No abstract

Herbivores usually consume a mere fraction of available plant biomass. Spatial patterns in feeding damage may be attributable to induced defences by the host plant; a damaged plant reacts by lowering its nutritional value, thereby forcing herbivores to move on before food gets worse. In this study, we test this general hypothesis on a specific model system: caterpillars of the alpine butterfly Parnassius smintheus feeding on lance-leaved stonecrop Sedum lanceolatum. We first describe spatial patterns in host distribution and feeding damage within alpine meadows. We then use laboratory experiments to test a key assumption behind the proposed mechanisms: that the host plant exhibits an induced response with a negative impact on larval performance, and that this response is activated with a delay. Finally, we relate the patterns observed to the actual behaviour of Parnassius larvae. Overall, we found the level of feeding damage to be low (on damaged plants, only 5% of all leaves were fed upon). Within meadows, both host plants and feeding damage were clumped at a small spatial scale. This pattern seemed directly explicable by the timing of the host's induced defence. Laboratory experiments revealed a delay of 1Á2 d before the defence reached a level affecting larval performance, and wild larvae switch plants more quickly than this. A simulation model demonstrated that the spatial distribution of host plant damage can be generated by a simple random walk, based on the empirically observed step frequency, length and turning angles. Hence, as the most parsimonious explanation for the observed level and pattern of host plant damage, we offer a scenario where induced changes in host-plant quality limits the time spent per plant, but the herbivore moves throughout the landscape without any particular directionality.

1 Using a grease-gap technique, we have investigated the effects of purine and pyrimidine nucleotides on the d.c. potential of the rat isolated superior cervical ganglion (SCG). 2 Of the purines tested, adenosine, adenosine 5'-triphosphate (ATP), P,y-methylene-adenosine 5'-triphosphate (P,y-MeATP) at up to 300 gM produced concentration-dependent hyperpolarizations, whereas 2-methyl-thio-ATP (2-Me.S.ATP) and a,p-methylene-ATP (a,,B-MeATP) depolarized ganglia. Of the pyrimidines tested, uridine 5'-triphosphate (UTP) produced concentration-dependent depolarizations and cytosine 5'-triphosphate (CTP) at 1000 tLM produced considerably smaller but significant depolarizations. In contrast uridine 5'-monophosphate (UMP) at 1000 AM hyperpolarized ganglia. The relative order of potency of purines and pyrimidines to depolarize ganglia was:-UTP> az,-MeATP>> CTP> 2-Me.S.ATP and to hyperpolarize ganglia was:-adenosine = P,By-MeATP> ATP> UMP.3 The ability of purines and pyrimidines to alter the depolarizing response caused by muscarine and of purines to alter depolarization induced by y-aminobutyric acid (GABA) was determined. The relative order of potency of nucleotides in depressing submaximal depolarization caused by muscarine (100 nM) was: adenosine = ATP>P,y-MeATP whereas 2-Me.S.ATP, a,4-MeATP and UTP did not significantly alter depolarization caused by muscarine. At 100ZM 3,Ty-MeATP and adenosine but not ATP potentiated GABA-induced depolarizations. 4 Hyperpolarizations caused by adenosine, ATP, P,y-MeATP and UMP and depolarizations caused by aj-MeATP were enhanced in medium containing reduced concentrations of calcium (0.1 mM) and potassium (2 mM). In this medium 8-phenyltheophylline abolished hyperpolarizations caused by adenosine and reversed hyperpolarizations caused by ATP into depolarizations. Suramin (300 tLM), a P2-purinoceptor antagonist, significantly reduced the depolarizing response caused by a,t-MeATP and significantly increased hyperpolarizations caused by ATP and ,B,-MeATP. Suramin (300 AM) did not significantly alter depolarizations caused by l,l-dimethyl-4-phenylpiperazinium (10 ILM), potassium (3 mM) or muscarine (100 nM) and significantly potentiated depolarizations caused by UTP (100IM).5 It is concluded that the rat SCG contains PI-purinoceptors that hyperpolarize the ganglion and diminish sensitivity to muscarine, and P2X-purinoceptors that depolarize the SCG. There is also some evidence to suggest the presence of receptors for UTP, i.e., pyrimidinoceptors, which depolarize SCG neurones.

No abstract

1 The effects of pyrimidines and purines on the d.c. potential of the rat isolated superior cervical ganglion (SCG) have been examined by a grease-gap technique to determine the structure-activity requirements of the receptor activated by pyrimidines, i.e. a pyrimidinoceptor. 2 5-Aminoimidazole4-carboxamide-l-f-D-ribofuranosyl (ZTP), the pyrimidines, cytidine 5'-triphosphate (CTP), uridine 5'-triphosphate (UTP) and thymidine 5'-triphosphate (TTP) and the purines, adenosine 5'-triphosphate (ATP; in the presence of an Al-purinoceptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) (1 Mm)), adenosine 5'-0-(3-thiotriphosphate) (ATPyS), guanosine 5'-triphosphate (GTP), inosine 5'-triphosphate (ITP) depolarized ganglia in a concentration-dependent manner.The relative order of ZTP and purine 5'-triphosphates in depolarizing ganglia was ZTP>ATPyS > >ATP? ITP=GTP, and for the pyrimidine 5'-triphosphates UTP>TTP>CTP. Depolarizations evoked by ATPyS were followed by concentration-dependent hyperpolarizations at 100 and 1000 MM. 3 At concentrations of between 0.1 Mm and 1 mm, uridine 5'-diphosphate (UDP), uridine 5'-diphosphoglucose (UDPG) and uridine 5'-diphosphoglucuronic acid (UDPGA) evoked significant and concentration-dependent depolarizations, whereas uridine 5'-monophosphate (UMP), uridine and uracil were inactive or produced small (<45 pY) depolarizations. The relative order of potency of uridine analogues in depolarizing ganglia was UDP> UTP > UDPG > UDPGA > > uracil > UMP = pseudouridine uridine. At 3 and 10 mM, uridine produced concentration-dependent hyperpolarizations. Nikkomycin Z, a nucleoside resembling UTP (viz. the triphosphate chain at the 5'-position on the ribose moiety being replaced by a peptide), was inactive between 1 uM and 1 mM. Generally, a concentration of 10 mm was required before thymidine, 6-azathymine, 6-azauracil or 6-azauridine depolarized ganglia. 4 Suramin (300 Mm), a P2-purinoceptor antagonist, significantly depressed depolarizations evoked by a,fi-methylene-ATP (a,fi-MeATP; 100 Mm), ATPyS (100 Mm), CTP (1 mM), GTP (1 mM), ZTP (30 MM) and ATP (300 MM) in the presence of DPCPX (1 yM). Suramin reversed a small depolarization evoked by UMP (1 mM) into a small hyperpolarization. In contrast depolarizations evoked by UDP, UTP, UDPG (all at 100 Mm) and TTP (300 Mm) were unaltered or enhanced by suramin. 5 It is concluded that the rat SCG contains distinct nucleotide receptors including a P2-purinoceptor (activated by a,f,-MeATP, ATP, GTP, ITP and ZTP) and a pyrimidinoceptor (activated by UTP, UDP, UDPG, UDPGA and TTP). The pyrmidinoceptor on rat SCG neurones had specific structure activity requirements with the di-and triphosphates of uridine being the most effective depolarizing agonists examined.