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PubMed1991

Localization of cholinergic differentiation factor/leukemia inhibitory factor mRNA in the rat brain and peripheral tissues.

Sympathetic neurons display considerable plasticity in the neurotransmitter and neuropeptide phenotypes they express in vitro and in vivo. The cholinergic differentiation factor (CDF, also known as leukemia inhibitory factor, LIF) induces cultured rat sympathetic neurons to become cholinergic, without affecting their survival or growth. To understand the role of this factor in normal development, it is essential to determine where it is produced in situ. To localize CDF/LIF mRNA, a semiquantitative, reverse transcription-polymerase chain reaction method was employed. Actin and tubulin mRNA were used as internal controls, and two different sets of CDF/LIF primers were compared. In postnatal rat peripheral tissues, CDF/LIF mRNA was selectively localized in the target area of developing, sympathetic cholinergic neurons; the mRNA was not detected in the targets of sympathetic noradrenergic neurons. This finding supports the hypothesis that CDF/LIF is a target-derived neuronal differentiation factor. In postnatal rat brain, CDF/LIF mRNA is localized selectively in two parts of the visual system, visual cortex and superior colliculus. Thus, CDF/LIF may play a role in this system as well.

Aging↗
PubMed1988

Sex hormone-binding globulin in the diagnosis of peripheral tissue resistance to thyroid hormone: the value of changes after short term triiodothyronine administration.

Thyroid hormone is one of several factors that modulate the level of sex hormone-binding globulin (SHBG) in serum. SHBG levels are usually elevated in thyrotoxicosis and have been reported to be normal in a few patients with generalized resistance to thyroid hormone (GRTH). This study was designed to determine whether basal serum SHBG levels or the SHBG response to short term T3 administration could be used as an index of thyroid hormone action and thus serve as a test for the evaluation of patients suspected of having peripheral tissue resistance to thyroid hormone. Serum SHBG, total T4, free T4 index (FT4I), total T3, and TSH levels were measured in 21 normal subjects, 28 hypothyroid patients, 20 thyrotoxic patients, and 10 patients with GRTH. Excluding patients with GRTH, serum basal SHBG values were correlated with FT4I values (r = 0.66; P less than 0.0001). Mean SHBG levels in the patients with GRTH [37.6 +/- 16.2 (+/- SD) nmol/L] were not significantly different from those in the normal subjects (35.1 +/- 19.3 nmol/L) or hypothyroid patients (26.3 +/- 17.1 nmol/L), but were significantly lower than those in the thyrotoxic group (64.7 +/- 19.2 nmol/L; P less than 0.001). All 10 patients with GRTH had basal SHBG values in the normal range, but 7 of 20 (35%) thyrotoxic patients also had normal basal SHBG values. T3 was given orally for three sequential 3-day periods at doses of 50, 100, and 200 micrograms daily to 7 normal subjects, 11 hypothyroid and 3 thyrotoxic patients, and all 10 patients with GRTH. The serum SHBG concentration was measured on the last day at each dosage level. During T3 administration, SHBG levels increased in all individuals with normal tissue responsiveness. The increase above the basal value (delta SHBG) at each T3 dose was similar in normal, hypothyroid, and thyrotoxic individuals (non-resistant subjects). After administration of 50 micrograms T3 daily, the mean delta SHBG level was decreased [-2.9 +/- 5.3 (+/- SD) nmol/L] in the resistant patients and increased (4.0 +/- 4.9 nmol/L; P less than 0.005) in the nonresistant subjects. After administration of 100 micrograms T3 daily, the mean delta SHBG was -4.5 +/- 6.8 nmol/L in the resistant patients and 8.6 +/- 5.1 nmol/L (P less than 0.0001) in the nonresistant subjects. Serum SHBG decreased by more than 2 nmol/L in 6 of 10 (60%) resistant patients, but in no nonresistant subject.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1999

Effect of vitamin E intake on levels of vitamins E and C in the central nervous system and peripheral tissues: implications for health recommendations.

