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K Racké

Publications and source records attributed to K Racké.

At least 91 records · Page 5Linked to original sources
PubMed1987

Cholinergic modulation of the release of 5-hydroxytryptamine from the guinea pig ileum.

Isolated segments of the guinea pig ileum were vascularly perfused and the release of 5-HT and its metabolite 5-HIAA into the portal venous effluent determined by HPLC with electrochemical detection. Test substances were applied via the arterial perfusion medium. Oxotremorine inhibited concentration-dependently the release of 5-HT and 5-HIAA (by 47% at 1 mumol/l). Scopolamine (0.1 mumol/l) did not affect the release of 5-HT and 5-HIAA, but antagonized the effect of oxotremorine. In the presence of TTX (1 mumol/l), oxotremorine (1 mumol/l) increased the release of 5-HT by 150% and that of 5-HIAA by 220%. This increase was completely blocked by scopolamine. Hexamethonium (100 mumol/l) and TTX (1 mumol/l) reduced the release of 5-HT by 32 and 40%, respectively. DMPP (10 mumol/l) increased the release of 5-HT by 57%, and this effect was prevented by hexamethonium. Neither DMPP nor hexamethonium significantly affected the release of 5-HIAA. The enhancing effect of DMPP on 5-HT release was increased and prolonged in the presence of TTX or scopolamine. Nicotine (1, 10 or 30 mumol/l) alone did not cause a consistent increase in the release of 5-HT. However, in the presence of scopolamine nicotine increased the release of 5-HT by 57%. In conclusion, the release of intestinal 5-HT is facilitated via muscarine and nicotine receptors located on the enterochromaffin cells. Indirect evidence suggests that the release of 5-HT is additionally modulated by an as yet unknown inhibitory neurotransmitter released by muscarine receptor activation.

Animals↗
PubMed1987

Temperature-dependent effects of increased intraluminal pressure on serotonin release from the vascularly perfused guinea pig ileum.

Isolated segments of the guinea pig ileum were vascularly perfused and the release of endogenous serotonin into the portal effluent was measured. Peristalsis was induced by raising the intraluminal hydrostatic pressure by 500 Pa for 5 min. Serotonin release increased during peristalsis induced by fluid of 37 degrees C, but decreased when the temperature of the intraluminal fluid was between 13 degrees C and 22 degrees C. In the presence of naloxone (0.3 mumol/l) raising the intraluminal pressure with fluid of 37 degrees C caused an inhibition of the serotonin release which was blocked by scopolamine (0.1 mumol/l). Naloxone did not affect the inhibition of serotonin release during peristalsis caused by fluid of 19 degrees C, neither did indomethacin (1 mumol/l). In conclusion, liquid distension of the guinea pig isolated ileum elicits peristaltic activity, and affects the release of serotonin into the portal circulation. The changes in serotonin release depend on the temperature of the fluid passing through the intestinal lumen, whereas peristalsis is not affected by the temperature of the intraluminal fluid.

Animals↗
PubMed1987

GABAA and GABAB receptor-mediated inhibition of release of 5-hydroxytryptamine in the intermediate lobe of the rat pituitary gland.

Isolated neurointermediate lobes or neural lobes of the rat pituitary gland attached to the pituitary stalk were incubated in vitro and the spontaneous or electrically (pituitary stalk stimulation, 5 Hz, 1,500 pulses) evoked release of 5-hydroxytryptamine was determined. The evoked release of 5-hydroxytryptamine from the neurointermediate lobe was increased fivefold in the presence of the dopamine receptor antagonist (-)-sulpiride (1 microM). The evoked release of 5-hydroxytryptamine from the isolated neural lobe was not altered by (-)-sulpiride. The evoked release of 5-hydroxytryptamine from the isolated neural lobe in the presence of (-)-sulpiride was less than 5% of that from the combined neurointermediate lobe showing that most of the 5-hydroxytryptamine released from the combined neurointermediate lobe originated in the intermediate lobe. The evoked release of 5-hydroxytryptamine from the neurointermediate lobe in the presence of (-)-sulpiride showed a diurnal variation. It was three to five times higher between 9.30 and 14.00 h than between 8.30 and 9.30 h or between 14.00 and 16.00 h. The 5-hydroxytryptamine tissue content at the end of the incubation experiments also showed similar variations which were, however, less pronounced. The evoked release of 5-hydroxytryptamine from the neurointermediate lobe, in the presence of (-)-sulpiride, was reduced by the preferential GABAA receptor agonist muscimol or the selective GABAB receptor agonist (-)-baclofen in a concentration-dependent manner. Bicuculline, a selective GABAA receptor antagonist inhibited the effect of muscimol, but not that of (-)-baclofen. Bicuculline alone did not affect the release of 5-hydroxytryptamine from the gland. It is concluded that the release of 5-hydroxytryptamine in the intermediate lobe is influenced by both dopaminergic and GABAergic mechanisms.

