Ecofriendly Approach for the Control of a Common Insect Pest in the Food Industry, Combining Polymeric Nanoparticles and Post-application Temperatures.

One of the most common insect pests is Plodia interpunctella (Hübner) (Lepidoptera: Pyralidae), which affects different food commodities. A new effective approach for the management of insect pests is the development of new formulations based on essential oils (EO). However, few works informed about the relationship between insecticidal activity of EO or essential oils loaded polymeric nanoparticles (EOPN) and post-application temperature. In our work, palmarosa [Cymbopogon martinii (Roxb.) Watson], geranium (Geranium maculatum L.), and peppermint (Mentha piperita L.) oils were formulated in a polyethylene glycol 6000 matrix to obtain EOPN. Geranium and palmarosa EOPN had sizes of 259 and 191 nm, respectively; the encapsulation efficiency (EE) was close to 90%, and the samples were monodisperse. The sizes from peppermint EOPN were around 380 nm, with an EE of 72%, and were polidisperse. In a contact toxicity bioassay, the insecticidal effect of the oils was increased by all EOPN, with palmarosa oil being the most toxic. In addition, the oils and their nanoparticles showed a significantly negative temperature coefficient when applied by contact. In a fumigant bioassay, just palmarosa and peppermint EOPN enhanced the oil activity and palmarosa EO and EOPN showed the highest toxic effect. In this case, the EO and EOPN insecticidal activity was unaffected by environmental temperature variation.

Scavenging Activity of Dermestes maculatus (Coleoptera: Dermestidae) on Burned Cadaveric Tissue.

The aim of this work was to study the effect that fire exposure in tissues may have on Dermestes maculatus DeGeer (Dermestidae: Dermestini) taphonomic behaviour under controlled conditions. Two different times of fire exposure (treatments) were evaluated, 15 min and 30 min, after spraying pig trotters with gasoil. The pig trotters were provided to adult hide beetles and both were maintained at 24 ± 0.1°C, 55.4% ± 2% relative humidity, and a 12:12 h day/night cycle. An unburned pig trotter was used as a control for each treatment. Observations were made and photographs were taken every 4-5 days for 4 months. Qualitative and quantitative analyses were performed. Dermestes maculatus was able to feed and reproduce on burned tissues. Beetles in adult and larvae stages produced different types of marks in several kinds of tissues such as integumental, connective, and muscular, in the controls and treatments. Apparently, 15 min of burning the pig trotters were not sufficient enough to cause differences in the taphonomic marks with respect to the control, but post mortem burning for 30 min may have implicated changes (lesser insect damage represented by lesser number and surface of both depressions and holes were found with respect to the control; greater surfaces and diameters were noticed compared to those found in the unburned pig trotters). The shape of the marks was equal in the controls and treatments.

Cholinesterase activity during embryonic development in the blood-feeding bug Triatoma patagonica.

Triatoma patagonica Del Ponte (Hemiptera: Reduviidae), a vector of Chagas' disease, is widely distributed in Argentina and is found in sylvatic and peridomiciliary ecotopes, as well as occasionally in human dwellings after the chemical control of Triatoma infestans. Anti-cholinesteratic products can be applied in peridomiciliary areas and thus knowledge of cholinesterase activity during embryonic development in this species might contribute further information relevant to effective chemical control. Cholinesterase activity was characterized by reactions to eserine 10(-5) m, to increasing concentrations of substrate and to varying centrifugal speeds. Acetylcholinesterase activity was detected on day 4 and was significant from day 5. A reduction in cholinesterase activity towards acetylthiocholine (ATC) was observed on days 9 and 10 of development. Cholinesterase activity towards ATC and butyrylthiocholine (BTC) in homogenates of eggs was inhibited by eserine 10(-5) m. The shape of the curve indicating levels of inhibition at different concentrations of ATC was typical of acetylcholinesterase. Activity towards BTC did not appear to be inhibited by excess substrate, which parallels the behaviour of butyrylcholinesterases. Cholinesterase activity towards ATC was reduced in supernatant centrifuged at 15 000 g compared with supernatant centrifuged at 1100 g. The cholinesterase system that hydrolyzes mainly ATC seems to belong to the nervous system, as indicated by its behaviour towards the substrates assayed, its greater insolubility and the fact that it evolves parallel to the development of the nervous system. Knowledge of biochemical changes associated with the development and maturation of the nervous system during embryonic development would contribute to the better understanding of anti-cholinesteratic compounds with ovicidal action that might be used in control campaigns against vectors of Chagas' disease.