Vitamin E (alpha-gamma-tocopherol) is an important component in biological membranes. A decrease in its concentration imposes structural and functional damage to the cells. The object of this study was to assess the effect of a graded dietary vitamin E (E) intake on E concentration in specific regions of the brain, and its influence on vitamin C levels and neurological function. Following a 2-month period, rats supplemented with 5, 30, 60, 250 or 500 mg all-rac-alpha-tocopherol-acetate/kg diet (mg E/kg diet) exhibited a significant increase of E concentration in brain and peripheral tissues. However, while blood and liver showed a dose response increase in E concentration which correlated well with the different levels of E in the diet, the central nervous system (CNS) followed the same pattern of increase of vitamin E in brain tissue only when the diet was supplemented with 5, 30, or 60 mg E/kg diet. No further increase in E concentration was observed when the diet was supplemented with 250 or 500 mg E/kg diet. Similarly, the heart tissue showed a significant increase in its E concentration when the was enriched with 5, 30, or 60 mg E/kg diet, with no further increases at 250 or 500 mg. Vitamin C concentration in brain cortex and cerebellum, plasma, liver, and heart was reduced in the groups receiving 250 or 500 mg E/kg diet. Compared to the low E group, rats supplemented with the 60, 250 or 500 mg E/kg diet showed a significant enhancement in striatal dopamine (DA) release, but no differences were observed among the latter three groups.

Animals↗
PubMed1994

Binding of the anti-inflammatory steroid deflazacort to glucocorticoid receptors in brain and peripheral tissues. In vivo and in vitro studies.

Deflazacort (DFC) is a heterocyclic glucocorticoid with anti-inflammatory activity but with decreased side effects. In this study, we have evaluated the capacity of DFC and other glucocorticoids to reach the central nervous system (CNS) in vivo by measuring changes of [3H]dexamethasone (DEX) binding to glucocorticoid receptors (GR) in vitro. GR occupation was effected by DEX in the cerebral cortex, hippocampus, pituitary, liver and thymus, with DFC showing a similar profile except for the cerebral cortex. In contrast, corticosterone weakly occupied GR in the thymus, pituitary and hippocampus and methyl-prednisolone was active only in peripheral tissues. Furthermore, IC50 for DEX in vitro amounted to 15-17 nM in the hippocampus and liver, whereas IC50 for the active metabolite 21-deacetyl-DFC (21-OH-DFC) was 4 times higher. 21-OH-DFC bound to type II and was absent from type I GR. When tested in equipotent doses based on IC50 analysis, DFC and DEX similarly induced in vivo ornithine decarboxylase activity in hippocampus and liver, although body weight loss after chronic treatment was significantly less for DFC. The results show that DFC distributes on the CNS similarly to DEX, induces ornithine decarboxylase activity but presents less intensive catabolic effects, making it suitable for use as an anti-inflammatory steroid during chronic therapeutic regimes.

Animals↗
PubMed2006

Early resuscitation with polymerized bovine hemoglobin reverses acidosis, but not peripheral tissue oxygenation, in a severe hamster shock model.

Awake hamsters equipped with the dorsal window chamber preparation were subjected to hemorrhage of 50% of the estimated blood volume. Initial resuscitation (25% of estimated blood volume) with polymerized bovine hemoglobin (PBH) or 10% hydroxyethyl starch (HES) occurred in concert with an equivolumetric bleeding to simulate the early, prehospital setting (exchange transfusion). Resuscitation (25% of estimated blood volume) without bleeding was performed with PBH, HES, or autologous red blood cells (HES-RBCs). Peripheral microcirculation, tissue oxygenation, and systemic hemodynamic and blood gas parameters were assessed. After exchange transfusion, base deficit was -8.6 +/- 3.7 mmol/L (PBH) and -5.1 +/- 5.3 mmol/L (HES) (not significant). Functional capillary density was 17% +/- 6% of baseline (PBH) and 31% +/- 11% (HES) (P < 0.05) and arteriolar diameter 73% +/- 3% of baseline (PBH) and 90% + 5% (HES) (P < 0.01). At the end, hemoglobin levels were 3.7 +/- 0.3 g/dL with HES, 8.2 +/- 0.6 g/dL with PBH, and 10.4 +/- 0.8 g/dL with HES-RBCs (P < 0.01 HES vs. PBH and HES-RBCs, P < 0.05 PBH vs. HES-RBCs). Base excess was restored to baseline with PBH and HES-RBCs, but not with HES (P < 0.05). Functional capillary density was 46% +/- 5% of baseline (PBH), 62% + 20% (HES-RBCs), and 36% +/- 19% (HES) (P < 0.01 HES-RBCs vs. HES). Peripheral oxygen delivery and consumption was highest with HES-RBCs, followed by PBH (P < 0.05 HES-RBCs vs. PBH, P < 0.01 HES-RBCs and PBH vs. HES). In conclusion, the PBH led to a correction of base deficit comparable to blood transfusion. However, oxygenation of the peripheral tissue was inferior with PBH. This was attributed to its negative impact on the peripheral microcirculation caused by arteriolar vasoconstriction.

