Approach to Physiological Functions of Ethrel in the Ripening of Cotton Boll

Both leaf and boll of cotton can absorb ethrel and the acceptor releases ethylene rapidly. Ethrel absorbed by leaves can release ethylene in bolls, whereas that absorbed by bolls cannot release ethylene in leaves. Bolls treated with ethrel has two peaks in ethylene releasing. The first peak appears about two days after treatment, and the second appears before the splitting of boll. The control has only one peak in ethylene releasing which appears eight days later than the second peak of the bolls treated with ethrel. This coincides with the fact that ethrel enables bolls to split seven to ten days earlier. The releasing of ethylene by cotton bolls is closely related to temperature, and is accelerated with increasing temperature no matter cotton bolls are treated with ethrel or not.     

The controlled release of insulin-mimetic metal ions by the multifunction of chitosan

Vanadium, which is an insulin-mimetic metal ion, was efficiently adsorbed on chitosan (CS). The adsorption of vanadium on CS was affected by the vanadium/CS ratio and the initial concentration of vanadium in preparative medium under constant pH condition. The vanadium-CS complex was able to control vanadium release. Moreover, a consistent control of vanadium release was achieved by incorporation of the vanadium-CS complex into a CS gel. After implantation of the CS gel retaining the vanadium-CS complex into diabetic mice, insulin-mimetic efficacy was confirmed by observation of a steady reduction in blood glucose levels. The sustained vanadium release also contributed to minimization of the side-effects. Thus, CS gel retaining the vanadium-CS complex appears promising as a vehicle for vanadium with long-term action and a low toxicity leading to its clinical use.     

Models for pest control: Complementary effects of periodic releases of sterile pests and parasitoids

Four host-parasitoid models that incorporate the simultaneous or sequential release during each generation of sterile hosts and parasitoids for control or eradication of host species are presented. The models are based on two modifications of the Nicholson-Bailey model which incorporate density regulation either in the host larvae or via parasitoid oviposition. Parasitization of host larvae and adults forms another comparison. The models indicate that the release of sterile hosts alone is more efficient than release of parasitoids alone in controlling the hosts if population regulation is in the parasitoids; otherwise, the release of parasitoids alone is more efficient. The release of both steriles and parasitoids is much more efficient than the release of either alone for either suppressing or eradicating the hosts. This greater efficiency in combination rather than separately appears to be a special case of a more general principle, which is that two pest control methods will mutually complement each other if their optimal actions in reducing host numbers are at very different host densities. This is the case for sterile releases (optimal at low host densities) and parasitoid inundation (optimal at high host densities).     

Effects of age on the adrenergic cardiac neuroeffector junction

Although it is clear that adrenergic nervous system control of cardiac function decreases with age and that the effector organ fails to adjust to this decreased control, it is not completely evident which of the many mechanisms operant at the adrenergic-cardiac neuroeffector junction contribute to this state. Prejunctionally, it appears that norepinephrine content decreases with age and that adrenergic axonal degeneration occurs. Also, evidence is available to suggest that modulation by prejunctional alpha adrenergic receptors of norepinephrine release is altered with increasing age, as is neuronal uptake of norepinephrine. Postjunctionally, it appears that beta-adrenergic receptor sensitivity to agonists undergoes age-related alterations, and possibly post receptor mechanisms involved in receptor-response coupling. Other mechanisms, such as those involved in transmitter uptake into extraneuronal sites, adrenergic neuronal responsiveness to stimulation, transmitter release and turnover, calcium and prejunctional receptor modulation of transmitter release, postjunctional receptor development of supersensitivity or subsensitivity, need further elucidation in order to have an understanding of the factors that contribute to the breakdown of homeostatic mechanisms that regulate the heart.     

Neuropeptide Y does not inhibit the release of alpha-MSH from the pars intermedia of the rat adenohypophysis

Neuropeptide Y in concentrations from 10(-8) to 10(-6) M inhibits the release of alpha-MSH from the frog (Rana pipiens) pituitary in a reversible, sustained, and concentration-related manner. However, it does not inhibit the release of alpha-MSH from the rat pars intermedia. Thus, while neuropeptide Y may play a role in the control of alpha-MSH release in amphibia, it appears not to be a regulatory peptide for the mammalian pars intermedia.     

alpha-Tocopherol and protein kinase C inhibition enhance platelet-derived nitric oxide release.