An enriched environment restores normal behavior while providing cytoskeletal restoration and synaptic changes in the hippocampus of rats exposed to an experimental model of depression.

The exposure of rats to an enriched environment (EE) has several effects in common with the administration of antidepressants. However, there is still little information about the molecular underpinnings of these effects on rats subjected to experimental models of depression. The aim of this research was to evaluate the effects of EE on rats exposed to the learned helplessness paradigm (LH), a well-known model of the disease. We found that a 21 day exposure to EE reverts helplessness behavior to normal in LH animals. Inmunohistochemical labeling showed that this effect was accompanied by normalization of two structural proteins of hippocampal neurons to control values: the light neurofilament subunit (NFL) and the postsynaptic density 95 (PSD-95) protein, which were decreased in LH animals housed in standard cages. The decrease in the presynaptic protein synaptophysin (SYN) observed in LH animals remained unchanged after exposure to EE. There was no increase in neurogenesis as measured by quantification of double-labeled cells with 5-bromo-2'-deoxyuridine (BrdU) and the neuronal marker beta-tubulin class III. These results show that EE may have behavioral and synaptic effects on animals exposed to an experimental model of depression, and that such actions seem to be independent from neurogenesis.

Repellence and toxicity of Schinus molle extracts on Blattella germanica.

The biological activities of ethanol and petroleum ether extracts from leaves and fruits of Schinus molle against adults of Blattella germanica were examined by repellence test and topical application. All extracts produced significant repellent effect and mortality.

Biological activity of Schinus molle on Triatoma infestans.

Hexanic extracts from leaves and fruits of Schinus molle were tested for repellent and insecticidal properties against first instar nymphs and eggs of Triatoma infestans, the vector of Chagas' disease. Leaf and fruit extracts were highly repellent for first nymphs. Fruit extracts had also ovicidal activity.

Neuronal cytoskeletal alterations in an experimental model of depression.

It has been proposed that depression is associated with hippocampal morphological changes. The apical dendrite atrophy of hippocampal CA3 pyramidal neurons has been described in experimental models of depression. The aim of the present study was to determine which cytoskeletal components are involved in the morphological changes previously described in the hippocampus of depressed animals. The expression of different neuronal cytoskeletal markers was analyzed by immunohistochemistry in rats exposed to a learned helplessness paradigm, an experimental model of depression. Rats were trained with 60 inescapable foot shocks (0.6 mA/15 s) and escape latencies and failures were tested 4 days after training. Animals in which learned helplessness behavior persisted for 21 days were included in the depressed group. No foot shocks were delivered to control rats. Microtubule-associated protein 2 (MAP-2) and light (NFL; 68 kDa), medium (NFM; 160 kDa) and heavy (NFH; 200 kDa) neurofilament subunit immunostainings were analyzed employing morphometric parameters. In the depressed group, NFL immunostaining decreased 55% (P<0.05) and 60% (P<0.001) in CA3 and dentate gyrus, respectively. In the same areas, MAP-2, NFM and NFH immunostainings did not differ between depressed and control animals. Since NFL is present in the core of mature neurofilament, it is proposed that hippocampal depression-associated plastic alterations may be due to changes in the dynamics of the neurofilament assembly.

[Glutamatergic neurotransmission, depression and antidepressants]. / Neurotransmisión glutamatérgica, depresión y antidepresivos.

Depression is a psychiatric disorder that affects 20% of the population. Despite the efforts aimed to identify the mechanisms underlying its behavioral and affective symptoms, no consensus has been reached. In the last years two new theories, the glutamatergic and the genomic ones, have been proposed. Upon the first, the exposition to stressful stimuli increases hippocampal glutamatergic neurotransmission and triggers excitotoxic changes. The second one postulates that depression is closely correlated with neuronal atrophy due to a decrease in BDNF. The aim of this work is to review recent findings about the glutamatergic neurotransmission and its implication in animal models of depression, depressed patients and in both conditions after the antidepressant treatment. We also tried to identify possible links between these observations and the genomic theory.

