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Parasitic castration is an adaptive strategy where parasites usurp the hosts’ reproductive physiology to complete their life cycle. The alterations in the host traits vary in their magnitude, from subtle changes in the host morpho-physiology and behaviour to the production of complex aberrant phenotypes, which often depend on the host gender. The strepsipteran macroparasite Xenos vesparum induces dramatic behavioural and physiological changes in its female host, the paper wasp Polistes dominula , while its effect on the male phenotype is largely unknown. In this study we investigated how a single X. vesparum parasite influences the functional morphology of P. dominula male reproductive apparatus. We performed morphometry and ultrastructure characterization of corpora allata , testes, seminal vesicles and accessory glands in parasitized and unparasitized males, and also in young and old males to control for the effect of age on the natural deterioration of these organs. Our results show that age significantly affects the development of male reproductive apparatus. A low parasite load – one parasite per host is the common prevalence in the field – has only a marginal impact on the reproductive morphology of P. dominula males, affecting quantitatively but not qualitatively the protein content of male accessory glands. Thus, in male P. dominula wasps, X. vesparum appears to behave as a true “parasite”, in clear opposition to the role of “parasitoid” that it takes in female hosts where castration causes the reproductive death. [ABSTRACT FROM AUTHOR]

In previous studies onPolistes dominulapaper wasps, male size affects both mating success and territorial strategy. Larger males occupy exclusive territories at leks, i.e. landmarks where they achieve most copulations (Residents), while smaller males search for females in sub-optimal locations across territories as Transients. We here observed spatial and mating behaviour of a selected size-bimodal population of males, caught at leks and released in semi-natural conditions. Residents, mainly Large males, were more successful in sexual interactions with virgin females than Transients. Residents also engaged in ‘mate guarding’, reported here for the first time. On the other hand, some Small males achieved copulations inside their own territories, at foraging sites or by grasping females and falling on the ground. Both tactics of mate access – patrolling a territory for perched females or intercepting females – were successful, the former more than the latter, whereas size itself was irrelevant to sexual performance and mating success, regardless of our size-bimodal sample. Moreover, we carried out morphological analysis of male reproductive apparatus. Males with larger accessory glands, directly involved in reproductive success in many insects, mated more than males with smaller accessory glands, regardless of male body size. [ABSTRACT FROM AUTHOR]

Presents the results of a study which focused on the stripes display of captive hover-wasp males in both intra- andve populations of the same damselfy species, Ischnura elegans, with a range of androchrome frequencies. Ability of males to discriminate between androchrome and gynochrome female morphs; Proportion of gynochrome females to androchrome females.

Abstract: The effects of cholecystokinin (CCK) agonists and antagonists on spontaneous and electrically evoked endogenous GABA release from rat cerebral cortex slices were evaluated. Neither the nonselective and CCK[sub B]-selective receptor agonists CCK-8S (3-1,000 nM) and CCK-4 (3-1,000 nM), respectively, nor the selective CCK[sub B] and CCK[sub A] receptor antagonists GV 150013 (3-30 nM) and L-364,718 (10-100 nM), respectively, significantly affected spontaneous GABA release. CCK-8S (1-1,000 nM) and CCK-4 (1-1,000 nM) increased the electrically (5 and 10 Hz)-evoked GABA release. On the contrary, GV 150013 (10 and 30 nM) significantly decreased the electrically evoked GABA release only when the slices were stimulated at the higher 10 Hz frequency. The CCK-8S- and CCK-4-induced increases in electrically evoked GABA release were counteracted by GV 150013, but not by L-364,718. Furthermore, GV 150013 at 3 nM shifted to the right the CCK-4 concentration-response curve, whereas at the higher 10 nM concentration it dramatically flattened the curve. Finally, in cortical slices obtained from rats chronically treated with GV 150013, the concentration-response curve of CCK-4 was shifted to the left and the peak effect of the peptide was significantly higher than that observed in naive animals. These results suggest that CCK increases electrically evoked, but not spontaneous, endogenous GABA release from rat cortical slices, possibly by activating local CCK[sub B] receptors. In addition, chronic treatment with the novel CCK[sub B] receptor antagonist GV... [ABSTRACT FROM AUTHOR]

Investigates the sexually selected vigilance behavior of the grey partridge `Perdix perdix.' Factors which influence the choice of mate selected; Findings of studies conducted; Methodology used in studies.

