A review on colorimetric methods for determination of organophosphate pesticides using gold and silver nanoparticles.

This review (with 99 refs.) summarizes the progress that has been made in colorimetric (i.e. spectrophotometric) determination of organophosphate pesticides (OPPs) using gold and silver nanoparticles (NPs). Following an introduction into the field, a first large section covers the types and functions of organophosphate pesticides. Methods for colorimetric (spectrophotometric) measurements including RGB techniques are discussed next. A further section covers the characteristic features of gold and silver-based NPs. Syntheses and modifications of metal NPs are covered in section 5. This is followed by overviews on enzyme inhibition-based assays, aptamer-based assays and chemical (non-enzymatic) assays, and a discussion of specific features of colorimetric assays. Several Tables are presented that give an overview on the wealth of methods and materials. A concluding section addresses current challenges and discusses potential future trends and opportunities. Graphical abstractSchematic representation of organophosphate pesticide determinations based on aggregation of nanoparticles (particular silver or gold nanoparticles). This leads to a color change which can be determined visually and monitored by a red shift in the absorption spectrum.

Enhanced Fos expression in glutamic acid decarboxylase immunoreactive neurons of the mouse periaqueductal grey during opioid withdrawal.

Previous studies using c-Fos immunohistochemistry suggest that a sub-population of neurons in the midbrain periaqueductal gray region is activated during opioid withdrawal. The neurochemical identity of these cells is unknown but cellular physiological studies have implicated GABAergic neurons. The present study investigated whether GABAergic neurons are activated in the mouse periaqueductal gray during opioid withdrawal using dual-antibody immunohistochemistry for Fos and glutamic acid decarboxylase. Both chronic opioid treatment and naloxone-precipitated opioid withdrawal increased Fos expression in the periaqueductal gray, with the greatest increase being four-fold in the caudal ventrolateral subdivision following withdrawal. Neurons stained for both Fos and glutamic acid decarboxylase were greatly enhanced in all subdivisions of the periaqueductal gray following withdrawal, particularly in the lateral and ventrolateral divisions where the increase was up to 70-fold. These results suggest that activation of a subpopulation of GABAergic interneurons in the periaqueductal gray plays a role in opioid withdrawal.

Inhibition of calcium channels by opioid- and adenosine-receptor agonists in neurons of the nucleus accumbens.

The pharmacological effects of opioid- and adenosine-receptor agonists on neural signalling were investigated by measuring drug actions on barium current flowing through calcium channels in acutely-dissociated neurons of the rat nucleus accumbens (NAc). Under whole-cell voltage clamp, opioids acted via mu, but not delta or kappa, receptors to partially inhibit barium current. Mean inhibition was 35+/-2% (+/-s.e.mean, n = 33) for methionine-enkephalin and 37+/-1% (n = 65) for the selective mu receptor agonist DAMGO, both measured at saturating agonist concentrations in neurons with diameter > or = 20 microm. EC(50) for DAMGO was 100 nM. Perfusion of naloxone reversed the current inhibition by DAMGO. Adenosine also partially inhibited barium current in these neurons. Mean inhibition was 28+/-2% (n = 29) for adenosine and 33+/-3% (n = 27) for the selective A1 receptor agonist N(6)CPA, both at saturating concentrations in neurons with diameter > or = 20 microm. EC(50) for N(6)CPA was 34 nM. Adenosine inhibition was reversed by perfusion of an A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine, while the selective A2A receptor agonist, CGS 21680, had no effect. Inhibition by opioids and adenosine was mutually occlusive, suggesting a converging pathway onto calcium channels. These actions involved a G-protein-coupled mechanism, as demonstrated by the partial relief of inhibition by strong depolarization and by the application of N-ethylmaleimide or GTP-gamma-S. Inhibition of barium current by opioids had their greatest effect in large neurons, that is, in presumed interneurons. In contrast, opioid inhibition in neurons with diameter < or = 15 microm was 11+/-2% (n = 26) for methionine-enkephalin and 11+/-4% (n = 17) for DAMGO, both measured at saturating agonist concentrations. Adenosine inhibition in neurons with diameter < or = 15 microm was 22+/-5% (n = 9). These results implicate the interneurons as a locus for the modulation of the excitability of projection neurons in the NAc during the processes of addiction and withdrawal.

Increased opioid inhibition of GABA release in nucleus accumbens during morphine withdrawal.

