Natural biological control of Chrysodeixis includens.

A wide variety of abiotic and biotic factors act on insect pests to regulate their populations. Knowledge of the time and magnitude of these factors is fundamental to understanding population dynamics and developing efficient pest management systems. We investigate the natural mortality factors, critical pest stages, and key mortality factors that regulate Chrysodeixis includens populations via ecological life tables. The total mortality caused by natural factors was 99.99%. Natural enemies were the most important mortality factors in all pest stages. The critical stages of C. includens mortality were second and fourth instars. The key mortality factors were predation by ants in the second instar and predation by Vespidae in the fourth instar. The elimination of these factors can cause an increase of 77.52 and 85.17% of C. includens population, respectively. This study elucidates the importance of natural enemies and other natural mortality factors in C. includens population regulation. These factors should be considered in developing and implementing C. includens management strategies and tactics in order to achieve effective and sustainable pest control.

Opiatergic participation in the thirst-inhibiting effect of acute third ventricle injections of cadmium (Cd2+) and lead (Pb2+).

We have previously demonstrated that acute third ventricle injections of both lead and cadmium prevent the dipsogenic response elicited by dehydration or by central injections of dipsogenic agents such as angiotensin II, carbachol and isoproterenol in rats. We have also shown that the antidipsogenic action of cadmium may be due, at least in part, to activation of thirst-inhibitory central serotonergic pathways. In the present paper we show that in Wistar male rats the antidipsogenic effect of both lead acetate (3.0 nmol/rat) and cadmium chloride (3.0 nmol/rat) may be partially dependent on the activation of brain opiatergic pathways since central injections of naloxone (82.5 nmol/rat), a non-selective opioid antagonist, blunt the thirst-inhibiting effect of these metals. One hundred and twenty minutes after the second third ventricle injections, dehydrated animals (14 h overnight) receiving saline + sodium acetate displayed a high water intake (7.90 +/- 0.47 ml/100 g body weight) whereas animals receiving saline + lead acetate drank 3.24 +/- 0.47 ml/100 g body weight. Animals receiving naloxone + lead acetate drank 6.94 +/- 0.60 ml/100 g body weight. Animals receiving saline + saline drank 8.16 +/- 0.66 ml/100 g body weight whilst animals receiving saline + cadmium chloride drank 1.63 +/- 0.37 ml/100 g body weight. Animals receiving naloxone + cadmium chloride drank 8.01 +/- 0.94 ml/100 g body weight. It is suggested that acute third ventricle injections of both lead and cadmium exert their antidipsogenic effect by activating thirst-inhibiting opioid pathways in the brain.

Natriuretic and kaliuretic effects of central acute cadmium administration in rats.

We studied the acute effects of cadmium third ventricle injections on renal excretion of water, sodium and potassium in rats previously submitted to an oral water load equivalent to 10% of their body weight. Injections of cadmium chloride (0.03, 0.3, and 3.0 nmol/rat) significantly increased sodium and potassium renal excretion without changing urine flow. Pretreatment with losartan, an angiotensin II AT1 receptor antagonist (10.8 nmol/rat into the third ventricle 10 min before central cadmium administration) inhibits the natriuretic effect of this metal, being unable to reverse its kaliuretic effect. Pretreatment with gadolinium, a calcium-channel blocker (0.3 nmol/rat into the third ventricle 20 min before central cadmium administration) abolishes both the natriuretic and the kaliuretic response of cadmium. The data clearly show that cadmium injections into the third ventricle disturb central regulation of renal function leading to an increased renal loss of sodium and potassium. It is also evident that the natriuretic action of the metal depends on an increase in brain angiotensin II release. Also, the functional integrity of calcium channels is required for the expression of both the natriuretic and the kaliuretic effects of the metal.