Animals↗
PubMed1987

Spontaneous release of endogenous 5-hydroxytryptamine and 5-hydroxyindoleacetic acid from the isolated vascularly perfused ileum of the guinea-pig.

The spontaneous release of 5-hydroxytryptamine and its metabolite 5-hydroxyindoleacetic acid from the enterochromaffin cells of the small intestine into the portal circulation was investigated in vitro using the vascularly perfused ileum of the guinea-pig. The release of 5-hydroxytryptamine decreased by 70% in a calcium-free medium and by 35% in the presence of tetrodotoxin. Inhibition of monoamine oxidase activity by pargyline (100 microM) had no effect on the spontaneous release of 5-hydroxytryptamine although it caused a 75% reduction in the outflow of 5-hydroxyindoleacetic acid. Imipramine (1 microM), an inhibitor of neuronal uptake of 5-hydroxytryptamine, reduced the 5-hydroxyindoleacetic acid outflow by 57% and increased the release of 5-hydroxytryptamine by 66%. The combination of both drugs showed no additional effect. The tissue content of 5-hydroxytryptamine and its metabolite was not changed after perfusion with the precursor L-tryptophan or monofluoromethyldopa, an inhibitor of the L-aromatic amino acid decarboxylase. The results show that the spontaneous release of 5-hydroxytryptamine and its metabolite reflects largely calcium-dependent exocytotic release of the amine. "Neuronal uptake" (into aminergic and/or enterochromaffin cells) followed by deamination appears to be the main pathway of 5-hydroxytryptamine catabolism in the guinea-pig ileum.

Animals↗
PubMed1986

Release of endogenous 5-hydroxytryptamine from the intermediate lobe of the rat pituitary gland is inhibited by endogenous dopamine.

The release of endogenous 5-hydroxytryptamine (5-HT) from the in vitro incubated neurointermediate lobe (NIL) of the rat hypophysis was measured by HPLC with electrochemical detection. 5-HT release evoked by electrical stimulation of the pituitary stalk from the NIL, but not from the isolated neural lobe (NL) was enhanced in the presence of the dopamine receptor antagonist sulpiride (1 microM). The opiate receptor antagonist naloxone (1 microM) had no effect on the evoked release of 5-HT from the NIL or NL. In conclusion, the release of endogenous 5-HT from the intermediate lobe is under inhibitory control of endogenous dopamine.

Animals↗
PubMed1986

Endogenous opioids inhibit the in vitro release of endogenous dopamine preferentially in the neural lobe of the rat neurointermediate lobe.

The release of endogenous dopamine (DA) from the in vitro incubated combined neurointermediate lobe (NIL) or isolated neural lobe (NL) was studied. In the presence of the DA uptake inhibitor GBR 12921 (200 nM), electrical stimulation of the pituitary stalk caused an increase of the outflow of DA from the NIL in a frequency-dependent manner. Naloxone (1 microM) enhanced the DA release from the NIL evoked by electrical stimulation at 7 or 15 Hz by about 40%, but had no effect on DA release evoked by stimulation at 3 Hz. When the electrical stimulation was carried out at 15 Hz, the evoked DA release (expressed as fraction of the DA tissue content) from the NL amounted to only 15% of that from the combined NIL. Naloxone (1 microM) increased the evoked DA release from the isolated NL by 242%. Thus, the effect of naloxone on DA release from the combined NIL may be confined mainly to the NL. In conclusion, DA release from the NL is under inhibitory control of endogenous opioids released from the NL during stimulation at 7 or 15 Hz. Beta-Endorphin, known to be released spontaneously at a high rate from in vitro incubated NILs, appears to lack inhibitory effects on DA release from the NIL.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

Modulation by fenoldopam (SKF 82526) and bromocriptine of the electrically evoked release of vasopressin from the rat neurohypophysis. Effects of dopamine depletion.

