Restraint stress-induced changes in endogenous zinc release from the rat hippocampus

Itoh, Toshihiro; Saito, Takeshi; Fujimura, Morihiro; Watanabe, Sho; Saito, Kazuo

doi:10.1016/0006-8993(93)91283-x

Cited by 52 publications

(32 citation statements)

References 30 publications

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“…There are reports of increases in extracellular glutamate in response to relatively severe stress such as restraint, forced swimming or tail shock (Itoh, Saito, Fujimara, Watanabe & Saito, 1993;Keefe et al 1993;Lowy, Gault & Yamamoto, 1993;Moghaddam, 1993). In the present study we have used microdialysis in the striatum of freely moving rats to monitor both basal glutamate levels and changes resulting from mild physiological stimulation.…”

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confidence: 98%

The source of physiologically stimulated glutamate efflux from the striatum of conscious rats.

Miele

Boutelle

Fillenz

1996

The Journal of Physiology

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1. Glutamate in the extracellular compartment of the striatum of freely moving rats was monitored at 5 min intervals using microdialysis and an enzyme-based assay. 2. Basal levels of dialysate glutamate were 3-6 + 05 1uM. Local infusion through the dialysis probe of tetrodotoxin (TTX), cadmium chloride or magnesium chloride produced no reduction in basal levels of glutamate; with the latter two there was, instead, an increase. 3. Neuronal activation stimulated by induced grooming was accompanied by an increase in total glutamate efflux of 47 5 + 25-0% above basal level; this increase was not reduced by local infusion of 'ITX. 4. We propose that the ITX-insensitive release of glutamate in response to physiological stimulation is derived from glial cells and is a Ca2+-dependent mechanism triggered by a receptor-mediated release of Ca2+ from internal stores that spreads through the network of astrocytes.Glutamate is the main central excitatory transmitter in the vertebrate nervous system. This function has been extensively investigated using electrophysiological techniques. However glutamate, as well as being a neurotransmitter, has an additional role in energy and nitrogen metabolism. As a result, it is present in relatively high concentration in the cytoplasm of all neurones, as well as glia.

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confidence: 98%

The source of physiologically stimulated glutamate efflux from the striatum of conscious rats.

Miele

Boutelle

Fillenz

1996

The Journal of Physiology

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“…Superoxide dismutase may also be involved (38). "These changes may be irreversible" (37 (43,44), and brain Zn (45).…”

Section: Individual Ids Descriptionsmentioning

confidence: 99%

“…With (126)(127)(128) and chlorpyrifos with other OP pesticides (109,114 Zinc deficiency has been widely investigated in the last two decades and is now recognized to be a public health problem (132); a recent estimate is that 30% of the adult U.S. population is at risk. Zinc is centrally involved in multiple human systems (133), induding GABA and other neurotransmitter enabling (24,45,(134)(135)(136)(137), and in sequestering and defense against heavy metals and chemicals (138). Gestational Zn deficiency appears to damage hippocampal and other functions (44,45,139,140).…”

Section: Individual Ids Descriptionsmentioning

confidence: 99%

“…Zinc is centrally involved in multiple human systems (133), induding GABA and other neurotransmitter enabling (24,45,(134)(135)(136)(137), and in sequestering and defense against heavy metals and chemicals (138). Gestational Zn deficiency appears to damage hippocampal and other functions (44,45,139,140). Chronic Zn deficiency reduces the IRA by deactivation of thymulin (133,(141)(142)(143)(144) (19,(145)(146)(147)(148) (158), including the brain (158), and it can cross the blood-brain barrier (159).…”

Section: Individual Ids Descriptionsmentioning

confidence: 99%

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Integrated Defense System Overlaps as a Disease Model: With Examples for Multiple Chemical Sensitivity

Rowat¹

1998

Environmental Health Perspectives

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“…This phenomenon is not unique to uranium as previous -studies demonstrated that stress alters trace metal distribution and clearance. For example, brain zinc levels are reported to decrease by 30% following cold-restraint stress, while stress increases serum and urinary zinc levels (Spencer et al, 1985;Itoh et al, 1993;Izgut-Uysal et al, 2000). In a similar manner, stress might alter the subcellular distribution of uranium such that more metal is in a readily exchangeable state, resulting in decreased brain uranium and increased serum uranium.…”

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confidence: 99%

Multifactorial Assessment of Depleted Uranium Neurotoxicity

Jortner¹

2004

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Public reporting burden for this collection of Information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of Information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302, and Tables Abstracts Manuscripts Introduction This is a four-year study on the neurotoxic potential of depleted uranium (DU) in laboratory rats. Previous studies with Gulf War veterans and experimental animals exposed to embedded DU suggest that neurotoxicity may result from DU exposure (McDiarmid eta!. 2000; Pellmar eta/., 1999). The current investigation is designed to assess the neurotoxic potential of acute and chronic exposure to DU and the contribution of stress to expression of DU neurotoxicity and kinetics. All studies are being performed with adult male Sprague-Dawley rats. As noted in the Table below, the components of this project are as follows: 1-Dose-finding and preliminary toxicokinetic studies of DU. These were conducted in the Year 1 of the project 2-Pilot stress study-To obtain an optimal model of experimental stress for use in the acute and chronic DU exposure studies. This was done in Year 2 and Year 3. 3-Acute neurotoxicity of soluble DU (uranyl acetate)-To determine nervous system kinetics and toxicity of DU. This was a major focus in Year 3. The in-life portion was done, and the neurobehavioral and most of the neurochemical data were obtained and analyzed. Neuropathological studies of the brain were also performed in this year. Tissue uranium assays were done in part. 4-Long-term toxicity study-This will assess chronic exposures from implanted solid DU particles, a model of some Gulf War casualties. This study began in Year 3, and is in progress. STRESS THAT RESULTED IN MARKED, TRANSIENT ELEVATION OF PLASMA CORTICOSTERONE. CLINICAL, NEUROCHEMICAL AND PATHOLOGICAL STUDIES WERE UNDERTAKEN. MAJOR FINDINGS WERE TRANSIENT DECREASE IN DOPAMINE IN THE CAUDATE-PUTAMEN ON POST-DOSING DAY 3 IN THE HIGH DOSE, UNSTRESSED ANIMALS. THERE WERE DU-RELATED DECREASES IN MOTOR ACTIVITY, BODY WEIGHT GAIN AND FORELIMB GRIP STRENGTH. DU DOSE-RELATED RENAL TUBULAR NECROSIS WAS ALSO SEEN, AND MAY HAVE CONTRIBUTED TO THESE CLINICAL FINDINGS. STRESS HAD NO EFFECT ON THE RENAL DISEASE OR THE CLINICAL CHANGES, EXCEPT FOR A PROTECTIVE EFFECT IN THE GRIP STRENGTH. TASK 4, A LONG-TERM DU-IMPLANTATION/STRESS STUDY, WASMethods for both the acute and chronic (3, 4 -above) studies employed the following procedures. Inductively coupled plasma-mass spectrometry (ICP-MS) analysis to assess the kinetics of uranium in the cerebral cortex, hippocampus, striatum, and cerebellum at selected periods after DU administration. Neurotoxicity is as...

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Restraint stress-induced changes in endogenous zinc release from the rat hippocampus

Cited by 52 publications

References 30 publications

The source of physiologically stimulated glutamate efflux from the striatum of conscious rats.

The source of physiologically stimulated glutamate efflux from the striatum of conscious rats.

Integrated Defense System Overlaps as a Disease Model: With Examples for Multiple Chemical Sensitivity

Multifactorial Assessment of Depleted Uranium Neurotoxicity

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