The nucleus accumbens is a key component of the reward pathway that plays a role in addiction to many drugs of abuse, including psychostimulants and opioids. The effects of withdrawal from chronic morphine were examined in the nucleus accumbens using brain slices from morphine-treated animals. Recordings were made from interneurons in the shell of nucleus accumbens, and the presynaptic inhibition of GABA-A IPSCs by opioids was examined. In slices from control animals, opioids caused a maximal inhibition of 50%, forskolin increased the IPSC amplitude by less than twofold, and the maximal inhibition by opioids in the presence of forskolin was not changed. During withdrawal, however, forskolin caused approximately a fourfold increase in the amplitude of the IPSC, and the maximal inhibition by opioids was increased to 80%. The results indicate that transmitter release is increased during opioid withdrawal, particularly after the activation of adenylyl cyclase. The cAMP-dependent increase in transmitter release is potently inhibited by opioids, such that the overall effect of opioids is augmented during withdrawal. The induction of an opioid-sensitive cAMP-dependent mechanism that regulates transmitter release may be a critical component of acute opioid withdrawal.

Swim-stress but not opioid withdrawal increases expression of c-fos immunoreactivity in rat periaqueductal gray neurons which project to the rostral ventromedial medulla.

Expression of c-fos-like immunoreactivity has been used as a marker for neuronal activation and is elevated in the periaqueductal gray following stressful and noxious stimuli, and opioid withdrawal. The present study examined the staining of c-fos-like immunoreactivity following opiate withdrawal or swim-stress (2.5-3 min at 21 degrees C) in periaqueductal gray neurons of the rat which had projections to and through the rostral ventromedial medulla identified by microinjection of the retrograde tracer, Fast Blue, into the nucleus raphe magnus prior to development of morphine dependence. Both naloxone-precipitated withdrawal and swim-stress increased numbers of neurons expressing c-fos-like immunoreactivity in periaqueductal gray. Naloxone-precipitated withdrawal did not increase the number of double-labelled neurons in periaqueductal gray suggesting that neurons excited during opioid withdrawal do not project to the ventromedial medulla. In contrast, swim-stress produced increases in double-labelled neurons in periaqueductal gray suggesting that many periaqueductal gray neurons activated by swim-stress project to the ventromedial medulla. These findings suggest that naloxone-precipitated withdrawal does not activate ventrolateral periaqueductal gray neurons which are involved in descending inhibitory pathways, consistent with behavioural observations that naloxone-precipitated withdrawal is qualitatively opposite to electrical and chemical stimulation of the ventrolateral periaqueductal gray. The results are also consistent with a role of descending projections from periaqueductal gray in stress-induced antinociception.

The mu-opioid receptor antagonist D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP) [but not D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP)] produces a nonopioid receptor-mediated increase in K+ conductance of rat locus ceruleus neurons.

The somatostatin analogues D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP) and D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) have been used widely as selective antagonists of mu-opioid receptors. Actions of CTOP and CTAP on the membrane properties of rat locus ceruleus neurons were studied using intracellular recordings of membrane currents in superfused brain slices. CTOP increased a K+ conductance with an EC50 of 560 nM. The maximal conductance increase produced by CTOP (10 microM) was similar to that produced by high concentrations of the mu-opioid agonists D-Ala-Met-enkephalinglyol (1 microM) and Met-enkephalin (10 microM), as well as an alpha 2-adrenoceptor agonist (UK14304, 3 microM) and somatostatin (1 microM). The K+ current produced by CTOP was not antagonized by naloxone (1 microM), suggesting it was not mediated by mu-opioid receptors. The K+ currents induced by high concentrations of CTOP desensitized to 42% of the initial maximum after prolonged superfusion (t1/2 = 247 sec). In the presence of fully desensitized CTOP responses, somatostatin (1 microM) still produced near-maximal K+ currents; i.e., there was no cross-desensitization, which suggests that CTOP might act on a receptor distinct from somatostatin receptors. However, the converse did not apply; high concentrations of CTOP (30 microM) did not produce any additional current in the presence of desensitized somatostatin responses. No cross-desensitization was observed between CTOP (10-30 microM) and Met-enkephalin (30 microM) or nociceptin (3 microM) regardless of the order of drug application. Cyclo-(7-aminoheptanoyl-Phe-D-Trp-Lys-Thr[Bzl], antagonized both somatostatin-(KD = 10 microM) and CTOP-(KD = 8 microM) induced K+ currents with similar potency. Concentrations of CTOP (100 nM) that produced a small K+ current partially antagonized the actions of Met-enkephalin (10 microM) on mu-opioid receptors. In contrast to CTOP, CTAP produced no K+ current at concentrations of 300 nM and 1 microM and little current at 10 microM. CTAP potently antagonized K+ currents produced by the mu-opioid receptor agonist D-Ala-Met-enkephalin-glyol, with an equilibrium dissociation constant of 4 nM (Schild analysis). CTAP did not antagonize K+ currents produced by CTOP or somatostatin. These results demonstrate that CTOP is a potent and efficacious agonist at nonopioid receptors, whereas CTAP is a potent mu-opioid receptor antagonist with little nonopioid agonist activity in rat locus ceruleus neurons. The receptor activated by CTOP has yet to be fully resolved but seems to be similar to the somatostatin type 2 receptor or perhaps to a receptor closely related to somatostatin or opioid receptors.