Acidosis↗
PubMed1996

Evaluation of pituitary and peripheral tissue markers of thyroid hormone action in an Iranian family with resistance to thyroid hormone.

Resistance to thyroid hormone (RTH), an inherited syndrome of reduced sensitivity to thyroid hormone, is being detected with increased frequency. We report the first family with RTH identified in Iran. Goiter prompted thyroid evaluation, and nonsuppressed TSH associated with high free T4, suggested RTH as the etiology. The mother and all four of her children expressed the RTH phenotype associated with attention deficit and hyperactivity. Detailed clinical and laboratory studies before and following the administration of graded doses of L-T3 demonstrated relatively severe resistance to the hormone at the level of the thyrotrophs and peripheral tissues. Our data underscore the importance of evaluating the changes of various parameters of thyroid hormone action in response to thyroid hormone rather than their measurement at baseline or assessment of absolute levels.

Adolescent↗
PubMed1999

Endogenous proteins controlling amyloid beta-peptide polymerization. Possible implications for beta-amyloid formation in the central nervous system and in peripheral tissues.

We report that certain plasma proteins, at physiological concentrations, are potent inhibitors of amyloid beta-peptide (Abeta) polymerization. These proteins are also present in cerebrospinal fluid, but at low concentrations having little or no effect on Abeta. Thirteen proteins representing more than 90% of the protein content in plasma and cerebrospinal fluid were studied. Quantitatively, albumin was the most important protein, representing 60% of the total amyloid inhibitory activity, followed by alpha1-antitrypsin and immunoglobulins A and G. Albumin suppressed amyloid formation by binding to the oligomeric or polymeric Abeta, blocking a further addition of peptide. This effect was also observed when the incorporation of labeled Abeta into genuine beta-amyloid in tissue section was studied. The Abeta and the anti-diabetic drug tolbutamide apparently bind to the same site on albumin. Tolbutamide displaces Abeta from albumin, increasing its free concentration and enhancing amyloid formation. The present results suggest that several endogenous proteins are negative regulators of amyloid formation. Plasma contains at least 300 times more amyloid inhibitory activity than cerebrospinal fluid. These findings may provide one explanation as to why beta-amyloid deposits are not found in peripheral tissues but are only found in the central nervous system. Moreover, the data suggest that some drugs that display an affinity for albumin may enhance beta-amyloid formation and promote the development of Alzheimer's disease.

Amyloid beta-Peptides↗
PubMed1993

The effect of U-50,488H tolerance-dependence and abstinence on the levels of dynorphin (1-13) in brain regions, spinal cord, pituitary gland and peripheral tissues of the rat.

Male Sprague-Dawley rats were rendered tolerant to and physically dependent on U-50,488H, a kappa-opiate agonist, by injecting 25 mg/kg of the drug intraperitoneally twice a day for 4 days. Two sets of rats were used. Rats labeled as tolerant-dependent were injected with U-50,488H (25 mg/kg) 1 h before sacrificing on day 5, whereas the abstinent rats were sacrificed on day 5 without the injection of U-50,488H. Of all the tissues on day 5 without the injection of U-50,488H. Of all the tissues examined, the pituitary gland had the highest level of dynorphin (1-13), whereas the heart had the lowest level. The levels of dynorphin (1-13) increased in the hypothalamus, hippocampus and pons/medulla of U-50,488H tolerant-dependent rats, whereas in abstinent rats the levels of dynorphin (1-13) were elevated only in the midbrain. The levels of dynorphin (1-13) in the pituitary gland of U-50,488H tolerant-dependent or abstinent rats were unchanged. In peripheral tissues, the levels of dynorphin (1-13) in the heart of U-50,488H tolerant-dependent rats were increased. In the abstinent rats they were elevated in the adrenals, spleen, and the heart but were decreased in the kidneys. Compared to morphine tolerant-dependent and abstinent rats, significant differences in the levels of dynorphin (1-13) in tissues of 50,488H tolerant-dependent and abstinent rats were observed and may explain many pharmacological differences in the mu- and kappa-opiate induced tolerance-dependence and abstinence processes.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1978

Glucose metabolism in intact man: the responsiveness of splanchnic and peripheral tissues to insulin.

