Somatostatin selectively ablates post-inspiratory activity after injection into the Bötzinger complex

Area of Science:

• Neuroscience
• Respiratory Physiology

Background:

• Somatostatin (SST) neurons in the ventral respiratory column (VRC) are crucial for normal breathing patterns.
• The neuromodulatory effects of SST on VRC neurons are not well understood, with local administration known to induce apnoea.

Purpose of the Study:

• To investigate the cardiorespiratory effects of microinjecting Somatostatin (SST) into key respiratory subnuclei of the VRC.
• To characterize the impact of SST on the preBötzinger complex, Bötzinger complex, and rostral ventral respiratory group (rVRG).

Main Methods:

• Microinjections of varying SST concentrations (0.15, 0.45, 1.5 mM) into the Bötzinger complex, preBötzinger complex, and rVRG of anesthetized, paralyzed, and artificially ventilated rats.
• Recording of phrenic nerve discharge, vagal nerve activity, and sympathetic nerve activity to assess cardiorespiratory responses.

Main Results:

• SST microinjection into the Bötzinger complex altered phrenic nerve discharge from augmenting to apneustic, prolonged inspiration, and abolished post-inspiratory activity.
• Bilateral SST injection into the Bötzinger complex caused pronounced apneusis with variable inspiratory duration.
• SST in the preBötzinger complex induced bradypnoea and dose-dependent apnoea; in the rVRG, it reduced phrenic nerve amplitude and caused apnoea.

Conclusions:

• Somatostatin (SST) exerts a potent inhibitory effect on respiratory neurons throughout the VRC.
• A unique finding is that SST inhibition of the Bötzinger complex ablates post-inspiratory activity, leading to apneusis, a response not observed with other inhibitory agents.
• The precise mechanism underlying SST's effect on Bötzinger neurons requires further investigation.