Stabilization of the discharge rate of sympathetic preganglionic neurons

Polosa, Canio; Schondorf, R.; Laskey, W.

doi:10.1016/0165-1838(82)90088-1

Cited by 17 publications

(4 citation statements)

References 37 publications

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“…5, middle traces). The activity of single sympathetic preganglionic neurons in vivo is characterized by a lack of short interspike intervals (Polosa et al 1982; Kubota et al 1995); we therefore interpret this pattern as showing that each separated spike train was driven by a single preganglionic neuron. Autocorrelograms without a prominent central gap were taken to indicate that more than one preganglionic neuron was driving the activity.…”

Section: Resultsmentioning

confidence: 94%

Ganglionic transmission in a vasomotor pathway studied in vivo

Bratton

Davies

Jänig

et al. 2010

The Journal of Physiology

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Intracellular recordings were made in vivo from 40 spontaneously active cells in the third lumbar sympathetic ganglion of urethane-anaesthetized rats. In 38/40 cells ongoing action potentials showed strong cardiac rhythmicity (93.4 ± 1.9% modulation) indicating high barosensitivity and probable muscle vasoconstrictor (MVC) function. Subthreshold excitatory postsynaptic potentials (EPSPs) showed the same pattern. The 38 barosensitive neurons fired action potentials at 2.9 ± 0.3 Hz. All action potentials were triggered by EPSPs, most of which were unitary events. Calculations indicated that <5% of action potentials were triggered by summation of otherwise subthreshold EPSPs. 'Dominant' synaptic inputs with a high safety factor were identified, confirming previous work. These were active in 24/38 cells and accounted for 32% of all action potentials; other ('secondary') inputs drove the remainder. Inputs (21 dominant, 19 secondary) attributed to single preganglionic neurons fired at 1.38 ± 0.16 Hz. An average of two to three preganglionic neurons were estimated to drive each ganglion cell's action potentials. When cells were held hyperpolarized to block spiking, a range of spontaneous EPSP amplitudes was revealed. Threshold equivalent was defined as the membrane potential value that was exceeded by spontaneous EPSPs at the same frequency as the cell's original firing rate. In 10/12 cells examined, a continuum of EPSP amplitudes overlapped threshold equivalent. Small changes in cell excitability could therefore raise or lower the percentage of preganglionic inputs triggering action potentials. The results indicate that vasoconstrictor ganglion cells in vivo mostly behave not as 1:1 relays, but as continuously variable gates.

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Section: Resultsmentioning

confidence: 94%

Ganglionic transmission in a vasomotor pathway studied in vivo

Bratton

Davies

Jänig

et al. 2010

The Journal of Physiology

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“…A possible explanation for the increase in the number of infected SPNs as the survival time increases is that some SPNs could become infected through intraspinal axon collaterals. The existence of such collaterals has been suggested by several electrophysiological studies (Polosa et al, 1982; McKenna and Schramm, 1983; Dun and Mo, 1989), although anatomical results are less conclusive. Several collateralizations have been found in a minority of SPN axons in pigeon (Cabot and Bogan, 1987; Bogan and Cabot, 1991) and rat (Forehand, 1990) but have not been observed in cat (Dembowsky et al, 1985).…”

Section: Discussionmentioning

confidence: 95%

“…The postsynaptic targets of these intraspinal collaterals are unknown, although none of them was found to be recurrent onto the SPN of origin in pigeon (Cabot and Bogan, 1987; Bogan and Cabot, 1991). Collateral terminals could be presynaptic to dendrites of SPNs or dendrites of spinal INs; the latter possibility is suggested by electrophysiological data supporting the existence of spinal excitatory INs involved in the brainstem and reflex control of SPNs (Barman and Gebber, 1984), as well as inhibitory INs associated with SPN activity as part of recurrent inhibitory circuits modulating sympathetic outflow (McCall et al, 1977; Polosa et al, 1982). Further studies are needed to determine the existence of intraspinal communication among SPNs, directly or through INs, and its physiological role in the control of target‐specific sympathetic outflow.…”

Section: Discussionmentioning

confidence: 99%

Characterization of the central nervous system innervation of the rat spleen using viral transneuronal tracing

Cano

Sved

Rinaman

et al. 2001

J of Comparative Neurology

205

124

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Splenic immune function is modulated by sympathetic innervation, which in turn is controlled by inputs from supraspinal regions. In the present study, the characterization of central circuits involved in the control of splenic function was accomplished by injecting pseudorabies virus (PRV), a retrograde transynaptic tracer, into the spleen and conducting a temporal analysis of the progression of the infection from 60 hours to 110 hours postinoculation. In addition, central noradrenergic cell groups involved in splenic innervation were characterized by dual immunohistochemical detection of dopamine-beta-hydroxylase and PRV. Infection in the CNS first appeared in the spinal cord. Splenic sympathetic preganglionic neurons, identified in rats injected with Fluoro-Gold i.p. prior to PRV inoculation of the spleen, were located in T(3)-T(12) bilaterally; numerous infected interneurons were also found in the thoracic spinal cord (T(1)-T(13)). Infected neurons in the brain were first observed in the A5 region, ventromedial medulla, rostral ventrolateral medulla, paraventricular hypothalamic nucleus, Barrington's nucleus, and caudal raphe. At intermediate survival times, the number of infected cells increased in previously infected areas, and infected neurons also appeared in lateral hypothalamus, A7 region, locus coeruleus, subcoeruleus region, nucleus of the solitary tract, and C3 cell group. At longer postinoculation intervals, infected neurons were found in additional hypothalamic areas, Edinger-Westphal nucleus, periaqueductal gray, pedunculopontine tegmental nucleus, caudal ventrolateral medulla, and area postrema. These results demonstrate that the sympathetic outflow to the spleen is controlled by a complex multisynaptic pathway that involves several brainstem and forebrain nuclei.

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“…Many SPNs clearly receive inputs from the presympathetic neurons in the RVLM that play a major role in generating their activity (8,14,39). However, there may also be SPNs that discharge spontaneously to maintain sympathetic activity and rhythmicity at the spinal level (40,41).…”

Section: Electrophysiological Characteristics Of the Spnsmentioning

confidence: 99%