The first-instar larvae of strepsipteran parasites, commonly referred to as “triungulins”, are the host-seeking stage: they must locate, invade and successfully develop in the new host, in order to start their parasitic cycle. Little information is available about the behaviour of Xenos vesparum triungulins. They emerge in batches from the endoparasitic female infecting Polistes dominulus, the primary host, and reach the nest through a vector (a foraging wasp or the parasitised wasp itself). Once there, they have the possibility to penetrate into wasp immatures at different developmental stages. In this study, we performed preliminary analyses aimed to investigate which cues are important to direct triungulin movements during their brief stay in wasp nests. In laboratory conditions we selectively presented different stimuli to Xenos larvae: apparently, the host larva itself is attractive in an open arena, but not inside a confined space, nor are epicuticular compounds of wasp larvae able to control triungulin movements. These are more likely oriented by their gregarious behaviour, whereas light (positive phototaxy) may at a previous stage enhance their emergence via the brood canal opening in the female cephalothorax. [ABSTRACT FROM AUTHOR]

Using flow cytometry, the genome sizes of two species of Strepsiptera were studied: that of maleCaenocholax fenyesi texensisKathirithamby&Johnston (Myrmecolacidae) at 108 Mb, which is the smallest insect genome documented to date; and those of male and femaleXenos vesparumRossi (Stylopidae), which are 1C = 130 and 133 Mb, respectively. The genome sizes of the following were analysed for comparative purposes: (a) the Hessian fly,Mayetiola destructor(Say), which was previously reported to be the smallest among insects: the male measured at 1C = 121 Mb and the female at 1C = 158 Mb; and (b) the female parasitic, haplodiploid, microhymenopteran wasp,Trichogramma brassicaeBezdenko, which measured at 1C = 246 Mb. The hosts of the strepsipterans were also measured: maleSolenopsis invictaBuren, the red imported fire ant (host of maleC. f. texensis), which is 1C = 753.3 Mb, and femalePolistes dominulusChrist, the paper wasp (host ofX. vesparum), is 1C = 301.4 Mb. Endoreduplication (4C) of the genome of the thorax of the male strepsipteran, and higher levels of endoduplication (4, 8, 16C) in the body of the larger female was observed. In contrast, little or no endoreduplication was observed, either in the Hessian fly, or in the parasitic wasp. [ABSTRACT FROM AUTHOR]

Intracerebral microdialysis was employed in awake freely moving rats to investigate the effects of nociceptin/orphanin FQ receptor ligands on glutamate extracellular levels in the substantia nigra pars reticulata. Nociceptin/orphanin FQ, ineffective at 0.1 μM, induced a prolonged stimulation of nigral glutamate levels at 1 and 10 μM (mean effect of 137±9 and 167±13%, respectively, of basal values). These effects were prevented by the novel nociceptin/orphanin FQ receptor antagonist [Nphe1]nociceptin/orphanin FQ(1-13)NH2 (100 and 300 μM, respectively) but not by the non-selective opioid receptor antagonist naloxone (10 μM). [Nphe1]nociceptin/orphanin FQ(1-13)NH2 (100 μM) inhibited by itself glutamate outflow (maximal reduction to 71±4%) while naloxone was ineffective. The nociceptin/orphanin FQ receptor ligand [Phe1ψ(CH2-NH)Gly2]nociceptin/orphanin FQ(1-13)NH2 also facilitated glutamate outflow at 10 μM (mean effect of 145±10%). Intranigral perfusion with tetrodotoxin (1 μM) or with the dopamine D2 receptor antagonist raclopride (1 μM), failed to affect basal glutamate output and prevented the facilitatory effect of nociceptin/orphanin FQ (10 μM). However, perfusion with the GABAA receptor antagonist bicuculline (10 μM) increased local glutamate extracellular levels by itself and attenuated the effect of the peptide.Our data suggest that nociceptin/orphanin FQ increases glutamate extracellular levels in the substantia nigra pars reticulata via activation of nociceptin/orphanin FQ receptors located on non-glutamatergic, possibly dopaminergic and GABAergic, neuronal elements. [Copyright &y& Elsevier]

Discrimination among potential partners is a critical step in sexual selection to avoid wasting reproductive resources on an unsuitable mate. In the female-dominated hymenopteran societies males have often been regarded as ‘flying sperm containers’ spending all their time and energy in trying to acquire a mate. We investigated the male sexual preference for potential partners using as a model the primitively eusocial wasp Polistes dominula in which female caste is rather flexible and difficult to determine. By means of laboratory bioassays, we compared the males' behaviour towards females of different reproductive potential. Males were able to recognize female castes, strongly preferring reproductive females to workers, regardless of female age or health. The results show that in this species caste plays a key role in orienting male discrimination and preference, presumably through chemical cues, towards reproductive females both healthy and parasite-castrated. Overall, our study shows that social Hymenoptera males are not always ‘small mating machines’ eager to mate. [ABSTRACT FROM AUTHOR]