Platelet activation is tightly regulated by products of the endothelium and platelets including nitric oxide (NO). Excess vascular oxidative stress has been associated with impaired NO release, and antioxidant status has been shown to alter endothelium-derived NO bioactivity. Although physiological levels of a-tocopherol are known to inhibit platelet function, the effect of a-tocopherol on platelet NO release is unknown. Loading platelets with physiologic levels of a-tocopherol increased platelet NO production approximately 1.5-fold (Pa-tocopherol, platelet NO release increased 50% (Pa-Tocopherol-loaded platelets also produced 74% less superoxide as compared with control (Pa-tocopherol inhibited PKC-dependent eNOS phosphorylation as determined by immunoprecipitation. Lastly, platelets isolated from NOS3-deficient mice released 80% less superoxide as compared with control animals (P=0.011), and incubation of NOS III-deficient platelets with 500 mM a-tocopherol only caused a modest additional decrease in platelet superoxide release (NS). Thus, a-tocopherol appears to enhance platelet NO release both in vitro and in vivo through antioxidant- and PKC-dependent mechanisms.     

Diurnal patterns of dopamine release in chicken retina

The retinal dopaminergic system appears to play a major role in the regulation of global retinal processes related to light adaptation. Although most reports agree that dopamine release is stimulated by light, some retinal functions that are mediated by dopamine exhibit circadian patterns of activity, suggesting that dopamine release may be controlled by a circadian oscillator as well as by light. Using the accumulation of the dopamine metabolite dihydroxyphenylacetic acid (DOPAC) in the vitreous as a measure of dopamine release rates, we have investigated the balance between circadian- and light control over dopamine release. In chickens held under diurnal light:dark conditions, vitreal levels of DOPAC showed daily oscillations with the steady-state levels increasing nine-fold during the light phase. Kinetic analysis of this data indicates that apparent dopamine release rates increased almost four-fold at the onset of light and then remained continuously elevated throughout the 12h light phase. In constant darkness, vitreal levels of DOPAC displayed circadian oscillations, with an almost two-fold increase in dopamine release rates coinciding with subjective dawn/early morning. This circadian rise in vitreal DOPAC could be blocked by intravitreal administration of melatonin (10 nmol), as predicted by the model of the dark-light switch where a circadian fall in melatonin would relieve dopamine release of inhibition and thus be responsible for the slight circadian increase in dopamine release. The increase in vitreal DOPAC in response to light, however, was only partially suppressed by melatonin. The activity of the dopaminergic amacrine cell in the chicken retina thus appears to be dominated by light-activated input.     

Hydrogen ion changes of rhodopsin. pK changes and the thermal decay of metarhodopsin II380

The ionization changes during the photolysis of the visual pigment, cattle rhodopsin, have been measured by simultaneous recording of spectral and pH changes. The thermal intermediates of rhodopsin and pH changes were recorded over a pH range of 4.6–8.9.In the normal sequence of intermediate changes at pH values of 5.4–7.7, the proton uptake of rhodopsin during the metarhodopsin I₄₇₈ to II₃₈₀ reaction is followed by a proton release in the thermal decay of metarhodopsin II₃₈₀ to III₄₆₅. Below pH 5.4, no proton release is observed during the thermal decay of metarhodopsin II₃₈₀, and the metarhodopsin II₃₈₀ appears to thermally decay directly to N-retinylidene-opsin₄₄₀. Above pH 7.7, the major process appears to be a proton release and the final product is N-retinylidene-opsin₃₆₅.The ionization state of certain groups in rhodopsin appears to control the metarhodopsin I₄₇₈ to II₃₈₀ reaction and control the products in the thermal decay of metarhodopsin II₃₈₀. The pK changes of certain groups in rhodopsin may be the major factor in determining sequence of thermal intermediates and the values of the kinetic activation parameters. The reversing ionization changes may be important to the transduction process.     

