Decabromodiphenyl ether (BDE 209), the major congener in the high volume industrial flame retardant mixture "DecaBDE", has recently been shown to be metabolized by carp. To further explore this phenomenon, juvenile rainbow trout were exposed to BDE 209 via the diet for a five month period. Analysis of the whole body homogenate, liver, serum, and intestinal tissues revealed that BDE 209 accumulated in rainbow trout tissues and was most concentrated in the liver. In addition to BDE 209, several hepta-, octa-, and nonaBDE congeners also accumulated in rainbow trout tissues over the same period as a result of BDE 209 debromination. Based on the total body burden of the hepta- through decaBDE congeners, uptake of BDE 209 was estimated at 3.2%. Congener profiles were different among whole body homogenate, liver, and serum, with the whole body homogenates having a greater contribution of the debrominated biotransformation products. Extracts of the rainbow trout whole body homogenates were compared with extracts from a previous experiment with common carp. This comparison revealed that BDE 202 (2,2',3,3',5,5',6,6'-octabromodiphenyl ether) was a dominant debromination product in both studies. To determine whether the observed debromination was metabolically driven, liver microsomal fractions were prepared from both common carp and rainbow trout. Analysis of the microsomal fractions following incubation with BDE 209 revealed that rainbow trout biotransformed as much as 22% of the BDE 209 mass, primarily to octa- and nonaBDE congeners. In contrast, carp liver microsomes biotransformed up to 65% of the BDE 209 mass, primarily down to hexaBDE congeners. These microsomal incubations confirm a metabolic pathway for BDE 209 debromination.
The production and use of nonpolybrominated diphenyl ether (non-PBDE), brominated flame retardant (BFR) alternatives have been on the rise, although their assessment in environmental samples is largely understudied. In the present study, several non-PBDE BFRs were found in the egg pools of herring gulls (Larus argentatus) from seven colonies in the five Laurentian Great Lakes (collected in 1982 to 2006). Of the 19 BFRs monitored, hexabromobenzene (HBB), 1,2-bis(2,4,6-tribromophe-noxy)ethane (BTBPE), decabromodiphenyl ethane (DBDPE), and alpha-, beta-, gamma-, and delta-isomers of 1,2-dibromo-4-(1,2-dibromoeth-yl)cyclohexane (TBECH) were present in eggs from all the colonies with the highest detection frequencies of 100%, 54%, 9% and 97%, respectively. In 2005 and 2006 eggs, the concentrations of DBDPE were highest at three of the seven colonies (1.3 to 288 ng/g wet weight (ww)) and surpassed decabromodiphenyl ether (BDE-209). HBB (0.10 to 3.92 ng/g ww), BTBPE (1.82 to 0.06 ng/g ww), and Sigma-TBECH (0.04 to 3.44 ng/g ww; mainly the beta-isomer 52 to 100% of Sigma-TBECH) were detected at lower concentrations (and generally <
Electrophysiological studies were made on microcultures (300-500 Ism in diameter) in which solitary sympathetic principal neurons from newborn rats grew on previously dissociated rat heart cells. (1,6,7,8). In contrast, when the neurons are cultured in the presence of nonneuronal cells (e.g., from ganglia or heart), or in medium conditioned by such cells, the neuronal population synthesizes both AcCh and NE (2, 9), and many neurons form nicotinic cholinergic synapses on each other (6-8, 10, 11). These effects are graded. A higher proportion of conditioned medium or a greater number of nonneuronal cells gives a higher ratio of AcCh synthesis to catecholamine synthesis (12), a higher incidence of cholinergic transmission, and a higher proportion of synapses which lack small granular vesicles (13 (MacLeish, unpublished). He found that the incidence of detectable neuronmyocyte interaction was too low to be useful, perhaps in part because the endings of each neuron were sparsely distributed in the large field of myocytes; the few cases found all appeared to be cholinergic.It was plausible that the incidence of detectable interaction would increase if the innervation field of a given neuron was concentrated on a few cardiac myocytes. Thus, we made microcultures containing a single neuron and a small number of myocytes in an area only a fraction of a millimeter in diameter. In this paper, we report physiological observations on such microcultures; in the accompanying paper, Landis (15) reports electron microscopic observations on the same microcultures.In