Baroreceptor influence on the relationships between discharges of different sympathetic nerves of the cat.

Kocsis, Bernát

doi:10.1113/jphysiol.1995.sp020551

Cited by 19 publications

(9 citation statements)

References 29 publications

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“…In baroreceptor-innervated animals the cardiacrelated rhythmicity in SND bursts reflects the fundamental organization of sympathetic neural circuits (9,23,25). The present results demonstrate that the basic cardiac-related pattern of SND bursts is altered by cold stress.…”

Section: Discussionsupporting

confidence: 51%

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Cold stress alters characteristics of sympathetic nerve discharge bursts

Kenney

Claassen

Fels

et al. 1999

Journal of Applied Physiology

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Frequency-domain analyses were used to determine the effect of cold stress on the relationships between the discharge bursts of sympathetic nerve pairs, sympathetic and aortic depressor nerve pairs, and sympathetic and phrenic nerve pairs in chloralose-anesthetized, baroreceptor-innervated rats. Sympathetic nerve discharge (SND) was recorded from the renal, lumbar, splanchnic, and adrenal nerves during decreases in core body temperature from 38 to 30 degrees C. The following observations were made. 1) Hypothermia produced nonuniform changes in the level of activity in regionally selective sympathetic nerves. Specifically, cold stress increased lumbar and decreased renal SND but did not significantly change the level of activity in splanchnic and adrenal nerves. 2) The cardiac-related pattern of renal, lumbar, and splanchnic SND bursts was transformed to a low-frequency (0-2 Hz) pattern during cooling, despite the presence of pulse-synchronous activity in arterial baroreceptor afferents. 3) Peak coherence values relating the discharges between sympathetic nerve pairs decreased at the cardiac frequency but were unchanged at low frequencies (0-2 Hz), indicating that the sources of low-frequency SND bursts remain prominently coupled during progressive reductions in core body temperature. 4) Coherence of discharge bursts in phrenic and renal sympathetic nerve pairs in the 0- to 2-Hz frequency band increased during mild hypothermia (36 degrees C) but decreased during deep hypothermia (30 degrees C). We conclude that hypothermia profoundly alters the organization of neural circuits involved in regulation of sympathetic nerve outflow to selected regional circulations.

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Section: Discussionsupporting

confidence: 51%

“…Spectral analyses provide the following information (9,10,25,27). The autospectrum of a signal shows the relative power present at each frequency.…”

Section: General Procedures the Surgical Procedures And Experimentalmentioning

confidence: 99%

Cold stress alters characteristics of sympathetic nerve discharge bursts

Kenney

Claassen

Fels

et al. 1999

Journal of Applied Physiology

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show abstract

“…The frequency resolution was 0.2 Hz/bin. Spectral analyses provide the following information (17,21,22). The autospectrum of a signal shows the relative power present at each frequency.…”

Section: General Proceduresmentioning

confidence: 99%

Effects of midbrain and spinal cord transections on sympathetic nerve responses to heating

Kenney

Pickar

Weiss

et al. 2000

American Journal of Physiology-Regulatory, Integrative and Comp

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In the present study, we investigated the contributions of forebrain, brain stem, and spinal neural circuits to heating-induced sympathetic nerve discharge (SND) responses in chloralose-anesthetized rats. Frequency characteristics of renal and splenic SND bursts and the level of activity in these nerves were determined in midbrain-transected (superior colliculus), spinal cord-transected [first cervical vertebra (C1)], and sham-transected (midbrain and spinal cord) rats during progressive increases in colonic temperature (T(c)) from 38 to 41.6-41.7 degrees C. The following observations were made. 1) Significant increases in renal and splenic SND were observed during hyperthermia in midbrain-transected, sham midbrain-transected, C1-transected, and sham C1-transected rats. 2) Heating changed the discharge pattern of renal and splenic SND bursts and was associated with prominent coupling between renal-splenic discharge bursts in midbrain-transected, sham midbrain-transected, and sham C1-transected rats. 3) The pattern of renal and splenic SND bursts remained unchanged from posttransection recovery levels during heating in C1-transected rats. We conclude that an intact forebrain is not required for the full expression of SND responses to increased T(c) and that spinal neural systems, in the absence of supraspinal circuits, are unable to markedly alter the frequency characteristics of SND in response to acute heat stress.

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“…Shared inhibitory as well as excitatory inputs can cause cross-correlation peaks (Moore et al 1970). A second reason is that the postulated oscillators driving sympathetic nerve activity are able to function independently of baroreceptor signals (Gebber 1980(Gebber , 1990Kocsis 1995;Kocsis et al 1990;Taylor and Gebber 1975). Whether the proposed oscillator circuits are wholly or partly independent of baroreceptor signals, or even if they drift between those two states, their influence should be detectable as a baroreceptor-independent source of synchrony.…”

Section: Evidence For Common Synchronizing Inputsmentioning

confidence: 99%

Analysis of Firing Correlations Between Sympathetic Premotor Neuron Pairs in Anesthetized Cats

McAllen

Trevaks

Allen

2001

Journal of Neurophysiology

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The activity of sympathetic premotor neurons in the rostral ventrolateral medulla (subretrofacial nucleus) supports sympathetic vasomotor tone, but the factors that drive these premotor neurons' activity have not been determined. This study examines whether either direct interconnections between subretrofacial neurons or synchronizing common inputs to them are important for generating their tonic activity. Simultaneous extracellular single-unit recordings were made from 32 pairs of sympathetic premotor neurons in the subretrofacial nucleus of chloralose-anesthetized cats. Paired spike trains were either separated by spike shape from a single-electrode recording (14 pairs) or recorded from two electrodes less than 250 microm apart (18 pairs). All neurons were inhibited by carotid baroreceptor stimulation and most had a spinal axon proven by antidromic stimulation from the spinal cord. Autocorrelation, inter-spike interval, and cardiac cycle-triggered histograms were constructed from the spontaneous activity of each neuron, and cross-correlation histograms covering several time scales were generated for each neuron pair. No significant peaks or troughs were found in short-term cross-correlation histograms (2 ms bins, +/-100 ms range), providing no support for important local synaptic interactions. On an intermediate time scale (20 ms bins, +/-1 s range), cross-correlation revealed two patterns indicating shared, synchronizing inputs. Repeating peaks and troughs (19/32 pairs) were due to the two neurons' common cardiac rhythmicity, of presumed baroreceptor origin. Single, zero time-spanning peaks of 40--180 ms width were seen in 5/32 cases. Calculations based on the prevalence and strength of these synchronizing inputs indicate that most of the ensemble spike activity of the subretrofacial neuron population is derived from asynchronous sources (be they intrinsic or extrinsic). If synchronizing sources such as neuronal oscillators were responsible for more than a minor part of the drive, they would be multiple, dispersed, and weak.

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Baroreceptor influence on the relationships between discharges of different sympathetic nerves of the cat.

Cited by 19 publications

References 29 publications

Cold stress alters characteristics of sympathetic nerve discharge bursts

Cold stress alters characteristics of sympathetic nerve discharge bursts

Effects of midbrain and spinal cord transections on sympathetic nerve responses to heating

Analysis of Firing Correlations Between Sympathetic Premotor Neuron Pairs in Anesthetized Cats

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