Oestrogen and progesterone interactions in the control of gonadotrophin and prolactin secretion

Oestrogen and progesterone have marked effects on the secretion of the gonadotrophins and prolactin. During most of the oestrous or menstrual cycle the secretion of gonadotrophin is maintained at a relatively low level by the negative feedback of oestrogen and progesterone on the hypothalamic-pituitary system. The spontaneous ovulatory surge of gonadotrophin is produced by a positive feedback cascade. The cascade is initiated by an increase in the plasma concentration of oestradiol-17 beta which triggers a surge of luteinizing hormone releasing hormone (LHRH) and an increase in pituitary responsiveness to LHRH. The facilitatory action of oestrogen on pituitary responsiveness is reinforced by progesterone and the priming effect of LHRH. How oestrogen and progesterone exert their effects is not clear but the facilitatory effects of oestrogen take about 24 h, and the stimulation of LHRH release is produced by an indirect effect of oestradiol on neurons which are possibly opioid, dopaminergic or noradrenergic and which modulate the activity of LHRH neurons. In the rat, a spontaneous prolactin surge occurs at the same time as the spontaneous ovulatory gonadotrophin surge. The prolactin surge also appears to involve a positive feedback between the brain-pituitary system and the ovary. However, the mechanism of the prolactin surge is poorly understood mainly because the neural control of prolactin release appears to be mediated by prolactin inhibiting as well as releasing factors, and the precise role of these factors has not been established. The control of prolactin release is further complicated by the fact that oestradiol stimulates prolactin synthesis and release by a direct action on the prolactotrophes. Prolactin and gonadotrophin surges also occur simultaneously in several experimental steroid models. A theoretical model is proposed which could explain how oestrogen and progesterone trigger the simultaneous surge of LH and prolactin.     

Antigen-induced secretion in the optic gland of Octopus vulgaris.

The optic gland of the octupus responds to a variety of foreign proteins--1 to 2 days after the injection--by the mass production and release of a particulated material. In the electron microscope the antigen-induced substance shows as a non-membrane bound particle of size about 30 nm. When released into the blood it does not disintegrate instantly. The chemistry of this material, which is probably identical with the optic gland hormone, is not known. However, non-vesicular storage and release as well as the abundance of tubular mitochondria suggest that the hormone is a steroid. The optic gland hormone, which is known to control sexual maturation, feeding and death in Octopus, appears to be involved in a defence mechanism against non-octopus proteins.     

Contribution of cardiopulmonary baroreceptors to the control of the kidney.

The role of cardiopulmonary receptors in the control of renal sympathetic nerve activity and of renin release is reviewed. The evidence indicates that cardiopulmonary receptors with vagal afferents exert a tonic inhibition on both renal nerve activity and on renin release. The magnitude of this inhibition appears directly related to changes in blood volume. Atrial as well as ventricular receptors can influence the secretion of renin. Cardiopulmonary receptors with vagal afferents may also reflexly modulate renal prostaglandin secretion. There is preliminary evidence to suggest that cardiopulmonary receptors with sympathetic afferents can influence renal nerve activity. The limitations of previous studies are outlined and a direction for future studies is suggested. It is concluded that alterations in cardiopulmonary vagal afferent input and the resulting changes in renal nerve activity and in renin release are appropriate for the maintenance of blood volume homeostasis.     

Acquisition and social communication of stimulus recognition by Fish

In fish, behavior commonly designated as Pavlovian and/or instrumental conditioning, imprinting, and social learning often appears to reflect a phylogenetically adapted operation of a single underlying learning mechanism, a version of stimulus substitution. In this mechanism, a releasing stimulus comes to share control over the release of behavior with a previously neutral stimulus. In addition, control over the direction of released responses is simultaneously transferred. The outcome, as supported by review of the literature, is that recognition learning in fish seems to involve primarily the extension to new stimuli of control over the elicitation of preorganized unlearned responses.     

Hysteretic nature of NADH substrate inhibition of bovine liver glutamate dehydrogenase.

NADH substrate inhibition of bovine liver glutamate dehydrogenase appears to be eliminated at enzyme concentrations above 0.5mg/ml. Since the inhibition cannot be restored by preincubation of the enzyme with any substrate or product combination, the release of inhibition had previously been considered the result of enzyme polymerization. Benzene-saturated solutions, however, increase the extent of enzyme polymerization without affecting the NADH inhibition. These and related control measurements demonstrate that the release of substrate inhibition is the result of a hysteretic transition of an enzyme central and transitory complex.     