Single neurointermediate lobes were fixed by their stalks to a platinum wire electrode and incubated in Krebs-bicarbonate solution. Vasopressin release into the medium was determined by a radioimmunoassay. Vasopressin secretion was increased by electrical stimulation (15 Hz, 10 s trains with 10 s intervals for 10 min). Fenoldopam (SKF 82526) had a dual effect on vasopressin release, 30 nM decreasing (by 30%) and 3 microM increasing (by 32%) the evoked vasopressin secretion. The facilitatory effect of fenoldopam was antagonized in a concentration-dependent manner by flupenthixol but not by sulpiride. Sulpiride (1 microM) prevented the inhibitory effect of fenoldopam (30 microM). After pretreatment of the rats with the dopamine depleting agent, Ro4-1284 (2 mg/kg i.p. 1 h before the experiments), the evoked vasopressin release was decreased by 21% and the inhibitory effect of fenoldopam disappeared, but the facilitatory effect of fenoldopam was already seen at 30 nM. Similarly, bromocriptine (1-10 microM) decreased the evoked vasopressin release from untreated neurointermediate lobes by 30-40% but increased the vasopressin release by 30% after pretreatment with Ro4-1284. The present findings further support the concept that vasopressin from the neurohypophysis is modulated by dopaminergic mechanisms. Facilitatory effects are mediated via D 1 and inhibition via D 2 receptors. The presence of endogenous dopamine seems to be necessary for the inhibitory effects to occur.

Animals↗
PubMed1986

Release of endogenous 3,4-dihydroxyphenylethylamine and its metabolites from the isolated neurointermediate lobe of the rat pituitary gland. Effects of electrical stimulation and of inhibition of monoamine oxidase and reuptake.

Isolated rat neurointermediate lobes were incubated in vitro. The release of 3,4-dihydroxyphenylethylamine (dopamine, DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and methoxyphenylethanol (MOPET) was determined by HPLC with electrochemical detection. Under resting conditions, the outflow of metabolites was 35-50 times that of DA. HVA accounted for 50%, DOPAC for 45%, and MOPET for 5% of the metabolites. Although an equivalent of 40-50% of the tissue DA content was released per hour as metabolites, the tissue DA content was not reduced after 110 min of incubation. The spontaneous outflow of DA and its metabolites was not affected by the DA uptake inhibitor GBR 12921 (100 nM). Pargyline (10 microM) caused a time-dependent decrease of all metabolites (up to 90%). In the presence of GBR 12921 and pargyline, the spontaneous outflow of DA increased sevenfold. Removal of the intermediate lobe caused a 78% reduction in tissue DA content and a corresponding reduction of the outflow of metabolites. Electrical stimulation of the pituitary stalk (0.2 ms, 10 V, 15 Hz, three times for 1 min at intervals of 1 min) induced an increase in outflow of DA and all metabolites. DA accounted for 15%, HVA for 41%, DOPAC for 32%, and MOPET for 12% of the evoked release. The electrically evoked release of DA increased fourfold in the presence of GBR 12921 or pargyline and the effects of both drugs were additive. The evoked release of metabolites was not significantly affected by GBR 12921 but completely abolished by pargyline. In conclusion, oxidative deamination and O-methylation are important pathways for the catabolism of DA in the neurointermediate lobe.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

Dehydration increases the electrically evoked dopamine release from the neural and intermediate lobes of the rat hypophysis.