Opiatergic participation in the thirst-inhibiting effect of acute third ventricle injections of cadmium (Cd 2+ ) and lead (Pb 2+ )

We have previously demonstrated that acute third ventricle injections of both lead and cadmium prevent the dipsogenic response elicited by dehydration or by central injections of dipsogenic agents such as angiotensin II, carbachol and isoproterenol in rats. We have also shown that the antidipsogenic action of cadmium may be due, at least in part, to activation of thirst-inhibitory central serotonergic pathways. In the present paper we show that in Wistar male rats the antidipsogenic effect of both lead acetate (3.0 nmol/rat) and cadmium chloride (3.0 nmol/rat) may be partially dependent on the activation of brain opiatergic pathways since central injections of naloxone (82.5 nmol/rat), a non-selective opioid antagonist, blunt the thirst-inhibiting effect of these metals. One hundred and twenty minutes after the second third ventricle injections, dehydrated animals (14 h overnight) receiving saline + sodium acetate displayed a high water intake (7.90 ñ 0.47 ml/100 g body weight) whereas animals receiving saline + lead acetate drank 3.24 ñ 0.47 ml/100 g body weight. Animals receiving naloxone + lead acetate drank 6.94 ñ 0.60 ml/100 g body weight. Animals receiving saline + saline drank 8.16 ñ 0.66 ml/100 g body weight whilst animals receiving saline + cadmium chloride drank 1.63 ñ 0.37 ml/100 g body weight. Animals receiving naloxone + cadmium chloride drank 8.01 ñ 0.94 ml/100 g body weight. It is suggested that acute third ventricle injections of both lead and cadmium exert their antidipsogenic effect by activating thirst-inhibiting opioid pathways in the brain

Lead (Pb2+) and cadmium (Cd2+) inhibit the dipsogenic action of central beta-adrenergic stimulation by isoproterenol.

We have previously demonstrated that acute third ventricle injections of both Pb2+ and Cd2+ impair the dipsogenic response elicited by three different situations: dehydration and central cholinergic or angiotensinergic stimulation. beta-Adrenergic activation is part of the multifactorial integrated systems operating in drinking behavior control in the central nervous system. In the present study acute third ventricle injections of Pb2+ (3, 30 and 300 pmol/rat) or Cd2+ (0.3, 3 and 30 pmol/ rat) blocked the dipsogenic response induced by third ventricle injections of isoproterenol (ISO; 160 nmol/rat) in a dose-dependent manner. Normohydrated animals receiving ISO + NaAc (sodium acetate) or saline (controls) displayed a high water intake after 120 min (ISO+saline = 5.78 +/- 0.54 ml/100 g; ISO+NaAc = 6.00 +/- 0.6 ml/100 g). After the same period, animals receiving ISO but pretreated with PbAc at the highest dose employed (300 pmol/rat) drank 0.78 +/- 0.23 ml/100 g while those receiving ISO and pretreated with the highest dose of CdCl2 (30 pmol/rat) presented a water intake of 0.7 +/- 0.30 ml/100 g. Third ventricle injections of CdCl2 (3 nmol/rat) or PbAc (3 nmol/rat) did not modify food intake in rats deprived of food for 24 h. Thus, general central nervous system depression explaining the antidipsogenic action of the metals can be safely excluded. It is concluded that both Pb2+ and Cd2+ inhibit water intake induced by central beta-adrenergic stimulation.

Lead (Pb+) and cadmium (Cd2+) inhibit the dipsogenic action of central beta-adrenergic stimulation by isoproterenol

We have previously demonstrated that acute third ventricle injections of both Pb2+ and Cd2+ impair the dipsogenic response elicited by three different situations: dehydration and central cholinergic or angiotensinergic stimulation. beta-Adrenergic activation is part of the multifactorial integrated systems operating in drinking behavior control in the central nervous system. In the present study acute third ventricle injections of Pb2+ (3,30 and 300 pmol/rat) or Cd2+ (0.3, 3 and 30 pmol/rat) blocked the dipsogenic response induced by third ventricle injections of isoproterenol (ISO; 160 nmol/rat) in a dose-dependent manner. Normohydrated animals receiving ISO + NaAc (sodium acetate) or saline (controls) displayed a high water intake after 120 min (ISO + saline = 5.78 ñ O.54 ml/lOO g; ISO + NaAc = 6.00 ñ O.6 ml/lOO g). After the same period,animals receiving ISO but pretreated with PbAc at the highest dose employed (300 pmol/rat) drank O.78 ñ O.23 ml/lOO g while those receiving ISO and pretreated with the highest dose of CdCl(2)(30 pmol/rat) presented a water intake of O.7 ñ O.30 ml/lOO g. Third ventricle injections of CdCl(2) (3 nmol/rat) or PbAc (3 nmol/rat) did not modify food intake in rats deprived of food for 24 h. Thus, general central nervous system depression explaining the antidipsogenic action of the metals can be safely excluded. It is concluded that both Pb2+ and Cd2+ inhibit water intake induced by central beta-adrenergic stimulation.