Neurotransmisión glutamatérgica, depresión y antidepresivos / [Glutamatergic neurotransmission, depression and antidepressants]

Depression is a psychiatric disorder that affects 20

of the population. Despite the efforts aimed to identify the mechanisms underlying its behavioral and affective symptoms, no consensus has been reached. In the last years two new theories, the glutamatergic and the genomic ones, have been proposed. Upon the first, the exposition to stressful stimuli increases hippocampal glutamatergic neurotransmission and triggers excitotoxic changes. The second one postulates that depression is closely correlated with neuronal atrophy due to a decrease in BDNF. The aim of this work is to review recent findings about the glutamatergic neurotransmission and its implication in animal models of depression, depressed patients and in both conditions after the antidepressant treatment. We also tried to identify possible links between these observations and the genomic theory.

Neurotransmisión glutamatérgica, depresión y antidepresivos. / [Glutamatergic neurotransmission, depression and antidepressants]

Depression is a psychiatric disorder that affects 20

of the population. Despite the efforts aimed to identify the mechanisms underlying its behavioral and affective symptoms, no consensus has been reached. In the last years two new theories, the glutamatergic and the genomic ones, have been proposed. Upon the first, the exposition to stressful stimuli increases hippocampal glutamatergic neurotransmission and triggers excitotoxic changes. The second one postulates that depression is closely correlated with neuronal atrophy due to a decrease in BDNF. The aim of this work is to review recent findings about the glutamatergic neurotransmission and its implication in animal models of depression, depressed patients and in both conditions after the antidepressant treatment. We also tried to identify possible links between these observations and the genomic theory.

[New perspectives of the mechanism of action of antidepressants arised from genomic theory of depression]. / El mecanismo de acción de los antidepresivos a la luz de la teoría genómica de la depresión.

Depression is a highly prevalent condition in adult population. Research on the mechanism of action of antidepressant drugs is also expected to allow a better comprehension about its etiopathogenesis. First theories about neurobiology of depression pointed out the monoaminergic modifications elicited by antidepressants. However, these changes could not be correlated with the latency of action observed in their clinical use. In 1997, with the formulation of genomic theory of depression, old theories and new knowledge about cellular and molecular effects of antidepressant treatment became congruent. The main goal of this paper is to review this theory and the scientific papers in which it is supported. Scientific evidences against genomic theory of antidepressant action are also mentioned. CREB's participation in antidepressant response, as well as BDNF trophic effect and their intracellular signaling pathways are described, as many of these molecules could become targets for the action of new antidepressants.

Modulation by somatostatin of rat submandibular salivary secretion.

Although somatostatin (somatotrophin release inhibitory factor; SRIF) is a well-known inhibitory peptide, there are only a few reports of it acting as a positive modulator. In this work, the action of somatostatin upon rat submandibular protein secretion was studied. In vivo somatostatin infusion (35 microg/(kg h)) raised protein secretion stimulated by adrenergic and peptidergic agents. To rule out possible systemic effects of somatostatin, in vitro experiments were performed. Somatostatin (90 nmol/l) augmented protein release stimulated by noradrenaline (19 micromol/l) and substance P (10 micromol/l), but it did not affect isoprenaline (400 micromol/l)-induced protein release. Phenoxybenzamine (20 micromol/l) reduced the effect of somatostatin on noradrenaline-stimulated protein release. Propranolol (20 micromol/l) increased the noradrenaline-stimulated protein release and this effect was synergistic with the action of somatostatin. The absence of extracellular calcium did not significantly reduce somatostatin enhancement of agonist-induced secretion. Fluorescence measurements of the Ca(2+)-sensitive dye fluo3 showed that cytosolic calcium in acinar cells remained elevated during stimuli when somatostatin was present in the medium. It was concluded that somatostatin modulates rat submandibular protein secretion by prolonging the time that the cytosolic calcium signal remains high after stimulus.

Adaptive changes in the rat hippocampal glutamatergic neurotransmission are observed during long-term treatment with lorazepam.

RATIONALE: Chronic treatment with benzodiazepines induces tolerance to most of their pharmacological effects. The best-studied neurochemical correlation to this phenomenon involves GABAergic adaptive changes. However, some compensation by excitatory neurotransmission could also be postulated. OBJECTIVE: The aim of this work was to investigate the effect of chronic treatment with benzodiazepines on several parameters of hippocampal glutamatergic neurotransmission. METHODS: Rats were injected (IP) with a single dose or daily doses (21 days) of 1 mg/kg lorazepam (LZ) or vehicle. Thirty minutes after the last dose, animals were killed and parameters were measured in the dissected hippocampi. We determined one presynaptic parameter, in vitro glutamate release induced by a 60 mM K(+) stimulus. [(3)H]MK-801 binding to postsynaptic NMDA receptors and the NMDA-stimulated efflux of cGMP were also evaluated. RESULTS: While no changes were observed in any of the parameters after a single dose of the drug, we found an increase of 206% in in vitro glutamate release in chronically treated animals [two-way ANOVA: F(1,16)=6.22], together with an increment of 103% in the NMDA-stimulated cGMP efflux [two-way ANOVA: F(1,18)=14.05]. No changes either in K(D) or in B(max) values for [(3)H]MK-801 binding to hippocampal membranes were observed. CONCLUSIONS: Taken together, these changes strongly suggest that a compensatory increase in the glutamatergic response develops in the hippocampus during chronic treatment with LZ. Our findings might indicate a contribution of glutamatergic mechanisms to the tolerance to hippocampal-mediated effects of LZ, such as amnesic and anticonvulsant activities.

