Acetylcholine and central chemosensitivity: in vitro study in the newborn rat

https://doi.org/10.1016/0034-5687(90)90049-5Get rights and content

Abstract

In vitro experiments were performed in the superfused brainstem-spinal cord preparation of newborn rats in order to analyse the central respiratory effects of acetylcholine. The central motor output was assessed from recording electrical activity in nerves supplying respiratory muscles.

Acetylcholine added to the bathing medium induced dose-dependent increases in respiratory frequency which were blocked by muscarinic (but not nicotinic) antagonists and enhanced by physostigmine. These effects originated from the medullary ventral surface where chemosensitive structures have been previously located. The respiratory central chemosensitivity of the isolated brainstem was analysed using a CO2 free, pH 7.9 medium instead of the normal medium (bubbled with 5% CO2, pH 7.3). Decreases at the H+ and CO2 stimuli led to decreased inspiratory activity, resulting mainly from a decrease in the amplitude of the motor output. These responses were enhanced by atropine and diminished by physostigmine. These results obtained in vitro on the newborn rat suggest that cholinergic synapses are not directly involved in the genesis of respiratory rhythmicity but confirm previous results obtained in vitro in adult animal revealing that acetylcholine is implicated in the central respiratory chemosensitivity.

References (25)

  • N.B. Dev et al.

    A cholinergic mechanism involved in the respiratory chemosensitivity of the medulla oblongata in the cat

    Pflügers Arch.

    (1979)
  • A.S. Foutz et al.

    Persistence of central respiratory rhythmogenesis after maximal acetylcholinesterase inhibition in unanaesthetized cats

    Can. J. Physiol. Pharm.

    (1989)
  • Cited by (73)

    • Effects of acetylcholine on hypoglossal and C4 nerve activity in brainstem-spinal cord preparations from newborn rat

      2021, Respiratory Physiology and Neurobiology
      Citation Excerpt :

      As cholinergic neurons are mainly located outside the level of the slices (Picciotto et al., 2012; Ruggiero et al., 1990; Woolf, 1991), the remaining axons or terminals can still release ACh in the preBötC and XII nucleus. Consistent results were also obtained in experiments with brainstem-spinal cord preparation from newborn rats (Monteau et al., 1990; Wollman et al., 2016). Thus, activity of the choline acetyltransferase in newborn rat brain seems to be enough to show physiological function in the medulla.

    • Chemoreceptors, Breathing and pH

      2013, Seldin and Geibisch's The Kidney
    • Chemoreceptors, Breathing and pH

      2012, Seldin and Giebisch's The Kidney: Physiology and Pathophysiology
    • M3-receptor activation counteracts opioid-mediated apneusis, but the apneusis per se is not necessarily related to an impaired M3 mechanism in rats

      2011, Life Sciences
      Citation Excerpt :

      Further, it has been demonstrated that respiratory neurons receive muscarinic excitatory synaptic drives during hypercapnia (Takeda and Haji, 1991). The muscarinic receptor-mediated excitatory responses may agree with the result that ACh is involved in the respiratory neuronal excitation induced by CO2 (Monteau et al., 1990). It is generally accepted that opioids depress the chemosensitive neuronal pathways associated with the central response to hypercapnia (Pokorski et al., 1981).

    • Anandamide centrally depresses the respiratory rhythm generator of neonatal mice

      2010, Neuroscience
      Citation Excerpt :

      The central mechanisms through which AEA activation of CB1R affects the RRG are probably complex. AEA requires more than 5 min to significantly depress the RRG whereas NA, serotonin or acetylcholine affects the RRG within 1–2 min (Cayetanot et al., 2001; Monteau et al., 1990; Zanella et al., 2006). The latency of the effects of AEA suggests a special mode of action of the CB1R.

    View all citing articles on Scopus
    View full text