Calcium channel blockers inhibit the antidipsogenic effect of central injections of zinc in rats.

Previous data from our laboratory have indicated that acute third ventricle injections of Zn2+ elicit a significant antidipsogenic response in rats in three different situations; dehydration, and central angiotensinergic or cholineric stimulation. In the present study we analyzed whether this response depends on voltage-dependent calcium channels. Dehydrated (14 h of water deprivation, overnight) animals received 2-microliters i.c.v. injections of zinc acetate (Zn(Ac)2; 300 pmol/rat) after pretreatment with the voltage-dependent calcium channel blockers gadolinium (Gd3+; 0.03, 3.0 and 30 pmol/rat) or verapamil (VER; 0.027, 0.05 and 0.11 pmol/rat). Both blockers reserved the antidipsogenic effect of third ventricle injections of Zn2+ in a dose-dependent manner. After 120 min, animals pretreated with saline receiving Zn(Ac)2 drank 3.10 +/- 0.57 ml/100 g body weight while those pretreated with Gd3+ at the highest dose displayed a water intake of 5.45 +/- 0.41 ml/100 body weight (P < 0.01). Animals pretreated with the vehicle of VER receiving Zn(Ac)2 drank 3.15 +/- 0.45 ml/100 g while animals pretreated with VER at the highest dose receiving Zn(Ac)2 drank 6.16 +/- 0.62 ml/100 g (P < 0.01). The antidipsogenic effect of Zn(Ac)2 seems to be specific since the metal (same dose and injection procedures) did not modify food intake in rats after 24 h of food deprivation. It is suggested that Zn2+ exerts its antidipsogenic effect by activation of mechanism(s) depending on the functional integrity of voltage-dependent calcium channels.

Calcium channel blockers inhibit the antidipsogenic effect of central injections of zinc in rats

Previous data from our laboratory have indicated that acute third ventricle injections of Zn2+ elicit a significant antidipsogenic response in rats in three different situations: dehydration, and central angiotensinergic or cholinergic stimulation. In the present study we analyzed whether this response depends on voltage-dependent calcium channels. Dehydrated (l4 h of water deprivation, overnight) animals received 2-mul icv injections of zinc acetate (Zn(AC)2; 300 pmol/rat) after pretreatment with the voltage-dependent calcium channel blockers gadolinium (Gd3+;0.03, 3.0 and 30 pmol/rat) or verapamil (VER; 0.027, 0.05 and 0.11 pmol/rat). Both blockers reversed the antidipsogenic effect of third ventricle injections of Zn2+ in a dose-dependent manner. After 120 min, animals pretreated with saline receiving Zn(AC)2 drank 3.10 ñ 0.57 ml/100 g body weight while those pretreated with GD3+ at the highest dose displayed a water intake of 5.45 ñ O.41 ml/l00 g body weight (P<0.01). Animals pretreated with the vehicle of VER receiving Zn(AC)2 drank 3.15 ñ 0.45 ml/l00 g while animals pretreated with VER at the highest dose receiving Zn(AC)2 drank 6.16 ñ 0.62 ml/l00 g (P<0.01). The antidipsogenic effect of Zn(AC)2 seems to be specific since the metal (same dose and injection procedures) did not modify food intake in rats after 24 h of food deprivation. It is suggested that Zn2+ exerts its antidipsogenic effect by activation of mechanism(s) depending on the functional integrity of voltage-dependent calcium channels.