Read the full review for this F1000Prime recommended article: A high-throughput screening procedure for identifying mice with aberrant taste and oromotor function.

Many prey species (including plants) deter predators with defensive chemicals. These defensive chemicals act by rendering the prey's tissues noxious, toxic, or both. Here, I explore how predators cope with the presence of these chemicals in their diet. First, I describe the chemosensory mechanisms by which predators (including herbivores) detect defensive chemicals. Second, I review the mechanisms by which predators either avoid or tolerate defensive chemicals in prey. Third, I examine how effectively free-ranging predators can overcome the chemical defenses of prey. The available evidence indicates that predators have mixed success overcoming these defenses. This conclusion is based on reports of free-ranging predators rejecting unpalatable but harmless prey, or voluntarily ingesting toxic prey.

We examined the necessity of α-gustducin, a G protein α-subunit expressed in taste cells, to taste-mediated licking responses of mice to sapid stimuli. To this end, we measured licking responses of α-gustducin knock-out (Gus−/−) mice and heterozygotic littermate controls (Gus+/−) to a variety of ‘bitter’, ‘umami’, ‘sweet’, ‘salty’ and ‘sour’ taste stimuli. All previous studies of how Gus−/− mice ingest taste stimuli have used long-term (i.e. 48 h) preference tests, which may be confounded by post-ingestive and/or experiential effects of the taste stimuli. We minimized these confounds by using a brief-access taste test, which quantifies immediate lick responses to extremely small volumes of sapid solutions. We found that deleting α-gustducin (i) dramatically reduced the aversiveness of a diverse range of ‘bitter’ taste stimuli; (ii) moderately decreased appetitive licking to low and intermediate concentrations of an ‘umami’ taste stimulus (monosodium glutamate in the presence of 100 μM amiloride), but virtually eliminated the normal aversion to high concentrations of the same taste stimulus; (iii) slightly decreased appetitive licking to ‘sweet’ taste stimuli; and (iv) modestly reduced the aversiveness of high, but not low or intermediate, concentrations of NaCl. There was no significant effect of deleting α-gustducin on licking responses to NH₄Cl or HCl.

Herbivorous insects use a variety of physiological mechanisms to cope with noxious (i.e., unpalatable and/or toxic) compounds in their food plants. Here, I review what is known about this coping process, focusing on one species of caterpillar, the tobacco hornworm (Manduca sexta). Herbivorous insects possess both preingestive (i.e., chemosensory) and postingestive response mechanisms for detecting plant secondary compounds. Stimulation of either class of detection mechanism inhibits feeding rapidly by reducing biting rate and/or bite size. This aversive response is highly adaptive during encounters with secondary plant compounds that are toxic. The insect's dilemma is that many harmless or mildly toxic compounds also activate the aversive response. To overcome this dilemma, herbivorous insects employ at least three mechanisms for selectively deactivating their aversive response to relatively harmless secondary plant compounds: (1) the presence of carbohydrates can mask the unpalatable taste of some secondary plant compounds; (2) prolonged dietary exposure to some unpalatable secondary plant compounds can initiate long‐term adaptation mechanisms in the peripheral and central gustatory system; and (3) dietary exposure to toxic compounds can induce production of P450 detoxication enzymes. Thus, herbivorous insects utilize an integrated suite of physiological mechanisms to detect potentially toxic compounds in foods, and then selectively adapt to those that do not pose a serious threat to their growth and survivorship.