Late expiratory inhibition of stage 2 expiratory neurons in the cat--a correlate of expiratory termination

Abstract

1. Intracellular recordings were made from stage 2 expiratory bulbospinal neurons (E2Ns) in the caudal part of the ventral respiratory group in pentobarbitone-anesthetized cats, to characterize changes in neuronal input resistance (Rn) and synaptic inhibition occurring at the time of the expiratory-inspiratory phase transition of the respiratory cycle. 2. Rn was maximal between 30-90% of stage 2 expiration, but decreased significantly during the last 10% of stage 2 expiration. Mean normalized Rn for 60-90% of stage 2 expiration was 0.9 +/- 0.02, while mean Rn during the last 10% of stage 2 expiration was 0.68 +/- 0.09 (n = 8). This decrease in Rn began 200-300 ms before rapid hyperpolarization of E2N membrane potential and onset of phrenic nerve activity. 3. Under conditions of strong central respiratory drive, constant injection of positive current into E2Ns sometimes revealed a transient membrane hyperpolarization that straddled the expiratory-inspiratory phase transition. During this transient event, Rn was markedly reduced. 4. Intracellular injection of Cl- or NO3- ions into E2Ns produced reversal of chloride-dependent inhibitory synaptic potentials (IPSPs). Comparison of averages of membrane potential pattern over the whole respiratory cycle during control conditions and IPSP reversal revealed several periods of synaptic inhibition: 1) weak but progressively increasing synaptic inhibition during the second half of stage 2 expiration, 2) strong transient synaptic inhibition beginning 200-300 ms before the onset of phrenic nerve activity and ending shortly after the onset of phrenic nerve activity, and 3) strong but progressively decreasing synaptic inhibition throughout inspiration.(ABSTRACT TRUNCATED AT 250 WORDS)

Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating neurons

“…7). It was suggested that they play a role in the transition between expiration and inspiration (6,28,51). Lengthening of the interval between the biphasic discharges of type 2 neurons is consistent with lengthening of inspiration and expiration by opioids.…”

Rhythmic bursting of pre‐ and post‐inspiratory neurones during central apnoea in mature mice

“…Originally described by Cohen (1969), pre-inspiratory (PreI) neurones have recently been reported to play critical roles in both the initiation of inspiration (Smith, Ellenberger, Ballanyi, Richter & Feldman, 1991;Smith, Funk, Johnson & Feldman, 1995) and termination of expiration (Klages, Bellingham & Richter, 1993;Schwarzacher, Smith & Richter, 1995). Thus, the present study tests the hypothesis that PreI neurones inhibit PI neurones during PCF-induced PI apnoea thereby promoting the recommencement of inspiration.…”

“…PreI neurones may terminate expiration since the onset of the inspiratory-related inhibition of E neurones coincides with the pre-inspiratory period (Klages et al 1993;Paton, 1996b). On this basis, it was proposed that PreI neurones participate in an expiratory off-switch mechanism (Cohen, 1969;Klages et al 1993).…”

“…On this basis, it was proposed that PreI neurones participate in an expiratory off-switch mechanism (Cohen, 1969;Klages et al 1993). In addition, PreI neurones may also provide an excitatory drive for inspiration (Cohen, 1969;Johnson et al 1994;Schwarzacher et al 1995;Smith et al 1995).…”

Blockade of synaptic inhibition within the pre‐Bötzinger complex in the cat suppresses respiratory rhythm generation in vivo

“…In a specific type of respiratory neuron this is reflected by an alternation of excitatory synaptic drive mediated by glutamate and synaptic inhibition mediated by GABA and glycine (Schmid, Foutz & Denavit-Saubie, 1996). Synaptic inhibition results in reversible and irreversible switching off of phasic activities and shaping of neuronal discharge patterns (Richter, Camerer, Meesmann & R ohrig, 1979;Richter, 1982;Ballantyne & Richter, 1986; Remmers, Richter, Ballantyne, Bainton & Klein, 1986; Anders, Ballantyne, Bischoff, Lalley & Richter, 1991;Haji, Takeda & Remmers, 1992;Klages, Bellingham & Richter, 1993;Schmid et al 1996). Blockade of GABAergic and glycinergic mechanisms by systemic or local administration of receptor antagonists greatly disturbs rhythmic respiratory functions when studied under in vivo conditions (Hayashi & Lipsky, 1992) or under in vitro conditions in slice preparations that contain more rostral medullary and pontine structures (Paton, Ramirez & Richter, 1994;Paton & Richter, 1995).…”