Stabilization of Bursting in Respiratory Pacemaker Neurons

• DOI: 10.1523/jneurosci.23-08-03538.2003
• Publication Date: 2018-04-13T22:10:41Z
• Authors: Andrew K. Tryba; Fernando Peña; Jan-Marino Ramirez
• Keywords: Bursting

Synaptic and endogenous pacemaker properties have been hypothesized as principal cellular mechanisms for respiratory rhythm generation. This rhythmic activity is thought to originate in the pre-Bötzinger complex, an area that can generate fictive respiration when isolated brainstem slice preparations of mice. In preparations, external potassium concentration ([K+]o) typically elevated from 3 8 mm induce population activity. However, [K+](o) may not simply depolarize neurons but also change rhythm-generating by inducing or altering properties. To test this, we examined membrane potential (V(m)) nonpacemaker bursting before after blockade excitatory inhibitory synaptic input [K+]o artificial CSF (aCSF). Most (82%) ceased burst aCSF glutamatergic transmission. all these, was restored on additional glycinergic GABAergic inhibition. Thus, are suppressed inhibition, level which determine whether network rhythmicity generated (n = 12) 40) aCSF. aCSF, synaptically 22) continued over a wide range imposed V(m). Furthermore, V(m) significantly affected (p 0.1; n 10) changed mm, whereas nonpacemakers hyperpolarized < 0.001; 14). We conclude possess stabilize their against changes