Electrical and pharmacological properties of petrosal ganglion neurons that innervate the carotid body

Laboratorio de Neurobiología, Facultad de Ciencias Biológicas, P Universidad Católica de Chile, Casilla 114-D, Santiago 1, Chile.
Respiratory Physiology & Neurobiology (Impact Factor: 1.97). 08/2007; 157(1):130-9. DOI: 10.1016/j.resp.2006.12.006
Source: PubMed


The petrosal ganglion (PG) contains the somata of primary afferent neurons that innervate the chemoreceptor (glomus) cells in the carotid body (CB). The most accepted model of CB chemoreception states that natural stimuli trigger the release of one or more transmitters from glomus cells, which in turn acting on specific post-synaptic receptors increases the rate of discharge in the nerve endings of PG neurons. However, PG neurons that project to the CB represent only small fraction (roughly 20%) of the whole PG and their identification is not simple since their electrophysiological and pharmacological properties are not strikingly different as compared with other PG neurons, which project to the carotid sinus or the tongue. In addition, differences reported on the actions of putative transmitters on PG neurons may reflect true species differences. Nevertheless, some experimental strategies have contributed to identify and characterize the properties of PG neurons that innervate the CB. In this review, we examined the electrophysiological properties and pharmacological responses of PG neurons to putative CB excitatory transmitters, focusing on the methods of study and species differences. The evidences suggest that ACh and ATP play a major role in the fast excitatory transmission between glomus cells and chemosensory nerve endings in the cat, rat and rabbit. However, the role of other putative transmitters such as dopamine, 5-HT and GABA is less clear and depends on the specie studied.

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    • "The current model of chemoreception states that hypoxia induces the inhibition of K + channels, leading to glomus cell depolarization, entry of Ca 2+ through L-type Ca 2+ channels and the release of excitatory transmitters, which increase the discharge frequency of the nerve endings of chemosensory neurons. Glomus cells contain several molecules, such as ACh and ATP, that are candidates to act as excitatory transmitters between glomus cells and the nerve terminals (Iturriaga et al. 2007). "

    Experimental physiology 08/2014; 99(8). DOI:10.1113/expphysiol.2014.081042 · 2.67 Impact Factor
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    • "The CB initiates the hyperventilatory adjustments induced by hypoxia, but also increases the discharge of the sympathetic efferents to the heart, the splanchnic and renal vascular beds [38] [39]. The most accepted model of CB chemoreception states that hypoxia releases one -or more-excitatory transmitter(s) from the chemoreceptor cells, which in turn increases the discharge of petrosal neurons that projects to the NTS [40]. In addition to the cardiorespiratory responses, the stimulation of the CB chemoreceptor in conscious mammals activates the defense arousal areas, evoking defensive or even an escape reaction [3] [4]. "
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    ABSTRACT: The present work was aimed to evaluate the contribution of interception to the autonomic and behavioral responses to hypoxia. To address this issue, we studied whether the inactivation of the primary interoceptive posterior insular cortex (pIC) may disrupt the autonomic and behavioral effects of hypoxia in conscious rats. Rats were implanted with telemetric transmitters and microinjection cannulae placed bilaterally in the pIC. After one week, rats were injected with bupivacaine (26.5μM 1μL/side) and saline (1μL/side) into the pIC, and exposed to hypoxia (∼6% O2) for 150 s, and autonomic and behavioral responses were recorded. Hypoxia produces hypertension, tachycardia followed by bradycardia, and hypothermia. When O2 dropped to ∼8%, rats showed escape behavior. Baseline cardiovascular variables and the pattern of hypoxia-induced autonomic and behavioral responses were not disrupted by pIC inactivation. However, pIC inactivation produced a modest but significant temperature decrease, higher bradycardic and hypertensive responses to hypoxia, and a minimal delay in escape onset. In addition, we measured the hypoxia-induced Fos activation in the nucleus tractus solitarius (NTS), the periaqueductal gray matter (PAG) and the pIC, which are key components of the interoceptive pathway. Hypoxia increased the number of Fos-positive neurons in the NTS and PAG, but not in the pIC. Present results suggest that pIC is not involved in the hypoxia-induced behavioral response, which seems to be processed in the NTS and PAG, but has a role in the efferent control of autonomic changes coping with hypoxia.
    Behavioural brain research 07/2013; 253. DOI:10.1016/j.bbr.2013.07.015 · 3.03 Impact Factor
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    • "Among these molecules present in glomus cells, acetylcholine and adenosine triphosphate fulfill most of the criteria to be considered as the excitatory transmitters between the glomus cells and petrosal nerve ending (Iturriaga et al., 2007). However, other molecules such as dopamine, histamine, nitric oxide and endothelin-1 acts as modulators of the chemosensory process, acting on the glomus cells or controlling the vasomotor tone of the blood vessel (Iturriaga et al., 2007). More recently, it has been proposed that proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and interleukin 1β (IL-1β) are excitatory modulators of the chemoreception process in the rat carotid body (Lam et al., 2008, Liu et al., 2009, Shu et al., 2007). "

    Oxidative Stress and Diseases, 04/2012; , ISBN: 978-953-51-0552-7
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