Lesions to terminals of noradrenergic locus coeruleus neurones do not inhibit opiate withdrawal behaviour in rats.

The involvement of neurones of the locus coeruleus (LC) in expression of opiate withdrawal behaviour was tested in morphine-dependent rats using N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP4), a neurotoxin selective for noradrenergic terminals arising from LC. Lesions were validated by determination of cortical noradrenaline concentrations using gas chromatography-mass spectrometry, inhibition of the post-decapitation hindpaw reflex and dopamine-beta-hydroxylase immunohistochemistry. Lesions did not inhibit the expression of any naloxone-precipitated withdrawal signs. These results suggest no involvement of noradrenergic LC neurones in expression of the overt signs of opiate withdrawal, and raise the possibility that previous microinjection and electrolytic lesion studies were confounded by effects on nearby brain regions.

Increased fos-like immunoreactivity in the periaqueductal gray of anaesthetised rats during opiate withdrawal.

Staining of c-fos-like-immunoreactivity (CFIR) in neurones was used to study neuronal activation within subdivisions of periaqueductal gray (PAG), and in locus coeruleus and ventral tegmental area during opiate withdrawal in awake and anaesthetised, morphine-dependent rats. The number of CFIR containing neurones was significantly increased during naloxone-precipitated withdrawal in lateral and ventrolateral, particularly the caudal ventrolateral PAG. No changes were observed in dorsal-intermediate or dorsal-caudal PAG. In awake rats, a similar but more generalised increase in CFIR was observed in PAG following naloxone-precipitated withdrawal. Increases in ventral tegmental area and locus coeruleus during naloxone-precipitated withdrawal under anaesthesia varied greatly between animals. Induction of c-fos in lateral and ventrolateral PAG during withdrawal is consistent with known functions of these regions, involving the integration of autonomic and somatic components of defensive and escape behaviours which are characteristic signs of opiate withdrawal.

Australian funnel-web spider toxin, versutoxin, enhances spontaneous synaptic activity in single brain neurons in vitro.

Neurotoxins isolated from the venoms of Australian funnel-web spiders increase spontaneous action potential activity in a variety of excitable cells. In the present study intracellular recordings were made with microelectrodes (30-60 M omega, 2 M KCl) from locus coeruleus, mesencephalic nucleus of the trigeminal nerve and laterodorsal tegmental neurons in brain slices. Versutoxin, a polypeptide toxin isolated from the venom of Hadronyche versutus produced a profound increase in spontaneous synaptic activity impinging on neurons, which did not fully recover for up to 3 h after washout. The threshold concentration was 1.5 nM in locus coeruleus neurons, with increasing concentrations (up to 50 nM) producing larger effects. A modest increase in synaptic activity was observed in mesencephalic nucleus of the trigeminal nerve neurons during superfusion with 50 nM versutoxin. The increase in spontaneous synaptic activity was reversed by agents which block synaptic potentials impinging on locus coeruleus neurons, i.e., tetrodotoxin (100 nM), Co2+ (3 mM) or the combination of 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM) and bicuculline (30 microM). Threshold, peak amplitude, maximum rate of rise, duration, amplitude of afterhyperpolarisations and interspike intervals of action potentials in each type of neuron were unaffected by versutoxin. Voltage-current relationships were also unaffected. Calcium-dependent action potentials evoked in locus coeruleus neurons in the presence of tetrodotoxin were unaffected by versutoxin, as were depolarisations produced by exogenously applied glutamate. These results suggest that versutoxin increases spontaneous synaptic activity, but has no effect on the membrane properties of the soma of several types of rat brain neurons.