Chemical and biological properties of a protein-rich fraction of bacterial lipopolysaccharides. II. The in vitro rat peritoneal mast cell response.

Lipid A-associated protein (LAP) isolated from preparations of bacterial lipopolysaccharides (LPS, endotoxins) has been demonstrated to initiate the release of amines from rat peritoneal mast cells. The release at low concentrations of LAP requires both cellular energy and calcium, and thus appears to be a true secretory response. At higher concentrations the release is independent of these variables. The time required for maximal response is approximately 10 to 15 min at 37 degrees C. The response appears to be a general property of Escherichia coli LAP preparations since LAP isolated from three serotypes of these organisms all have similar activity. On the basis of heat lability at 100 degrees C, the ability of LAP to initiate mast cell secretion appears to be independent of its ability mitogenically to stimulate murine B lymphocytes.     

Control of luteinizing hormone-releasing hormone pulse generation in nonhuman primates

Summary 1. The pulsatile release of luteinizing hormone-releasing hormone (LHRH) is critical for reproductive function. However, the exact mechanism of LHRH pulse generation is unclear. The purpose of this article is to review the current knowledge on LHRH pulse generation and to discuss a series of studies in our laboratory.2. Using push-pull perfusion in the stalk-median eminence of the rhesus monkey several important facts have been revealed. There is evidence indicating that LHRH neurons themselves have endogenous pulse-generating mechanisms but that the pulsatility of LHRH release is also modulated by input from neuropeptide Y (NPY) and norepinephrine (NE) neurons. The release of NPY and NE is pulsatile, with their pulses preceding or occurring simultaneously with LHRH pulses, and the neuroligands NPY and NE and their agonists stimulate LHRH pulses, while the antagonists of the ligands suppress LHRH pulses.3. The pulsatile release of LHRH increases during the estrogen-induced LH surge as well as the progesterone-induced LH surge. These increases are partly due to the stimulatory effects of estrogen and progesterone on NPY neurons.4. An increase in pulsatile LHRH release occurs at the onset of puberty. This pubertal increase in LHRH release appears to be due to the removal of tonic inhibition from aminobutyric acid (GABA) neurons and a subsequent increase in the inputs of NPY and NE neurons to LHRH neurons.5. There are indications that additional neuromodulators are involved in the control of the LHRH pulse generation and that glia may play a role in coordinating pulses of the release of LHRH and neuromodulators.6. It is concluded that the mechanism generating LHRH pulses appears to comprise highly complex cellular elements in the hypothalamus. The study of neuronal and nonneuronal elements of LHRH pulse generation may serve as a model to study the oscillatory behavior of neurosecretion.     

Effect of the venom of Glycera convoluta on the spontaneous quantal release of transmitter

A neurotoxin able to increase the spontaneous release of transmitter was found in the venom glands of the polychaete annelid Glycera convoluta. We studied the effect of this venom on the frog cutaneous pectoris muscle, where its application produced a prolonged (20-h), high-frequency discharge of miniature potentials. After 5 h of action, the initial store was renewed several times but no detectable ultrastructural changes were observed. After 19 h of sustained activity, nerve terminals with their normal vesicular contents were infrequent; others were fragmented and contained swollen mitochondria, abnormal inclusions, and vesicles of various sizes. In the noncholinergic crayfish neuromuscular preparation, the venom triggered an important increase in spontaneous quantal release that subsided in 1 h. An activity higher than that in resting conditions then persisted for many hours. This high electrical activity was not accompanied by any detectable structural modifications after 3 h. In the torpedo electric organ preparation, the venom elicited a burst of activity that returned to control levels in 1 h. The release of ACh (evaluated by the efflux of radioactive acetate) paralleled the high electrical activity. No morphological changes or significant depletion of tissue stores were detected. The venom of Glycera convoluta appears to enhance considerably the release of transmitter without impairing its turnover. The venom effect is Ca++ dependent and reversible by washing, at least during the first hour of action. Because the high rate of transmitter release appears dissociated from the later-occurring structural modifications, it is possible that the venom mimics one component of the double mode of action proposed for black widow spider venom.     

