairs that had spontaneous fiber activities, 382 fiber pairs had firing positively correlated. Their temporal relationship was quantitatively evaluated by cross-correlogram. On average, correlated firing in a fiber pair occurred in scales of ∼40ms lasting for ∼11ms. The relative frequency distribution curves of correlogram parametrical values pertinent to the temporal features were best described by trimodal Gaussians, suggesting a correlated firing originated from three or less sources. Applications of bicuculline or gabazine (noncompetitive or competitive GABA(A) receptor antagonist) and/or strychnine (noncompetitive glycine receptor antagonist) increased, decreased, or did not change individual fiber activities. Antagonist-induced enhancement and attenuation of correlated firing were demonstrated by a respective increase and decrease of the peak probability of the cross-correlograms. Heterogeneity in antagonistic responses suggests that the inhibitory neurotransmission mediated by GABA(A) and glycine receptors is not essential for but can serve as a neural substrate to modulate synchronous firing behaviors. Plausible neural mechanisms were proposed to explain the temporal structures of correlated firing between sympathetic fibers.

journal_name

Neuroscience

journal_title

Neuroscience

authors

Su CK

doi

10.1016/j.neuroscience.2015.11.024

subject

Has Abstract

pub_date

2016-01-15 00:00:00

pages

227-46

eissn

0306-4522

issn

1873-7544

pii

S0306-4522(15)01013-1

journal_volume

312

pub_type

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