two previous studies (16, 17), explants of sympathetic ganglia were found to make functional contacts with explants of heart. METHODSSeveral methods for making microcultures suitable for electrophysiology and microscopy were successful, but none routinely so. The simplest method was, in brief, to apply 25 to 50 equally spaced droplets of dissolved collagen to a nonwetting polystyrene surface. When dried, these produced a grid (ca 50 mm2) of collagen islands, each island 300-500 Atm in diameter.Cardiac cells (myocytes and fibroblasts) were dissociated from hearts of newborn rats by use of collagenase (EC 3.4.24.3) (Worthington Type I; 1 mg/ml), and allowed to settle on the grid for about 2 hr. Almost all cells not adhering to the collagen islands could then be washed away with medium. Proliferation of the cardiac cells was suppressed after 1-2 days by y-irradiation (60Co; 5000 rads in 25-30 sec, where one rad equals 1 X 10-2 J/kg). One to 5 days later, principal neurons were dissociated from superior cervical ganglia of newborn rats (Charles River CD) as previously described (1,18), and plated at a density such that many islands received only one or a few neurons. The cultures were grown in L-15 CO2 medium (1) containing 5% adult rat serum or 10% fetal calf serum (Microbiological Associates, 14-414), but lacking bovine serum albumin and Methocel. Six platings (about 30 dishes per plating) were used in experiments reported here.For electrophysiological recordi...
A large percentage of patients with schizophrenia are characterized by an abnormality in P50 sensory gating. This abnormality has been shown to be genetically linked to the alpha-7 nicotinic receptor and is transiently reversed by acute nicotine administration. These observations have led to the development of pharmacological treatments designed to improve sensory gating. However, if normalization of P50 gating abnormalities is to guide drug development, then it becomes important to delineate the clinical correlates of enhanced P50 gating. We conducted a review of all available articles through March 2005 that have examined this issue. We found that, despite the prominent role that P50 abnormalities have played in our understanding of schizophrenia, there is a relative dearth of data examining P50 clinical correlates. There is evidence suggestive of an association between P50 and measures of attention, and multiple studies have failed to document a cross-sectional or longitudinal relationship between P50 and positive, negative, or other symptoms. These results suggest that considerably more work needs to be done to understand and validate the clinical significance of this impairment.
Drug dependence is characterized bydysregulation of brain reward systems and increased sensitivity to stress. Chronic exposure to drugs of abuse is associated with increased expression of the neuropeptide dynorphin, the endogenous ligand for kappa opioid receptors (KORs). Activation of KORs causes depressive- and aversive-like responses in rodents, raising the possibility that drug-induced upregulation of dynorphinplays a role independence-associated negative states. Here we used “binge” exposure to cocaine (3 daily intraperitoneal injections of 15 mg/kg for 14 days) to examine the development of dependence-like behavior in the intracranial self-stimulation (ICSS) test and the forced swim test (FST). When rats were tested immediately before their first scheduled injection of each day—a period of drug withdrawal corresponding to 20 hr after their last injection on the previous day—there were exposure-dependent increases in ICSS thresholds (a putative indicator of anhedonia) and decreases in latencies to immobility in the FST (a putative indicator of behavioral despair). Administration of the long-lasting KOR antagonist norBNI (20 μg, intracerebroventricular) before the beginning of the binge regimen attenuated the development of cocaine withdrawal-induced anhedonia in the ICSS test. In contrast, administration of norBNI in the midst of the binge regimen had no effect on expression of cocaine withdrawal-induced anhedonia in the ICSS test, although it did attenuate despair-like behavior in the FST. These data suggest that blockade of KORs before exposure to a stressor (in this case, cocaine withdrawal or forced swimming) can attenuate the development of stress-induced behavioral adaptations.
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