Selective Alterations of Opiate Receptor Subtypes in Mono sodium Glutamate-Treated Rats

Neonatal treatment of rats with monosodium glutamate (MSG) has been demonstrated to destroy cell bodies of neurons in the arcuate nucleus including the brain beta-endorphin (B-END) system. The effects on opiate receptors of the loss of B-END is unknown. Neonatal rats were treated with MSG as previously described. After reaching maturity (7-9 months), MSG-treated rats and litter-matched untreated control rats were decapitated and brains dissected into brain regions. Opiate receptor assays were run with [ 3 H]morphine (mu receptor ligand) and [ 3 H]D-alanine 2 -D-leucine 5 (DADL) enkephalin (delta receptor ligand) for each brain region for both MSG and control rats simultaneously. Scatchard plot analyses showed a selective increase in delta receptors in the thala-mus only. No corresponding change in mu receptors in the thalamus was found. The cross-competition IC 50 data supported this conclusion, showing a loss in the potency of morphine in displacing [ 3 H]DADL enkephalin in the thalamus of MSG-treated rats. This shift in delta receptors produced an IC 50 displacement pattern in thalamus, ordinarily a mu-rich area, similar to that of striatum or cortex, delta-rich areas, again indicating an increase in delta receptors. Similar changes in delta receptors in other brain regions were not found. These results represent one of the few examples of a selective and localized shift in delta with no change in mu sites. Furthermore, the delta increase may reflect an up-regulation of the receptors in thalamus after chronic loss of the endogenous opioid B-END.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65552/1/j.1471-4159.1983.tb08126.x.pd

Adenylyl cyclases types 1 and 8 promote pro-survival pathways after ethanol exposure in the neonatal brain

Although a wide range of developmental disabilities following fetal alcohol exposure are observed clinically, the molecular factors that determine the severity of these sequelae remain undefined. In mice exposed to ethanol, deletion of adenylyl cyclases (ACs) 1 and 8 exacerbates the neuroapoptosis that occurs in a prolonged post-treatment period; however, it remains unclear whether AC1 and AC8 are critical to the primary or secondary mechanisms underlying ethanol-induced neurodegeneration. Here we demonstrate that mice lacking AC1 and AC8 (DKO) display significantly increased apoptosis in the striatum, a region sensitive to neuroapoptosis in the acute post-treatment period, compared to WT controls. The enhanced neuroapoptotic response observed in the striatum of DKO mice is accompanied by significant reductions in phosphorylation of known pro-survival proteins, insulin receptor substrate-1 (IRS-1), Akt and extracellular signal-regulated kinases (ERKs). These data suggest that AC1/AC8 are crucial activators of cell survival signaling pathways acutely following ethanol exposure and represent molecular factors that may directly modulate the severity of symptoms associated with Fetal Alcohol Syndrome

Evaluation of striped bass stocks in Virginia, monitoring and tagging studies, 1999-2003 Annual report, 1 September 1999 - 31 October 2000

To document continued compliance with Federal law, the Anadromous Fishes Program of the Virginia Institute of Marine Science (VIMS) has monitored the size and age composition, sex ratio and maturity schedules of the spawning striped bass stock in the Rappahannock River since December 1981 utilizing commercial pound nets and, since 1991, variable-mesh experimental gill nets. Spawning stock assessment was expanded to include the James River in 1994 utilizing 11 commercial fyke nets and variable-mesh experimental gill nets. The use of fyke nets was discontinued after 1997. In conjunction with the monitoring studies, tagging programs have been conducted in the James and Rappahannock rivers since 1987 . These studies were established to document the migration and relative contribution of these Chesapeake Bay stocks to the coastal population and to provide a means to estimate inter-year survival rates (S). With the reestablishment of fall recreational fisheries in 1993, the tagging studies were expanded to include the York River and western Chesapeake Bay to provide a direct estimation of the resultant fishing mortality (F). This document reports the results of our tagging and monitoring activities during the period 1 September 1999 through 31 October 2000. It includes an assessment of the biological characteristics of striped bass taken from the 2000 spring spawning run, estimates of annual survival based on annual spring tagging, and the results of the fall 1999 directed mortality study that is cooperative with the Maryland Department of Natural Resources. The information contained in this report is required by the Atlantic States Marine Fisheries Commission and is used to implement a coordinated management plan for striped bass in Virginia, and along the eastern seaboard

Evaluation of striped bass stocks in Virginia, monitoring and tagging studies, 1999-2003 Annual report, 1 September 2000 - 31 October 2001

This report presents the results of striped bass (Marone saxatilis) tagging and monitoring activities in Virginia during the penod 1 September 2000 through 31 October 2001. It includes an assessment of the biological characteristics of striped bass taken from the 2001 spring spawning run, estimates of annual survtval based on annual spring tagging, and the results of the fall 2000 directed mortality study that is cooperative with the Maryland Department of Natural Resources. The information contained in this report is required by the Atlantic States Marine Fisheries Commission and is used to implement a coordinated management plan for striped bass in Virginia, and along the eastern seaboard

Behavioral Consequences of NMDA Antagonist-Induced Neuroapoptosis in the Infant Mouse Brain

