Neuron inspiratory

Inspiratory neurons of the VRG augment inspiratory activity. These neurons descend to the spinal cord where they stimulate neurons that supply the accessory muscles of inspiration including those that innervate the scalenus and sternocleidomastoid muscles. Contractions of these muscles cause a more forceful inspiration. 

Interval between the successive groups of action potentials of the inspiratory neurons, which determines the rate or frequency of breathing (as the interval shortens, the breathing rate increases)... 

Pulmonary stretch receptors are responsible for initiating the Hering-Breuer reflex. These stretch receptors are located within the smooth muscle of large and small airways. They are stimulated when the tidal volume exceeds 1 1. Nerve impulses are transmitted by the vagus nerve to the medullary respiratory center and inhibit the inspiratory neurons. The primary function of these receptors and the Hering-Breuer reflex is to prevent overinflation of the lungs. 

ATP is released extracellularly in the ventrolateral medulla during hypercapnia because of activation of central chemoreceptors. The action of hypercapnia is on P2 receptors localized in close proximity to the VLM inspiratory neurons. But the cellular sources of ATP released are yet to be investigated (Spyer and Thomas, 2000 Spyer et al., 2004, Gourine, 2005). 

Shao, X. M., and Feldman, J. L. (2000), Acetylcholine modulates respiratory pattern Effects mediated by M3-like receptors in prcBoizinger complex inspiratory neurons. Neurophysiol 83, 1243-1252. 

Respiratory rhythmicity is an emergent property of the RCPG resulting from mutual inhibition of inspiratory and expiratory related neurons. A minimal model due to Duffin [1991] postulated the early-burst inspiratory (I) neurons and Botzinger complex expiratory (E) neurons to be the mutually inhibiting pair. Adaptation of the I neurons (e.g., by calcium-activated potassium conductance) results in sustained relaxation oscillation in the network under constant chemical excitation. Both neuron groups are assumed to have monosynaptic inhibitory projections to bulbospinal inspiratory (Ir) output neurons (Figure 11.3). The model equations are ... 

FIGURE 11.3 A minimal neural network model of RCPG. I and E denote respectively the early-burst inspiratory neurons and Botzinger complex expiratory neurons P is a fictive adaptation neuron S is an excitation neuron or pacemaker cell. Not shown is the bulbospinal output neuron (1 ). Numbers denote connection strengths. (From Masakazu and coworkers [1998]. With permission.)... 

The two-phase Dufifin model may be extended to a three-phase pattern by incorporating other respiratory-related neurons. Richter and coworkers [Richter et al., 1986 Ogilvie et al., 1992] have proposed a three-phase RCPG model with mutual inhibition between / neurons and postinspiratory, late-inspiratory, and E neurons, all with adaptations. Botros and Bruce [1990] have described several variants of the Richter model with varying connectivity patterns, with and without adaptation. 

Lipski, J. and Voss, M.D. 1990. Gating of peripheral chemoreceptor input to medullary inspiratory neurons role of Botzinger complex neurons. In H. Acker, A. Trzebski, R.G. O Regan et al. (Eds.), Chemoreceptors and Chemoreceptor Reflexes, pp. 323-329, New York, Plenum Press. 

Oku, Y, Tanaka, I., and Ezure, K. 1992. Possible inspiratory off-switch neurones in the ventrolateral medulla of the cat. NeuroReport3 933. 

The primary center, located in the medulla, is made up of a complex of interconnected neurons that are part of the reticular system. Although the neurons are not condensed to form typical nuclei, it is possible to distinguish, on the basis of stimulation by microelectrodes, neurons that generate impulses responsible for inspiration from neurons generating impulses that lead to expiration. Therefore, we speak of an inspiration and an expiration center. Researchers believe that these centers are widely interconnected, and that inspiratory neurons are intermingled with expiratory neurons. 

The pneumotaxic center is in the upper pons. From it, neuron impulses are generated, periodically inhibiting the inspiratory center. Consequently, the continued excitation of the inspiratory center is converted into a rhythmic discharge inspiration followed by rest (expiration). 

From this brief discussion, it seems obvious that the rhythmicity of respiration must reside in some specific properties of the neurons of the inspiratory center. The exact mechanism of rhythmicity is not yet known, but three theories have been proposed (1) spontaneous rhythmic discharge of the inspiratory center neuron (2) continued discharge of the neurons of the respiratory center with periodic inhibition from other centers (3) low excitability of the neurons of the inspiratory center with periodic excitation by discharges generated in other neurons. 

In certain cold-blooded species, the brain stem continues to discharge impulses to the respiratory muscles after all afferent paths have been disconnected. This spontaneous activity of the respiratory neurons is controlled by the combined activation of the inspiratory and expiratory centers. 

The primary control resides in the inspiratory center, and the expiratory center acts in a secondary fashion by intermittently interrupting the respiratory discharge. The excited inspiratory center is believed to send impulses to the pneumotaxic center, which stimulates neurons in the expiratory center to discharge impulses that inhibit the inspiratory center. 

The neurons of the medullary reticular formation appear to be in some way connected with neurons in the hypothalamus. Indeed, hypothalamic depression may lead to decreased bicarbonate and electrically invoked inspiratory responses [51]. 

Takeda M, Matsumoto S. Medullary post-inspiratory neuronal and diaphragm post-inspiratory activity during spontaneous augmented breaths in anesthetized rats. Brain Res 1997 758 218-222. 

Mironov SL, Richter DW. H poxic modulation of L-type Ca(2-F) chaimels in inspiratory brainstem neurones intracellular signalling pathways and metabotropic glutamate receptors. Brain Res 2000 869 166-77. 

Mironov SL, Richter DW. Intracellular signalling pathways modulate K(ATP) channels in inspiratory brainstem neurones and their hypoxic activation involvement of metabotropic receptors, G-proteins and cytoskeleton. Brain Res 2000 853 60-67. Cummins TR, Jiang C, Haddad GG. Human neocortical excitability is decreased during anoxia via sodium channel modulation. J Clin Invest 1993 91 608-615. Mironov SL, Richter DW. Cytoskeleton mediates inhibition of the fast Na+ current in respiratory brainstem neurons during hypoxia. Eur J Neurosci 1999 11 1831-1834. Mironov SL, Richter DW. Oscillations and hypoxic changes of mitochondrial variables in neurons of the brainstem respiratory centre of mice. J Physiol 2001 533 227-236. Mazza E Jr, Edelman NH, Neubauer JA. Hypoxic excitation in neurons cultured fi om the rostral ventrolateral medulla of the neonatal rat. J Appl Physiol 2000 88 2319-2329. 

---