摘要:

Abstract:The time course and magnitude of the effects of product loss on the measurement of local cerebral glucose utilization (LCGU) by the 2‐[14C]deoxyglucose (DG) method were studied by determination of LCGU in 38 rats with 25–120 min experimental periods after a [14C]DG pulse and in 45 rats with experimental periods of 2.5–120 min during which arterial plasma [14C]DG concentrations (CP*) were maintained constant. LCGU was calculated by the operational equation, which assumes no product loss, with the original set of rate constants and with a new set redetermined in the rats used in the present study; in each case the rate constants were those specific to the structure. Data on local tissue14C concentrations andCP* were also plotted according to the multiple time/graphic evaluation technique (“Patlak Plot”). The results show that with both pulse and constant arterial inputs of [14C]DG the influence of the rate constants is critical early after onset of tracer administration but diminishes with time and becomes relatively minor by 30 min. After a [14C]DG pulse calculated LCGU remains constant between 25 and 45 min, indicating a negligible effect of product loss during that period; at 60 min it begins to fall and declines progressively with increasing time, indicating that product loss has become significant. WhenCP* is maintained constant, calculated LCGU does not change significantly over the full 120 min. The “Patlak Plots” reinforced the conclusions drawn from the time courses of calculated LCGU; evidence for loss of product was undetectable for at least 45 min after a pulse of [14C]DG and for at least 60 min after onset of a constant arterial inp

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1990.tb13316.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:X‐ray microprobe analysis was used to determine the effects of axotomy on distribution and concentration (millimoles of element per kilogram dry weight) of Na, P, Cl, K, and Ca in frozen, unfixed sections of rat sciatic nerve. Elemental concentrations were measured in axoplasm, mitochondria, and myelin at 8, 16, and 48 h after transection in small‐, medium‐, and large‐diameter fibers. In addition, elemental composition was determined in extraaxonal space (EAS) and Schwann cell cytoplasm. During the initial 16 h following transection, axoplasm of small fibers exhibited a decrease in dry weight concentrations of K and Cl, whereas Na and P increased compared to control values. Similar changes were observed in mitochondria of small axons, except for an early, large increase in Ca content. In contrast, intraaxonal compartments of larger fibers showed increased dry weight levels of K and P, with no changes in Na or Ca concentrations. Both Schwann cell cytoplasm and EAS at 8 and 16 h after injury had significant increases in Na, K, and Cl dry weight concentrations, whereas no changes, other than an increase in Ca, were observed in myelin. Regardless of fiber size, 48 h after transection, axoplasm and mitochondria displayed marked increases in Na, Cl, and Ca concentrations associated with decreased K. Also at 48 h, both Schwann cell cytoplasm and EAS had increased dry weight concentrations of Na, Cl, and K. The results of this study indicate that, in response to nerve transection, elemental content and distribution are altered according to a specific temporal pattern. This sequence of change, which occurs first in small axons, precedes the onset of Wallerian degeneration in transected

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1990.tb13317.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:A new technology called in vivo spectrophotometry was applied to the quantitative determination of the variations in local acetylcholinesterase (AChE) activities. Repeated measurements of the enzyme activities in the same live animal allowed the study of the in vivo inhibition of AChE by amitriptyline. Interactions between AChE and this tricyclic antidepressant were investigated at the striatal level in anesthetized rats. In this anesthetized model, AChE assays were shown to be stable for ∼8 h. The dose‐effect relationship was explored in the 2.5‐ to 50‐mg/kg amitriptyline range. A reversible inhibition was observed after acute amitriptyline administration. The maximum of inhibition appeared between 90 and 210 min after the intoxication and reached up to 22% for the 50‐mg/kg dose. The threshold dose was established as 8 mg/kg. Evidence for an indirect interaction between tricyclic antidepressant and AChE was demonstrated when the total integrity of the biological system was

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1990.tb13318.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:A single intraventricular injection into adult rats of 100 mouse lethal doses of tetanus toxin (TeTox) produces a marked intracellular redistribution of Ca2+/phosphatidylserine (PtdSer)‐dependent protein kinase C (PKC) activity. Changes are particularly pronounced in hypothalamus, hippocampus, and spinal cord structures. Translocation of PKC from the inactive cytosolic compartment to a membrane‐bound active form is followed by a time‐dependent reduction in both total activity and enzyme protein. The down‐regulation of PKC activity in the hypothalamus is accompanied by a marked increase in a Ca2+/PtdSer‐independent kinase activity, predominantly in the cytosolic fraction. Our data identify PKC as a possible indirect target for TeTox and suggest that down‐regulation of the enzyme may provide a clue for tetanus ne