Abstract: The effects of 5-hydroxytryptamine (5-HT) on neuronal excitability, evaluated as depolarization-induced firing rate, and on amino acid release, measured as electrically-evoked [3H]GABA and [3H]d-aspartate efflux, were investigated in rat primary cortical neuronal cultures. 5-HT displayed a concentration-dependent, bimodal effect on neuronal excitability: at 3–10μM it increased excitability through 5-HT2A receptors, and was blocked by the selective 5-HT2A antagonist MDL 100907, whereas at 30–100μM it reduced excitability through 5-HT1A receptors, and was, in turn, blocked by the selective 5-HT1A antagonist WAY 100135. The electrically-evoked [3H]GABA efflux was concentration-dependently inhibited by 5-HT (pEC50 =4.74) and such inhibition was prevented by WAY 100135, but not by GR 55562, a selective 5-HT1D/B receptor antagonist. Conversely, 5-HT concentration-dependently increased stimulus-evoked [3H]d-aspartate efflux (pEC50 =4.71). The increase was facilitated by methiothepin and was reversed into inhibition by ICS 205930, a selective 5-HT3 receptor antagonist. In the presence of ICS 205930, the inhibition induced by 5-HT was prevented by the selective 5-HT1D/B receptor antagonist GR 55562, but not by WAY 100135. These findings suggest that 5-HT inhibits GABA release through 5-HT1A receptors and exerts a dual modulation on glutamate release, mostly facilitatory (through 5-HT3 receptors) but also inhibitory (through 5-HT1D/B receptors), leading to a prevalently positive modulation of the excitatory signal by amino acid neurotransmitter containing neurons. [Copyright &y& Elsevier]

Abstract: Superfused rat cerebral cortex slices were submitted to a continuous electrical (5Hz) stimulation and treated with sodium azide (1–10mM) in the presence of 2mM 2-deoxyglucose (“chemical ischemia”). Presynaptic cholinergic activity, evaluated as acetylcholine release, was inhibited depending on the sodium azide concentrations and on the length of application (5–30min). Following a 5-min treatment with 10mM sodium azide, acetylcholine release was reduced to 45±2.3%; simultaneously, there was a 15- and 10-fold increase in glutamate and nitric oxide effluxes, respectively. After restoring normal superfusion conditions, acetylcholine release recovered to 70±3.1% of the controls; the N-methyl-d-aspartate receptor antagonist MK-801 (10μM) as well as the nitric oxide scavengers, haemoglobin (20μM) and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide (150μM), improved the recovery in presynaptic activity, showing that both glutamate and nitric oxide play detrimental roles in chemical ischemia. On the other hand, the post-ischemic recovery was worsened by the guanylylcyclase inhibitor 1H-[l,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (10μM), suggesting that the activation of such a pathway plays a neuroprotective role and that the nitric oxide-induced harmful effects depend on different mechanisms. Chemical ischemia-evoked nitric oxide efflux partly derived from its calcium-dependent endogenous synthesis, since both the intracellular calcium chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (1mM), and the nitric oxide synthase inhibitor, N ω-nitro-l-arginine methyl ester (100μM), substantially prevented sodium azide effects. Nitric oxide efflux was only weakly reduced by MK-801 and was not modified by either the L-type calcium channel blocker, nifedipine (10μM) or the N-type calcium channel blocker ω-conotoxin (0.5μM), thus suggesting a prevailing intracellular calcium-dependence of nitric oxide production, although a partial extracellular calcium source cannot be ruled out. These findings show that sodium azide plus 2-deoxyglucose treatment is a useful protocol to induce brain ischemia in vitro and underline the involvement of nitric oxide in the complex events following the ischemic insult. [Copyright &y& Elsevier]

The effects of nociceptin/orphanin FQ (N/OFQ) and endomorphin-1 (EM-1) on glutamate and GABA release, intracellular calcium, neuronal excitability and glutamate current were investigated in rat primary cortical neuronal cultures. Through their specific receptors N/OFQ and EM-1 (0.02–1 μM) inhibited the electrically evoked outflow of [3H]D-aspartate at most to -50% and that of [3H]GABA to -30%. In addition, at 1 μM, both peptides induced a decrease of the firing rate caused by electrical depolarization.N/OFQ 1–10 μM did not influence either the electrically evoked calcium influx or the glutamate-evoked currents, whereas EM-1 1 μM significantly inhibited them. Thus, in cortical neurons in culture, both N/OFQ and EM-1 inhibited the secretory process and neuronal excitability but EM-1 also affected calcium influx and cell body responsiveness to glutamate. Consequently, EM-1 appeared to dampen this excitatory signal more then N/OFQ did. [Copyright &y& Elsevier]