Presynaptic regulation of acetylcholine release in the CNS

The release of ACh appears to be under the control of autoreceptors localized on cholinergic nerve terminals. Moreover, the process can be regulated by transmitters other than ACh or by modulators either through receptor-mediated or carrier-mediated mechanisms. In this chapter we report on our recent results concerning the regulation of the release of ACh by ACh itself, 5-HT and GABA in the rat hippocampus. In particular it will be shown: 1) that the release of the cholinergic transmitter can be inhibited through muscarinic receptors of the M3 subtype; 2) that 5-HT can interact with ACh by depressing ACh release through the activation of receptors of the 5-HT1B subtype; 3) that the release of ACh can be enhanced by GABA by a novel mechanism involving a selective penetration of the amino acid into the cholinergic terminals.     

Differential effects of naloxone on basal and stress-induced release of ACTH and prolactin in the male rat

The effect of i.v. injection of various doses of naloxone (NAL) on plasma adrenocorticotropin (ACTH) and prolactin (Prl) in conscious animals bearing an indwelling intrajugular catheter was assessed. The effects were evaluated in animals which were left undisturbed and in others subjected to either restraint or ether stress. The results revealed that the dose of 3 mg/kg of NAL significantly reduced basal Prl levels, whereas a dose of 6 mg/kg of NAL was required to block completely either ether or restraint stress-induced release of Prl. The behavior of ACTH contrasted with that of Prl. There was no effect whatsoever of the 3 mg/kg dose of NAL on either resting or stress-induced ACTH levels, whereas a 6 mg/kg or 12 mg/kg dose of NAL elevated resting ACTH levels and only partially attenuated the further elevation induced by stress in these animals. The results clearly indicate a NAL sensitive step in the control of resting and stress-induced Prl release but indicate that the control of resting and stress-induced release of ACTH is different in that the predominantly millimicron receptor blocker, NAL, can elevate ACTH at high doses and can only partially block the response to stress. In contrast to Prl where opioid peptide control is solely stimulatory, this control of ACTH secretion appears to have both stimulatory and inhibitory features.     

Dopamine Depletion Preferentially Impairs D1 over D2-Receptor Regulation of Striatal In Vivo Acetylcholine Release

The roles of D2 and D1 dopaminergic receptors on the regulation of striatal acetylcholine (ACh) release in vivo were examined for a period of 120 min after acute (2 h) or prolonged (16 h) depletion of brain dopamine (DA) by alpha-methyl-p-tyrosine. The reduction of DA transmission did not affect basal ACh output after 2 h but markedly lowered ACh release by 16 h (50%). Acute alpha-methyl-p-tyrosine pretreatment prevented the reduction of ACh release by the D1 antagonist SCH 23390 and its increase by the D2 antagonist, remoxipride, consistent with a drastic reduction of DA transmission at both DA receptors. However, 16 h after alpha-methyl-p-tyrosine, the effect of remoxipride on ACh release was restored, but SCH 23390 still had no effect, suggesting that the D2 inhibitory tone on ACh release had recovered, whereas the reduction of the D1 facilitatory influence persisted. The D1 facilitatory control of ACh neurotransmission thus appears to be more sensitive than the D2 inhibitory control to a reduction in DA transmission. The new model of DA-ACh interaction resulting from these data casts fresh light on the relationship between changes in DA transmission and extrapyramidal motor function.     

Aging alterations in the modulation of central dopaminergic cilioinhibition by etorphine in the marine mussel,Mytilus edulis: Decrease in the inhibition of presynaptic dopamine release

1. This report further demonstrates that etorphine influences presynaptic dopamine release, which in turn centrally modulates peripheral cilioinhibition. 2. In older animals cilioinhibition has become enhanced due to a lack of responsiveness to endogenous opioids which results in greater dopamine release, causing a higher level of cilioinhibition as demonstrated by challenging the visceral ganglia with etorphine or destroying the dopaminergic component with 6-hydroxydopamine. 3. Only the central cilioinhibitory, not the peripheral inhibitory response, mechanism appears to be altered in older animals. Thus, the alteration appears in the central integrative mechanisms involved with regulating ciliary activity. 4. The KCl-stimulated release of dopamine is unaltered in both young and old organisms, whereas the opiate inhibition of the KCl-stimulated release of dopamine is reduced in older organisms. Thus, the aging-associated alteration is associated with a specific process. 5. The reduction of opioid influence and the resulting enhanced cilioinhibitory activity may make the organisms more susceptible to environmental stress.