El mecanismo de acción de los antidepresivos a la luz de la teoría genómica de la depresión / [New perspectives of the mechanism of action of antidepressants arised from genomic theory of depression]

Depression is a highly prevalent condition in adult population. Research on the mechanism of action of antidepressant drugs is also expected to allow a better comprehension about its etiopathogenesis. First theories about neurobiology of depression pointed out the monoaminergic modifications elicited by antidepressants. However, these changes could not be correlated with the latency of action observed in their clinical use. In 1997, with the formulation of genomic theory of depression, old theories and new knowledge about cellular and molecular effects of antidepressant treatment became congruent. The main goal of this paper is to review this theory and the scientific papers in which it is supported. Scientific evidences against genomic theory of antidepressant action are also mentioned. CREB’s participation in antidepressant response, as well as BDNF trophic effect and their intracellular signaling pathways are described, as many of these molecules could become targets for the action of new antidepressants.

El mecanismo de acción de los antidepresivos a la luz de la teoría genómica de la depresión. / [New perspectives of the mechanism of action of antidepressants arised from genomic theory of depression]

Depression is a highly prevalent condition in adult population. Research on the mechanism of action of antidepressant drugs is also expected to allow a better comprehension about its etiopathogenesis. First theories about neurobiology of depression pointed out the monoaminergic modifications elicited by antidepressants. However, these changes could not be correlated with the latency of action observed in their clinical use. In 1997, with the formulation of genomic theory of depression, old theories and new knowledge about cellular and molecular effects of antidepressant treatment became congruent. The main goal of this paper is to review this theory and the scientific papers in which it is supported. Scientific evidences against genomic theory of antidepressant action are also mentioned. CREBs participation in antidepressant response, as well as BDNF trophic effect and their intracellular signaling pathways are described, as many of these molecules could become targets for the action of new antidepressants.

Effect of oral L-arginine administration for three weeks in two kidney-two clip hypertensive rats.

Nitric oxide (NO) has been identified as an effective vascular relaxant. This study analyses the contribution of the precursor L-arginine (L-arg) by oral administration in two kidney-two clip hypertension in the rat (2K-2C). Two groups were studied: sham (SH, n=21) and hypertensive (HT, n=15). After 4 weeks of surgery, a group of rats remained as controls (SHc and HTc, respectively), while others were supplemented with L-arg (1.25 g/L) in drinking water (SHa and HTa) for 3 weeks. Blood pressure was significantly increased in 2K-2C rats but remained unchanged after L-arg treatment. Plasma nitrite/nitrate concentrations were not different among groups. The contractile response of aorta to KCl, serotonin and the protein kinase C (PKC) stimulant, phorbol 12,13-dibutyrate (PDBu) was also evaluated. Higher contractile responses to PDBu (p<0.001) and lower relaxation to acetylcholine (Ach 10(-6) M, p<0.05 and 10(-5)M, p<0.02) were observed in aortic rings of HTc vs SHc; L-arg supplementation significantly diminished tension development to all agonists (p<0.05) but failed to modify the lower relaxation to Ach in HTa. Thromboxane (TxA(2)) - synthesis in rings of HTc was higher than in SHc under basal conditions (p<0.05). In the groups with supplement of L-arg, PDBu significantly stimulated prostacyclin (PGI(2)) synthesis more in HTa rats than in SHa ones (p<0.05). To conclude: 1) L-arg fails to modify hypertension development in 2K-2C rats; and 2) L-arg exerts a beneficial effect on the vascular wall, by reducing contractility in rings from HTa rats; it also improved PGI(2) synthesis under PDBu stimulation. 3) greater PKC activation and TxA(2) production rather than lower NO availability might result in systemic hypertension in 2K-2C rats.