Background: Exposure to NMDA glutamate antagonists during the brain growth spurt period causes widespread neuroapoptosis in the rodent brain. This period in rodents occurs during the first two weeks after birth, and corresponds to the third trimester of pregnancy and several years after birth in humans. The developing human brain may be exposed to NMDA antagonists through drug-abusing mothers or through anesthesia. Methodology/Principal Findings: We evaluated the long-term neurobehavioral effects of mice exposed to a single dose of the NMDA antagonist, phencyclidine (PCP), or saline, on postnatal day 2 (P2) or P7, or on both P2 and P7. PCP treatment on P2 + P7 caused more severe cognitive impairments than either single treatment. Histological examination of acute neuroapoptosis resulting from exposure to PCP indicated that the regional pattern of degeneration induced by PCP in P2 pups was different from that in P7 pups. The extent of damage when evaluated quantitatively on P7 was greater for pups previously treated on P2 compared to pups treated only on P7. Conclusions: These findings signify that PCP induces different patterns of neuroapoptosis depending on the developmental age at the time of exposure, and that exposure at two separate developmental ages causes more severe neuropathological and neurobehavioral consequences than a single treatment

Evaluation of Striped Bass Stocks in Virginia: Monitoring Studies, 1993-1998 Completion Report 1 September 1997 - 31 October 1998

To document continued compliance with Federal law, the Virginia Institute of Marine Science (VIMS) Anadromous Program (AP) has monitored the size and age composition, sex ratio and maturity schedules of the spawning striped bass stock in the Rappahannock River since December 1981 utilizing commercial pound nets and, since 1991, variable-mesh experimental anchored gill nets. Spawning stock assessment was expanded to include the James River in 1994 utilizing extant commercial fyke nets and variable-mesh experimental gill nets. The use of fyke nets was discontinued after 1997. Tagging programs have been conducted in the James and Rappahannock rivers since 1987 in conjunction with the monitoring studies. These studies were established to document the migration and relative contribution of these Chesapeake Bay stocks to the coastal population and to provide a mean to estimate inter-year survival rates (S). The tagging studies were expanded to the York River and western Chesapeake Bay to provide a direct estimation of the resultant fishing mortality (F) with the re-establishment of fall recreational fisheries in 1993 . Because of low stock levels of striped bass in the recent past, and the variable nature of their population dynamics, Chesapeake Bay stocks may or may not be contributing their full potential to the coastal population which supports the fisheries north of Chesapeake Bay. Therefore, the information contained in this report is important to the development and implementation of a coordinated management plan for striped bass in Virginia, and along the eastern seaboard

Evaluation of striped bass stocks in Virginia, monitoring and tagging studies, 1999-2003 Annual report, 1 August 2002 - 31 August 2003

This report presents the results of striped bass (Marone saxatilis) tagging and monitoring activities in Virginia during the period 1 August 2002 through 31 August 2003. It includes an assessment ofthe biological characteristics of striped bass taken from the 2003 spring spawning run, estimates of annual survival based on annual spring tagging, and the results ofthe fall2002 directed mortality study that is cooperative with the Maryland Department of Natural Resources. The information contained in this report is required by the Atlantic States Marine Fisheries Commission and is used to implement a coordinated management plan for striped bass in Virginia, and along the eastern seaboard

Alcohol-induced apoptosis of oligodendrocytes in the fetal macaque brain

BACKGROUND: In utero exposure of the fetal non-human primate (NHP) brain to alcohol on a single occasion during early or late third-trimester gestation triggers widespread acute apoptotic death of cells in both gray and white matter (WM) regions of the fetal brain. In a prior publication, we documented that the dying gray matter cells are neurons, and described the regional distribution and magnitude of this cell death response. Here, we present new findings regarding the magnitude, identity and maturational status of the dying WM cells in these alcohol-exposed fetal NHP brains. RESULTS: Our findings document that the dying WM cells belong to the oligodendrocyte (OL) lineage. OLs become vulnerable when they are just beginning to generate myelin basic protein in preparation for myelinating axons, and they remain vulnerable throughout later stages of myelination. We found no evidence linking astrocytes, microglia or OL progenitors to this WM cell death response. The mean density (profiles per mm(3)) of dying WM cells in alcohol-exposed brains was 12.7 times higher than the mean density of WM cells dying by natural apoptosis in drug-naive control brains. CONCLUSIONS: In utero exposure of the fetal NHP brain to alcohol on a single occasion triggers widespread acute apoptotic death of neurons (previous study) and of OLs (present study) throughout WM regions of the developing brain. The rate of OL apoptosis in alcohol-exposed brains was 12.7 times higher than the natural OL apoptosis rate. OLs become sensitive to the apoptogenic action of alcohol when they are just beginning to generate constituents of myelin in their cytoplasm, and they remain vulnerable throughout later stages of myelination. There is growing evidence for a similar apoptotic response of both neurons and OLs following exposure of the developing brain to anesthetic and anticonvulsant drugs. Collectively, this body of evidence raises important questions regarding the role that neuro and oligo apoptosis may play in the human condition known as fetal alcohol spectrum disorder (FASD), and also poses a question whether other apoptogenic drugs, although long considered safe for pediatric/obstetric use, may have the potential to cause iatrogenic FASD-like developmental disability syndromes

Evaluation of striped bass stocks in Virginia, monitoring and tagging studies, 1999-2003 Annual report, 1 September 2001 - 31 October 2002

This report presents the results of striped bass (Marone saxatilis) tagging and monitoring activities in Virginia during the penod 1 September 2001 through 31 October 2002. It includes an assessment of the biological characteristics of striped bass taken from the 2002 spring spawning run, estimates of annual survtval based on annual spring tagging, and the results of the fall 2001 directed mortality study that is cooperative with the Maryland Department of Natural Resources. The information contained in this report is required by the Atlantic States Marine Fisheries Commission and is used to implement a coordinated management plan for striped bass in Virginia, and along the eastern seaboard