Thermal tolerance of the invasive red-bellied pacu and the risk of establishment in the United States.

Indigenous red-bellied pacu, Piaractus brachypomus, populations are in decline due to overfishing. Once ignored by aquaculturists because of their perceived low economic value, renewed aquaculture efforts in Central and South America aim to relieve fishing pressures on natural pacu populations. In the southern United States pacu aquaculture for the aquarium trade has raised concerns that accidental release could lead to establishment of overwintering populations outside captivity-a threat accentuated by the average 6 °C increase in shallow-water temperatures predicted by the end of the century. In the present study, Critical and Chronic Thermal Methodology was used to quantify red-bellied pacu thermal tolerance niche requirements. The data suggest that red-belllied pacu are a thermophilic species capable of tolerating low and high chronic temperatures of 16.5 °C and 35 °C, respectively. Critical thermal minimum and maximum temperatures of fish acclimated near their chronic limits are 10.3 and 44.4 °C. Red-bellied pacu aquaculture in the United States is concentrated in subtropical Florida regions that encourage rapid growth and reproduction, but carry an increased risk of establishing reproducing populations in local freshwater systems. The thermal niche data show that the risk of bioinvasion can be reduced or eliminated by adopting an approach whereby aquaculture potential is integrated with environmental temperature constraints.

Evidence for functional, inhibitory, histamine H3 receptors in rat carotid body Type I cells.

The Type I cells are the sensory elements of the carotid bodies and play a critical role in defining the ventilatory response to hypoxia and hypercapnia. Type I cells release multiple neurotransmitters during a chemosensory stimulus resulting in increased firing of the carotid sinus nerve and modification of the breathing pattern. While much is known about the actions of individual neurotransmitters in this system, very little is known about how multiple neurotransmitters may integrate to shape the output of the carotid body. Recent data has indicated that the neurotransmitter histamine does not excite isolated Type I cells despite being released during hypoxia and its receptors being present on the Type I cells. Here the hypothesis that histamine might modulate an excitatory neurotransmitter such as acetylcholine was tested. Using calcium imaging techniques it was found that histamine attenuated calcium signaling events initiated by the muscarinic acetylcholine receptor agonist acetyl-beta-methylcholine via an H3 receptor mediated mechanism. In summary, these results suggest that when acetylcholine and histamine are co-released from Type I cells in response to chemostimuli, histamine may attenuate or modulate the excitatory presynaptic actions of acetylcholine.

Presynaptic regulation of isolated neonatal rat carotid body type I cells by histamine.

The type I cells are the chemoreceptive elements of the carotid bodies and are critical in defining the ventilatory response to hypoxia and hypercapnia. Recent evidence has suggested that histamine is released by the carotid body in response to hypoxia and acts as an excitatory neurotransmitter. Here we use isolated neonatal rat type I cells to assess the presynaptic actions of histamine and define the receptor subtypes that mediate them. All four histamine receptor subtypes are expressed on the type I cells, however activation of these receptors with histamine or selective agonists caused no rise in intracellular calcium ([Ca(2+)](i)) and histamine did not augment calcium entry or modulate macroscopic currents evoked in type I cells. Thus activation of histamine receptors on type I cells is unlikely to provide a presynaptic positive feedback mechanism during chemotransduction and any excitatory role attributed to the actions of histamine is likely to come from a postsynaptic effect on the carotid sinus nerve (CSN).

Ion channel regulation by AMPK: the route of hypoxia-response coupling in thecarotid body and pulmonary artery.

Vital homeostatic mechanisms monitor O2 supply and adjust respiratory and circulatory function to meet demand. The pulmonary arteries and carotid bodies are key systems in this respect. Hypoxic pulmonary vasoconstriction (HPV) aids ventilation-perfusion matching in the lung by diverting blood flow from areas with an O2 deficit to those rich in O2, while a fall in arterial pO2 increases sensory afferent discharge from the carotid body to elicit corrective changes in breathing patterns. We discuss here the new concept that hypoxia, by inhibiting oxidative phosphorylation, activates AMP-activated protein kinase (AMPK) leading to consequent phosphorylation of target proteins, such as ion channels, which initiate pulmonary artery constriction and carotid body activation. Consistent with this view, AMPK knockout mice exhibit an impaired ventilatory response to hypoxia. Thus, AMPK may be sufficient and necessary for hypoxia-response coupling and may regulate O2 and thereby energy (ATP) supply at the whole body as well as the cellular level.