Dual probe microdialysis was employed in conscious rats to investigate whether endogenous dopamine is involved in the stimulation of glutamate release in the substantia nigra pars reticulata following striatal NMDA receptor activation. Intrastriatal perfusion with NMDA (1 and 10 µm) facilitated nigral glutamate release (dizocilpine- and tetrodotoxin-sensitive). The D[sub 2] dopamine receptor antagonist raclopride increased spontaneous nigral glutamate release and caused a leftward shift in the NMDA sensitivity, lowering NMDA effective concentrations to submicromolar levels. Conversely, the D[sub 1] antagonist SCH23390 prevented the effect of NMDA (1 µm) and caused a rightward shift in the NMDA sensitivity. It was tested whether the antagonist effects were due to dopamine receptor blockade or increased tone on D[sub 1]/D[sub 2] receptors. SCH23390 prevented the raclopride-induced enhancement of spontaneous but not NMDA-evoked glutamate release while raclopride left unchanged the SCH23390-induced inhibition. The physiopathological relevance of the dopaminergic modulation was strengthened by perfusing NMDA in the dopamine-depleted striatum of hemiparkinsonian rats. Nigral glutamate responsiveness to NMDA was enhanced as with raclopride. We conclude that endogenous striatal dopamine regulates both spontaneous and NMDA-induced nigral glutamate release via an opposite control mediated by D[sub 1] facilitatory and D[sub 2] inhibitory receptors. Alterations of this control may subserve the motor symptoms of Parkinson's disease. [ABSTRACT FROM AUTHOR]

Abstract The effect of metabotropic glutamate receptor agonists and antagonists on KCl (20 mm)-induced endogenous acetylcholine release from rat striatal synaptosomes was investigated. The group I agonist (S)-3,5-dihydroxyphenylglycine (DHPG), 1–1000 nm, potentiated in a concentration-dependent way the KCl-induced acetylcholine release, reaching maximal efficacy at 100 nm (+93 ± 14%). The effect of DHPG (10 nm) was counteracted by coapplication of (7-hydroximino)cyclopropan-b-chromen-1a-carboxylate (CPCCOEt), 10 µm, a metabotropic glutamate receptor type one selective antagonist, and 2-methyl-6-(phenylethynyl)pyridine (MPEP), 10 µm, a metabotropic glutamate receptor type five selective antagonist, but not by application of either antagonist alone. The group II agonist (2S, 1′R, 2′R, 3′R)-2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV), 1–1000 nm, inhibited in a concentration-dependent way the KCl-induced acetylcholine release displaying maximal efficacy at 300 nm (-32 ± 2%). The effect of DCG-IV 300 nm was counteracted by the group II selective antagonist (2S)-α-ethylglutamic acid (EGLU), 300 µm. The group III agonist l-amino-4-phosphonobutyric acid (L-AP4) failed to alter the KCl-induced acetycholine release up to 300 µm. We conclude that metabotropic glutamate receptors belonging to group I and II are located on the axon terminals of striatal cholinergic interneurons, their activation resulting in facilitation and inhibition, respectively, of acetylcholine release. [ABSTRACT FROM AUTHOR]

Abstract Dual probe microdialysis was employed in freely moving 6-hydroxydopamine (6-OHDA) hemilesioned rats to investigate the effects of blockade of N-methyl-D-aspartate (NMDA) receptors in the dorsolateral striatum on glutamate (Glu) release from the ipsilateral substantia nigra pars reticulata (SNr). Perfusion for 60 min with the NMDA antagonist dizocilpine (0.1 and 1 μm) in the dopamine (DA)-denervated striatum stimulated nigral Glu release (peak effect of 139 ± 7% and 138 ± 9%, respectively). The lower (0.01 μm) and higher (10 μm) concentrations were ineffective. In sham-operated rats, dizocilpine failed to affect nigral Glu release up to 1 μm but induced a prolonged stimulation at 10 μm (153 ± 9% at the end of perfusion). The present results show that DA-deficiency in the striatum of hemiparkinsonian rats is associated with increased responsivity of nigral Glu release to striatal NMDA receptor blockade. This suggests that changes of NMDA receptor mediated control of the striatofugal pathways occur during Parkinson's disease (PD). [ABSTRACT FROM AUTHOR]