Man controls his blood sugar concentration within rather narrow limits, despite wide latitude in the content and timing of meals. Man does not eat constantly; rather, he alternates between periods of "feasting" and "fasting." It is a useful generalization that the metabolic environment is altered such that forces promoting substrate storage are dominant during the postprandial period and forces that encourage substrate mobilization are prominent during food-free intervals. In this report, we shall primarily examine the role of insulin, the hormone of carbon storage, in maintaining glucose homeostasis during a 24-hr period. In particular, we wish to highlight (A) possible important differences in the dose response curves of insulin in splanchnic and peripheral tissues and (B) the modulating influences of hyperglycemia and glucagon on insulin's effects across the splanchnic bed.

Adipose Tissue↗
PubMed1989

Accelerated norepinephrine turnover in peripheral tissues after ventromedial hypothalamic stimulation in rats.

To obtain evidence for a functional connection between the ventromedial hypothalamic nucleus (VMH) and the sympathetic nervous system, effects of electrical stimulation of the VMH, the lateral hypothalamic area (LH) and the paraventricular hypothalamic nucleus (PVN) on norepinephrine (NE) turnover in the heart, liver, pancreas, spleen, submandibular gland and the interscapular brown adipose tissue were examined in anesthetized rats. Stimulation of the VMH elicited a 3-8-fold increase in the rate of NE turnover in all organs examined, whereas stimulation of the LH or the PVN had no appreciable effects. The effect of VMH stimulation was abolished after sympathetic ganglionic blockade with hexamethonium. Epinephrine turnover in the adrenal gland was accelerated by stimulation of not only the VMH but also the LH. It was concluded that the VMH is intimately associated with sympathetic facilitation in peripheral tissues.

Animals↗
PubMed1999

Epidural analgesia reduces the release of amino acids from peripheral tissues in the ebb phase of the metabolic response to major upper abdominal surgery.

The purpose of this prospective cohort study was to compare metabolic effects of epidural or patient controlled analgesia (PCA) in patients undergoing major upper abdominal surgery. Seventeen patients undergoing major upper abdominal surgery were included: 10 received perioperative epidural analgesia (Group I) and the remainder received morphine via a PCA device for postoperative analgesia (Group II). A number of measures compared between one day preoperatively (day 1) and day 2 postoperatively included femoral arterial and venous blood concentrations of glucose, lactate, pyruvate and amino acids. In addition, the relevant flux values were measured from the products of the respective arteriovenous substrate concentration differences and calf blood flow. The efflux of lactate from peripheral tissues was greater in Group II than in Group I (P < 0.01): glucose and pyruvate efflux did not differ between groups. There was no difference between groups in mean individual and total flux of amino acids on day-1. However increased efflux between day-1 and day 2 was found for alanine, valine, isoleucine, leucine, phenylalanine, lysine, arginine in both groups, and for serine, glycine, tyrosine and histidine in Group II (P < 0.05). The efflux of glycine, methionine, amino benzoic acid, alanine, and lysine was less in Group I than Group II on day 2 (P < 0.05). There was a significant difference in the total amino acid flux on day 2 (Group I = -1.2 mumol. (100 ml tissue)-1.min-1 cf Group II = -2.5 mumol. (100 ml tissue)-1.min-1; P = 0.04). In conclusion, perioperative epidural analgesia was associated with a reduced postoperative amino acid efflux two days following major upper abdominal surgery.

Amino Acids↗
PubMed1983

Use of a monoclonal antibody for comparative studies of monoamine oxidase B in mitochondrial extracts of human brain and peripheral tissues.

Monoamine oxidase B (MAO B; EC 1.4.3.4) activity in detergent extracts of mitochondria from autopsy brain (gray matter and medulla), liver, lung, and kidney from a single individual and from pooled, human platelets could be immunoprecipitated by a monoclonal anti-human platelet MAO B antibody (MAO-1C2) in combination with appropriate secondary reagents. MAO A activity, which was detected in brain, liver, lung, and kidney, was not immunoprecipitated under the same conditions. All MAO B-containing extracts, regardless of tissue source, inhibited immunoprecipitation of [3H]pargyline-labeled human platelet MAO, and the shapes of the inhibition curves were identical. The concentration of immunologically detectable MAO B protein in the extracts was estimated from immunoprecipitation competition data by reference to a standard curve relating observed inhibition of immunoprecipitation to the concentration of catalytically active platelet MAO added (estimated from [3H]pargyline binding data). MAO B protein concentrations measured by this radioimmunoassay were similar to concentrations of active MAO B as measured by pargyline binding. These results demonstrate that in the brain and peripheral tissues studied, molecules with MAO B activity share a unique antigenic determinant and similar catalytic efficiency. They also extend previous observations that MAO B molecules extracted from mitochondria bear an antigenic determinant which is not present on MAO A molecules. These results demonstrate the validity of a new competitive radioimmunoassay for active plus inactive MAO B concentration in human platelet extracts and extracts of mitochondria from human tissues. This radioimmunoassay should complement [3H]pargyline binding assays and enzyme activity assays in studies designed to clarify the mechanisms of genetic, disease, and treatment factors which lead to differences in MAO B function among individuals.

Adult↗
PubMed1990

Serum concentrations of thyroid hormones and activity of iodothyronine deiodinase in peripheral tissues of the house musk shrew, Suncus murinus.

Serum concentrations of thyroid hormones and the properties of iodothyronine deiodinase in tissues of the house musk shrew, Suncus murinus, were examined and compared with those of the rat. Serum concentrations of thyroxine (T4) and 3,3',5'-tri-iodothyronine (rT3) were higher, while the serum concentration of 3,5,3'-tri-iodothyronine (T3) was lower in the shrew than in the rat. Among liver, kidney, skeletal muscle, heart, brown adipose tissue (BAT), spleen, lung, testes and thymus homogenates of the shrew, T(4)5'-deiodinase (5'D) activity was highest in BAT, and rT3 5'D activity was highest in both the liver and BAT. Intermediate or low T3 5-deiodinase activity was noted in all tissues examined. Activity of 5'D for T4 and rT3 in liver and kidney was much lower, while that of BAT was much higher in the shrew than in the rat. Liver and kidney 5'D may be type-I and that of BAT may be type-II in the shrew, judging from its response to 6-n-propyl-2-thiouracil and iopanoic acid and substrate preference. Thus 5'D of the shrew was similar to that of the rat in type, but was different with respect to its activity in some peripheral tissues. This difference may have relevance to the low T3 state of the shrew.

Adipose Tissue, Brown↗
PubMed1996

Cloning of human cDNA encoding a novel heptahelix receptor expressed in Burkitt's lymphoma and widely distributed in brain and peripheral tissues.

Using PCR with degenerate primers and screening of a human B-cell lymphoblast cDNA library, a full-length cDNA encoding a 375-amino-acid protein was isolated. It contains seven regions of hydrophobic amino acids probably representing membrane-spanning domains of a novel heptahelix receptor, tentatively named CMKRL2. It shows nearly 30% overall identity with the high-affinity IL8 receptor and similar degree of homology with other chemoattractant receptors, including the "fusin" coreceptors for HIV1. Measurements of various transduction pathways following application of a panel of chemokines to transfected cells failed to evoke any reproducible response. Although the natural ligand for CMKRL2 could, thus, not be identified, receptor expression in spleen and lymph nodes as well as in Burkitt's lymphoma (irrespective of EBV status) supports a functional role in activated B-cells. Receptor message was ubiquitously distributed in normal peripheral tissues and CNS, suggesting that CMKRL2 is expressed in widespread cell populations, such as macrophages and neuroglia.

Adenylyl Cyclases↗
PubMed1990

Identification of cells in rat brain and peripheral tissues expressing mRNA for members of the nerve growth factor family.

Cells expressing mRNA for hippocampus-derived neurotrophic factor (HDNF/NT-3) or brain-derived neurotrophic factor (BDNF) were identified by in situ hybridization. In the rat brain, HDNF mRNA was predominantly found in pyramidal neurons in CA1 and CA2 of the hippocampus. Lower levels of HDNF mRNA were found in granular neurons of the dentate gyrus and in neurons of the taenia tecta and induseum griseum. BDNF mRNA-expressing cells were more widely distributed in the rat brain, with high levels in neurons of CA2, CA3, and the hilar region of the dentate gyrus, in the external and internal pyramidal layers of the cerebral cortex, in the claustrum, and in one brainstem structure. Lower levels were seen in CA1 and in the granular layer of the hippocampus, in the taenia tecta, and in the mammillary complex. In peripheral tissues, HDNF mRNA was found in glomerular cells in the kidney, secretory cells in the male rat submandibular gland, and epithelial cells in secondary and tertiary follicles in the ovary. Cells expressing BDNF mRNA were found in the dorsal root ganglia, where neurons of various sizes were labeled.

Animals↗
PubMed2000

Expression analysis of BACE2 in brain and peripheral tissues.

Beta-site amyloid precursor protein cleaving enzyme (BACE) is a novel transmembrane aspartic protease that possesses all the known characteristics of the beta-secretase involved in Alzheimer's disease (Vassar, R., Bennett, B. D., Babu-Khan, S., Kahn, S., Mendiaz, E. A., Denis, P., Teplow, D. B., Ross, S., Amarante, P., Loeloff, R., Luo, Y., Fisher, S., Fuller, J., Edenson, S., Lile, J., Jarosinski, M. A., Biere, A. L., Curran, E., Burgess, T., Louis, J. -C., Collins, F., Treanor, J., Rogers, G., and Citron, M. (1999) Science 286, 735-741). We have analyzed the sequence and expression pattern of a BACE homolog termed BACE2. BACE and BACE2 are unique among aspartic proteases in that they possess a carboxyl-terminal extension with a predicted transmembrane region and together they define a new family. Northern analysis reveals that BACE2 mRNA is expressed at low levels in most human peripheral tissues and at higher levels in colon, kidney, pancreas, placenta, prostate, stomach, and trachea. Human adult and fetal whole brain and most adult brain subregions express very low or undetectable levels of BACE2 mRNA. In addition, in situ hybridization of adult rat brain shows that BACE2 mRNA is expressed at very low levels in most brain regions. The very low or undetectable levels of BACE2 mRNA in the brain are not consistent with the expression pattern predicted for beta-secretase.

Amino Acid Sequence↗
PubMed1984

3-Aminopicolinate inhibits phosphoenolpyruvate carboxykinase in hepatocytes and increases release of gluconeogenic precursors from peripheral tissues.

3- Aminopicolinate , a hyperglycemic agent that activates purified phosphoenolpyruvate carboxykinase in the presence of Fe2+, inhibits glucose synthesis from lactate, pyruvate, asparagine, monomethyl succinate, or glutamine but does not affect that from fructose, dihydroxyacetone, sorbitol, or glycerol in hepatocytes isolated from rats fasted for 24 h. Lactate production from monomethyl succinate by hepatocytes is also inhibited by 3- aminopicolinate . This compound elevates the concentrations of pyruvate, malate, and aspartate but decreases that of phosphoenolpyruvate in hepatocytes incubated with lactate plus pyruvate. In rats, the ability of 3- aminopicolinate to elevate blood glucose concentration is unimpaired by renalectomy . The drug does not significantly affect glycemia in functionally hepatectomized rats but accelerates blood lactate and pyruvate accumulation to higher maximum concentrations even when kidney function is also ablated. It is concluded that 3- aminopicolinate inhibits phosphoenolpyruvate carboxykinase in hepatocytes, that the reported stimulation of renal glutaminase and glutamine gluconeogenesis by this compound does not contribute significantly to its hyperglycemic property, and that the drug increases gluconeogenic substrate supply from peripheral tissues.

Animals↗
PubMed1998

Effect of post-mortem delay on density of tachykinin receptors in rat peripheral tissues.

The effect of post-mortem delay on the affinity and density of tachykinin NK1 and NK2 receptors was examined in the rat submandibular gland and gastric fundus, respectively, using saturation binding studies with the radioligands [125I]Bolton-Hunter [Sar9, Met(O2)11]SP and [125I][Lys5, Tyr(I2)7, MeLeu9, Nle10]NKA(4-10). For NK1 receptors, no significant changes were seen in either Kd (control 375 +/- 35 pM, n = 5; 32 h post-mortem 390 +/- 59 pM, n = 5) or Bmax (control 96 +/- 16 fmol/mg protein, n = 5; 32 h post-mortem 62 +/- 10 fmol/mg protein, n = 5). For NK2 receptors, no alterations were seen up to 16 h post-mortem. However, significant (p < 0.001) changes were seen at 32 h post-mortem (n = 4), where values for Kd were increased (3.0 +/- 0.2 nM) and those for Bmax were reduced (42 +/- 5.9 fmol/mg protein), relative to control (Kd = 1.3 +/- 0.2 nM; Bmax = 208 +/- 30 fmol/mg protein, n = 5). These changes are probably related to observed histological deterioration. This study demonstrates the stability of tachykinin receptors in these peripheral tissues and indicates the suitability of post-mortem tissue as a valid control in future tachykinin receptor studies.

Animals↗