Chapters authored
Role of the Dorso- and Ventrolateral Pons in Cardiorespiratory Hypothalamic Defense Responses
Stimulation of discrete sites throughout the hypothalamus elicits autonomic and somatic responses. This chapter will stand out the cardiorespiratory changes evoked from stimulation of specific areas within the caudal hypothalamus: the perifornical area and the dorsomedial nucleus. The stimulation of these regions, known as the hypothalamic defense area (HDA), produces a pattern of visceral and somatic changes characteristic of the defense reaction, which includes tachypnea, tachycardia and a pressor response. A close review of the literature demonstrates that the changes observed during this defensive behavioral response are partially mediated by the interactions with pontine regions. These include the parabrachial complex, located in the dorsolateral pons, and the A5 region, located in the ventrolateral pons. Specific glutamatergic stimulation of cell bodies located within the parabrachial complex and A5 region evokes cardiorespiratory responses similar to those observed during stimulation of the HDA. This functional interaction suggests a possible role of glutamate pontine receptors in the modulation of the HDA response. This chapter describes the most important evidences confirming the implication of the dorso- and ventrolateral pons in the control of cardiorespiratory autonomic responses evoked from the perifornical and dorsomedial hypothalamus and the role of glutamate in this interaction.
Part of the book: Hypothalamus in Health and Diseases
A5 and A6 Noradrenergic Cell Groups: Implications for Cardiorespiratory Control
Central pontine A5 and A6 noradrenergic cell groups are two of the main sources of noradrenaline release at the spinal cord, at the level of the superficial dorsal horn, the motoneuron pools of the ventral horn, lamina X and the thoracic and sacral intermediolateral cell columns. Noradrenergic ascending or descending pathways originating in the A5 or A6 noradrenergic cell groups are highly sensitive to stress and to other high-arousal states. These noradrenergic groups present extensive projections that play a key role in the modulation of all antinociceptive and autonomic responses elicited by painful or threatening situations. Depending on the locations of these projections, different possible roles for each noradrenergic cell groups are suggested. The A6 noradrenergic cell group might have the greatest effect on somatosensory transmission and the A5 group on sympathetic function. Consistent with this, stimulation of central noradrenergic pathways evokes an array of stresslike and antinociceptive effects, including changes in blood pressure, heart rate and respiratory rate. In addition, it also produces an increase in excitability, which leads to a high degree of arousal and a potentiation of cortical and subcortical mechanism generating the necessary cognitive, behavioral and autonomic responses to confront these physical or psychological situations.
Part of the book: Autonomic Nervous System
Central Control of the Larynx in Mammals
Speech is a complex process that requires the coordination of multiple structures of the phonatory system regulated by the central nervous system. Specifically, the larynx is the key point necessary for the vocal folds to come into contact to convert the air that comes out of our lungs into sound. Vocal emission involves the genesis of a precise and prolonged expiration that provides an adequate pressure/air flow component to generate a subglottic pressure compatible with vocalization. The starting point for voluntary vocal production is the laryngeal motor cortex (LMC), a common structure in mammals, although the specific location within the cortex differs in humans. LCM projects to the periaqueductal gray matter (PGM), which leads to pontomedullary structures to locate the generators of laryngeal-respiratory motor patterns, necessary for vocal emission. All these regions present a high expression of FOXP2 transcription factor, necessary for brain and lung development that is closely related to vocalization. These central structures have in common that not only convey cardiorespiratory responses to environmental stress but also support vocalization. At clinical level, recent studies show that central circuits responsible for vocalization present an overactivity in certain speech disorders such as spasmodic dysphonia due to laryngeal dystonia.
Part of the book: Autonomic Nervous System