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1990.tb13319.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:With use of biologically active125I‐labelled δ‐dendrotoxin, a putative K+‐channel ligand, homogeneous, noninteracting, high‐affinity acceptors (KD= 0.32 ± 0.07 nM;Bmax= 0.33 ± 0.04 pmol/mg) were observed in synaptosomes from guinea‐pig cortex. This binding was antagonised noncompetitively by α‐dendrotoxin, an inhibitor of certain fast‐activating, voltage‐gated K+channels. Chemical cross‐linking of the δ‐dendrotoxin‐acceptor complex in synaptosomes yielded two specifically labeled polypeptides with molecular masses of 69 and 82 kilodaltons. Although α‐dendrotoxin prevents the labelling of both these bands, it cross‐linked only a single protein with a molecular mass of 69 kilodaltons. It is concluded that δ‐dendrotoxin interacts with a distinct site on the olig

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1990.tb13320.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:The external plexiform layer of the olfactory bulb is among the brain regions where insulin receptors are most abundant. In vitro binding of porcine125I‐insulin to membranes of dendrodendritic synaptosomes isolated from adult rat olfactory bulbs was studied to test the hypothesis that dendrodendritic synapses are major insulin‐receptive sites in the external plexiform layer of olfactory bulbs. Of the specific insulin binding sites present in a total particulate fraction from the olfactory bulbs, approximately half were recovered in the dendrodendritic synaptosome fraction. The only other subcellular fraction to which substantial insulin binding was observed was the conventional (axodendritic/axosomatic) synaptosome fraction. Analysis of equilibrium binding of insulin to dendrodendritic synaptosomal membranes, at total insulin concentrations of 0.5‐1,000 nM, revealed binding site heterogeneity consistent with a two‐site model for insulin binding to a high‐affinity (KD= 6 nM), low‐capacity (Bmax= 110 fmol/mg of protein) site and a low‐affinity (KD= 190 nM), high‐capacity (Bmax= 570 fmol/mg of protein) site. The results indicate that the intense labeling of the external plexiform layer of the olfactory bulb in autoradiographic studies of insulin binding can be attributed to insulin receptors on dendrodendritic synaptic membranes

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1990.tb13321.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:A phosphatidylinositol 4‐phosphate (PIP) kinase (EC 2.7.1.68) was purified from bovine brain membranes in a six‐step procedure involving solubilization of the enzyme with 170 mMNaCl followed by chromatography on diethylaminoethyl‐cellulose, phosphocellulose, Ultrogel AcA44, hydroxylapatite, and ATP‐agarose. The enzyme preparation was nearly homogeneous and was purified 5,600‐fold with a final specific activity of 85 nmol/min/mg of protein and a yield of 20%. Its molecular mass was 110 kilodaltons, as estimated by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis. The enzyme was specific for PIP; phosphorylation of phosphatidylinositol and diacylglycerol was n

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1990.tb13322.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Abstract:Binding of125I‐ω‐conotoxin GVIA and [3H]nitrendipine to membranes from bovine adrenal medulla was investigated to test for the presence of N‐ and L‐type Ca2+channels in adrenal chromaffin cells. Saturable, high‐affinity binding sites for125I‐ω‐conotoxin and [3H]nitrendipine were detected in a membrane fraction from adrenal medulla. [3H]Nitrendipine binding sites were found to have aKDof 500 ± 170 pMand aBmaxof 26 ± 11 pmol/g of protein.125I‐ω‐Conotoxin binding sites had aKDof 215 ± 56 pMand aBmaxof 105 ± 18 pmol/g of protein, about four times the number of sites found for [3H]nitrendipine.125I‐ω‐Conotoxin binding was potently inhibited by unlabeled toxin and Ca2+but was unaffected by dihydropyridines, verapamil, and diltiazem. [3H]Nitrendipine binding was not affected by ω‐conotoxin, whereas it was inhibited by other dihydropyridines. Bay K 8644 potentiated K+‐evoked cytosolic Ca2+transients measured by fura‐2 fluorescence, and this potentiation was completely blocked by nifedipine. In contrast, ω‐conotoxin had no effect on Bay K 8644‐evoked Ca2+transients. Thus, the binding sites for ω‐conotoxin and for nitrendipine appear to be different. The results confirm the presence of L‐type Ca2+channels and open the possibility of N‐type Ca2+channels as the ω‐c

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1990.tb13323.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1990.tb13326.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1990.tb13327.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY