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Biomedical subjects

R Gamse

Publications and source records attributed to R Gamse.

52 records · Page 3Linked to original sources
PubMed1981

Effect of capsaicin pretreatment on capsaicin-evoked release of immunoreactive somatostatin and substance P from primary sensory neurons.

Release of immunoreactive somatostatin (I-SRIF) and immunoreactive substance P (I-SP) was studied from slices prepared from upper dorsal horn (UDH) and lower dorsal plus ventral horn (LDH-VH) of rat spinal cord. Superfusion with capsaicin (10 microM) led to release of I-SRIF and I-SP from UDH slices but not from LDH-VH slices. The capsaicin-evoked release of I-SP was 6 fold higher than that of I-SRIF. A pulse of 60 mM K+ applied after the capsaicin pulse caused release of I-SRIF and I-SP from UDH as well as LDH-VH slices. Pretreatment of rats with capsaicin (125 mg/kg, s.c.) led to a nearly 40% depletion of I-SP in slices from UDH only. Capsaicin-evoked release from these slices was reduced by 81% for I-SRIF and by 79% for I-SP. Release evoked by K+ remained unchanged. These results indicate that capsaicin causes release of both I-SRIF and-I-SP and that this release is most likely restricted to primary sensory neurons. The marked reduction of the release of I-SP after systemic capsaicin pretreatment may well represent one of the, or even the reason for the insensitivity of capsaicin pretreated rats towards chemogenic pain.

Animals↗
PubMed1981

Substance P in tumors: pheochromocytoma and carcinoid.

Immunoreactive substance P (I-SP) was measured in two pheochromocytomas and a carcinoid of the caecum. The pheochromocytomas contained 1,5 and 50 pmol/g I-SP respectively. An HPLC analysis I-SP and catecholamines were enriched in the chromaffin granule fraction. The carcinoid contained 2900 pmol/g I-SP. About 40% of the immunoreactivity behaved like substance P on gel filtration, HPLC and in bioassays (fall in rabbit blood pressure and contraction of the guinea-pig ileum which was abolished by specific tachyphylaxis to substance P). These results indicate that authentic substance P is present in carcinoids and pheochromocytomas and that in the latter it is most likely stored in chromaffin granules.

Adrenal Gland Neoplasms↗
PubMed1980

Distribution of substance P in the rat gastrointestinal tract--lack of effect of capsaicin pretreatment.

A new method for extraction of immunoreactive substance P (I-SP) from rat intestine including pulverization of tissue frozen in liquid nitrogen and extraction with acid acetone is described. Using this method, amounts of I-SP in the rat intestine were found to be higher than previously reported. The highest concentrations of I-SP were found in the small intestine. Capsaicin pretreatment of newborn or adult rats had no effect on intestinal I-SP concentrations indicating that intrinsic SP neurones are capsaicin-insensitive.

Animals↗
PubMed1980

Release of immunoreactive somatostatin from hypothalamic cells in culture: inhibition by gamma-aminobutyric acid.

Primary cultures of dispersed hypothalamic cells were prepared from embryonic rats to study the release of immunoreactive somatostatin. The immunoreactive somatostatin content of these cultures increased during the first 2 weeks after plating and was readily measurable for several weeks thereafter; this material was characterized by gel permeation and reverse-phase chromatography. Depolarization of the cells with 60 mM K+ or with veratridine resulted in a calcium-dependent release of immunoreactive somatostatin which cochromatographed with synthetic somatostatin on reverse-phase chromatography. Tetrodotoxin blocked the veratridine-evoked release. However, even in the absence of exogenous stimuli, immunoreactive somatostatin was released by the cells into the medium. More than 70% of this tonic release was found to be calcium dependent and to be inhibited by tetrodotoxin, indicating that spontaneous electrical activity in the cultures leads to a release of immunoreactive somatostatin. gamma-Aminobutyric acid inhibited the tonic release of immunoreactive somatostatin and this was reversed by bicuculline. These findings support the hypothesis that gamma-aminobutyric acid inhibits somatostatin release in vivo.

Animals↗
PubMed1980

Effect of capsaicin pretreatment on substance P binding to synaptic vesicles.

Newborn or adult rats were pretreated with 50 mg kg-1 capsaicin. At the age of 2 to 4 months, binding of 125I-labelled Tyr8-substance P to synaptic vesicles prepared from different regions of the nervous system was examined. In both groups, capsaicin pretreatment led to a significant decrease in the number of binding sites in dorsal roots and spinal cord without having an effect on affinity. This decrease parallels the depletion of the substance P content (Gamse et al., 1980) and can be explained by degeneration of primary sensory neurons in newborn treated rats and by depletion of vesicles in adult treated rats.

Aging↗
PubMed1980

Decrease of substance P in primary afferent neurones and impairment of neurogenic plasma extravasation by capsaicin.

1 Rats were pretreated with capsaicin (50 mg/kg, s.c.) on the 2nd, 10th, or 20th day of life. Three months later immunoreactive substance P (I-SP) was determined in skin, sensory nerves and the central nervous system. Neurogenic plasma extravasation was also examined.2 Pretreatment at the age of 2 or 10 days resulted in a decrease (26 to 69%) of I-SP in skin, saphenous and vagus nerve, dorsal roots, dorsal half of the spinal cord, and medulla oblongata. The I-SP content of the ventral half of the spinal cord, of midbrain, hypothalamus, striatum, cortex, and cerebellum remained unchanged. Neurogenic plasma extravasation was inhibited by more than 80%.3 In contrast to this irreversible effect of capsaicin on newborn rats, pretreatment of 20 day old rats led to reversible depletion of I-SP and to reversible impairment of neurogenic plasma extravasation.4 Capsaicin pretreatment of adult rats caused a marked depletion of I-SP in the skin of the hind paw and an impairment of neurogenic plasma extravasation. A similar decrease of I-SP was seen after chronic denervation of the skin.5 Intra-arterial infusion of substance P (threshold dose 5 x 10(-13) mol/min) or physalaemin induced dose-dependent plasma extravasation. Somatostatin, vasoactive intestinal polypeptide, caerulein and the enkephalin-analogue FK 33-824 were ineffective in doses 100 fold higher.6 The results indicate that the action of capsaicin on substance P neurones is restricted to primary sensory neurones. Since in every case a decreased substance P content of the skin was associated with impaired neurogenic plasma extravasation, it is suggested that release of substance P is involved in neurogenic plasma extravasation.

Animals↗
PubMed1979

Nociceptive threshold after neonatal capsaicin treatment.

The nociceptive threshold as determined by the reaction time in the hot-plate and tail-flick tests was measured 3 to 4 months after pretreatment of young rats with capsaicin (50 mg kg-1 s.c.). The reaction time in the tail-flick test was prolonged in rats pretreated with capsaicin on the 2nd day of life. Capsaicin pretreatment up to the 10th day of life also resulted in a prolonged reaction time in the hot-plate test whereas capsaicin pretreatment after the 10th day of life was without effect. The elevation of the nociceptive threshold after neonatal capsaicin pretreatment most likely follows from degeneration of afferent nerve fibres activated by noxious stimuli.

Animals↗
PubMed1979

Indirect evidence for presynaptic location of opiate receptors on chemosensitive primary sensory neurones.

1. Rats were pretreated with 50 mg/kg s.c. capsaicin or solvent on the second day of life; 5 months later 3H-diprenorphine binding to homogenates of the whole spinal cord or of the upper dorsal horn of the spinal cord was investigated. 2. Capsaicin pretreatment resulted in a 17% decrease of opiate binding sites in the whole spinal cord and a 37% decrease in the upper dorsal horn with no change in their affinity. 3. Since neonatal capsaicin pretreatment causes degeneration of chemosensitive primary sensory neurones it is concluded that some opiate receptors are located presynaptically on the central terminals of these neurones.

Animals↗
PubMed1979

Substance P in the vagus nerve. Immunochemical and immunohistochemical evidence for axoplasmic transport.

1. The presence of immunoreactive substance P (I-SP) in the vagus nerve of 5 species was demonstrated by radioimmunoassay. Different amounts of SP per unit weight were found: Guinea pig greater than cat greater than rabbit, rat and cattle. 2. Infranodose ligations of the vagus nerve of cats and rabbits caused an accumulation of I-SP proximal but not distal to the ligation. The results obtained by radioimmunoassay and immunohistochemistry indicate a somatofugal axoplasmic transport of SP. 3. Double ligation experiments revealed that about 37% of I-SP of the cat vagus nerve are mobile. The transport rate of this mobile I-SP was found to be 170 mm per day. 4. Locally applied colchicine resulted in a similar accumulation of I-SP as after ligations. This is evidence favouring the involvement of microtubuli in the axoplasmic transport of SP. 5. Immunohistochemical data show that SP-fibers account for about 10% of the axons in the cat vagus nerve. Most of these SP-fibers seem to be unmyelinated. 6. Supranodose extracranial ligations of the cat vagus nerve led to an accumulation of I-SP on both sides of the ligature. Part of the SP-fibers are, therefore, afferent and their cell bodies are located in the nodose ganglion. The presence of efferent SP-fibers cannot be excluded.

Animals↗
PubMed1979

Substance P: characteristics of binding to synaptic vesicles of rat brain.

1. The binding of substance P (SP) to synaptic vesicles from rat brain was studied by use of the 125I-Tyr8-analogue of SP. 2. The pH dependence of the binding of both peptides to the lipid extractable fraction of synaptic vesicles was shown to be comparable. 3. The binding of 125I-Tyr8-SP shows a rate constant of association (k1 = 6.6 x 10(6) M-1 S-1), a rate constant of dissociation (k-1 = 6.4 x 10(-4) S-1) and gives a KD of 1 x 10(-10) M. Kd derived from equilibrium studies was 3.2 x 10(-10) M. 4. The binding of 125I-Tyr8-SP to lipids of synaptic vesicles was shown to be reversible, saturable and highly specific. 5. The kinetic data suggest one population of binding sites with a maximal number of 0.8 pmol per mg protein of the synaptic vesicle preparation. 6. Unlabeled SP and the (2--11)-, (3--11)- and (4--11)-analogues of SP inhibit the binding of 125I-Tyr8-SP in a decreasing order in a competitive way when added in excess. Tyr8-SP and eledoisin did not interfere with the binding of 125I-Tyr8-SP whereas uperolein and neurotensin caused a partial inhibition. Physalaemin and D-Ala2-D-Met5-enkephalin enhance the binding of 125I-Tyr8-SP in a cooperative way.

Animals↗
PubMed1978

The intestine as source of immunoreactive substance P in plasma of the cat.

1. Substance P (SP) was measured in acid acetone extracted plasma of cats using a sensitive radioimmunoassay. The immunoreactive material was submitted to ion exchange chromatography and at least 90% of immunoreactivity co-chromatographed with synthetic SP. 2. The level of immunoreactive SP (I-SP) in extracted plasma of the cat was 69.3 +/- 9.8 fmol/ml with values ranging from 2.5 to 165 fmol/ml. Evisceration of the cats caused a decrease of I-SP levels from 70.8 +/- 30.8 fmol/ml to 20.8 +/- 9.9 15 min and to 26.8 +/- 19.7 fmol/ml 60 min after the operation. 3. Ligation of intestinal blood vessels led to a fall in I-SP levels from 58.7 +/- 11.5 to 25.9 +/- 4.1 fmol/ml within 15 min. 4. No difference between I-SP values in portal (71.8 +/- 11.2 fmol/ml) and peripheral plasma (68.3 +/- 12.1 fmol/ml) was found under the conditions in which these experiments were performed. 5. It is concluded that a major part of circulating immunoreactive SP originates from the intestine.

Animals↗
PubMed1977

Lack of algesic effect of substance P on paravascular pain receptors.

1. Substance P (synthetic or extracted for intestine or central nervous system) is devoid of an algesic effect on paravascular pain receptors. 2. The algesic effect of a AP-containing acetone HCl-extract from spinal cord is explained by its high content of potassium ions. 3. SP-containing preparations which include an ammonium sulphate precipitation in the extraction procedure are algesic due to content of this salt. 4. SP-containing extract from intestine were found to be contaminated with a bradykinin-like peptide of high algesic potency. 5. These findings are discussed with regard to the restricted value of earlier results about central actions of SP-containing tissue extracts and with regard to the role of SP as a possible neurotransmitter.

Animals↗