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The pre-Bötzinger complex (preBötC) is a cluster of interneurons in the ventrolateral medulla of the brainstem. This complex has been proven to be essential for the generation of respiratory rhythm in mammals. The exact mechanism of the rhythm generation and transmission to motor nuclei remains controversial and the topic of much present research. Several synthetic compounds have been shown to act on neurons specific to the preBötC, most being selective agonists or antagonists to receptor subtypes on neurons in the vicinity. Since many of these neurons express GABA, glutamate, serotonin and adenosine receptors, chemicals custom tailored to bind at these sites are most effective at altering respiratory rhythm. Adenosine modulates the preBötC output via activation of the A1 and A2A receptor subtypes. An adenosine A1 receptor agonist has been shown to depress preBötC rhythmogenesis independent of the neurotransmitters GABA and glycine in "in vitro" preparations from 0-7 day old mice. Another synthetic drug specific to the adenosine A2A receptor subtype is CGS-21680 that has been shown to cause apneas in 14-21 day old rat pups ''in vivo''. For this reason, it has been used as a model to study pathological conditions such as apnea of prematurity and SIDS in neonatal infants. ==Description== The pre-Bötzinger complex (pre-BötC), a projection of the Botzinger complex, plays an important role in regulating respiration in mammals.〔 It is one of the four cell groups of the Ventral Respiratory Group (VRG). It is hypothesized that the pre-Bötzinger complex is the main location of the rhythmic pattern generation circuitry involved in breathing. It also contains pacemaker cells and nonpacemaker cells that initiate spontaneous breathing. Research is being conducted on the mechanisms involved, but it is currently unclear as to how this interneuron system is regulated. Rhythmogenesis, the generation of rhythm, is modulated by membrane properties and synaptic interactions occurring in interneurons, intrinsically-bursting pacemaker neurons, and follower neurons within the pre-Bötzinger complex. Together these neurons make up an intrinsic network that is capable of being regulated by a vast range of neurotransmitters, amino acids, and chemical signals, such as adenosine, GABA, and glycine.〔 The pre-Bötzinger complex produces two types of breathing rhythms under normal levels of oxygen. In eupnea, or normal breathing, the pre-BötC generates a rhythm that is fast and low in amplitude.〔 Sighs, on the other hand, consist of a slow and large amplitude rhythm. Each type of rhythm is generated by the same neurons in the pre-Bötzinger complex, but through different mechanisms, receptors, and ion currents that are controlled by changes in the behavior or environment of the organism. Under low levels of oxygen, the pre-Bötzinger complex needs to rearrange the activity of its neurons and requires the assistance of other brain structures, like the pons, to generate gasping. Gasping is characterized by a rhythm that has faster rise, shorter bursts, and lower frequency. The pre-BötC is capable of generating stable respiratory rhythms with varying degrees of oxygenation and throughout varying conditions of its environment using network reconfiguration and neuromodulation.〔 The structure contains a core network within a larger network of interconnected nuclei that function to maintain respiratory rhythms and the neuroplasticity and state-dependency of breathing. Two key features of the pre-BötC are its stability and its ability to adapt to changing environmental and behavioral conditions. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Pre-Bötzinger complex」の詳細全文を読む スポンサード リンク
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