The effect of dehydration on dopamine (DA) release from the neural and intermediate lobes of the rat pituitary gland after electrical stimulation of the pituitary stalk was studied in vitro. The amount of DA released from pituitary lobes of dehydrated rats (no water for 72 h), in which the hormone secretion from the hypophysis, especially the neural lobe, is known to be greatly enhanced, was significantly higher when compared with that from control tissues. In control and dehydrated rats the evoked DA release from the intermediate lobe was higher than that from the neural lobe. After dehydration, the stimulus-evoked DA release from the neural lobe increased by more than 200%, whereas that from the intermediate lobe increased by only 60%, indicating a preferential activation of the DA system of the neural lobe. There was a decrease in DA released per pulse from the combined neuro-intermediate lobe of control rats with increasing number of stimulation pulses. In contrast, DA release per pulse from the neuro-intermediate lobe of dehydrated rats showed a tendency to increase with increasing number of pulses. As the availability of newly synthesized DA is believed to be the limiting factor for transmitter release, the present observations suggested a higher in vitro DA synthesis rate in the tissues from dehydrated rats. This agrees with in vivo results of Alper and his colleagues who found an increased accumulation of L-3,4-dihydroxyphenylalanine (DOPA) in neuro-intermediate lobes of dehydrated rats after inhibition of DOPA-decarboxylase.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

Release of endogenous 5-hydroxytryptamine from the neural and the intermediate lobe of the rat pituitary gland evoked by electrical stimulation of the pituitary stalk.

A calcium-dependent release of 5-hydroxytryptamine from the neural and intermediate lobe of the rat pituitary gland has been demonstrated following electrical stimulation of the pituitary stalk with stimulation parameters thought to evoke propagated action potentials. The 5-hydroxytryptamine release from the intermediate lobe was double that from the neural lobe. The mass of the intermediate lobe of the rat is about 80% of that of the neural lobe [Holzbauer, Racké, Mann, Cooper, Cohen, Krause and Sharman (1984) J. Neural Transm. 59, 91-104]. The relatively high overflow of 5-hydroxytryptamine from the intermediate lobe agrees with immunohistochemical studies in which a larger number of 5-hydroxytryptamine fibres were seen in the intermediate lobe than in the neural lobe. The present results have demonstrated that the rat hypophysis contains neuronal 5-hydroxytryptamine. They also suggest that this amine may act as a neurotransmitter substance in the neural and intermediate lobe.

Animals↗
PubMed1985

Evidence for exocytotic release of dopamine beta-hydroxylase from rabbit heart and of vasopressin from rat neurohypophyses during homogenization and fractionation. Effects of gadolinium ions, cytochalasin B, gallopamil and different temperatures.

Isolated rabbit hearts were perfused according to a modified Langendorff method for 1 h (unstimulated hearts). In different hearts, release of dopamine beta-hydroxylase activity into the transmyocardial fluid draining the interstitium was evoked by electrical field stimulation for six periods of 1 min at 30 min intervals (stimulated hearts). The hearts were then homogenized and fractionated into 100,000 g supernatant and sedimented at 4 degrees C. In homogenates from unstimulated hearts, the soluble dopamine beta-hydroxylase (determined in the supernatant) accounted for 17% of the total dopamine beta-hydroxylase (determined in the homogenate). In stimulated hearts the soluble fraction of dopamine beta-hydroxylase was reduced by 65%. The dopamine beta-hydroxylase released into the transmyocardial fluid by electrical stimulation, expressed as fraction of the total activity, corresponded well to the loss of enzyme from the supernatant demonstrating that the soluble dopamine beta-hydroxylase determined from the supernatant represents the releasable pool. Gadolinium ions (Gd3+) added to the homogenization medium of unstimulated hearts reduced the soluble fraction of dopamine beta-hydroxylase up to 63%, with the maximum effect at 200 microM. Similarly, when neurohypophyses were homogenized and spun at 0-4 degrees C, the fraction of vasopressin in the soluble phase was about 50% of the total. Gd3+ reduced this fraction by maximally 60%, an effect which was accompanied by an increase of vasopressin in the sedimentable fraction. When cytochalasin B (10 microM) was present during the homogenization of the hearts the soluble fraction of dopamine beta-hydroxylase was reduced to the same extent as in the presence of Gd3+. However, cytochalasin B had no effect on the distribution of vasopressin in the soluble and sedimentable fractions of homogenates of neurohypophyses. Gallopamil, when present during the homogenization of the hearts at a maximum effective concentration of 1 microM, reduced the soluble fraction of dopamine beta-hydroxylase by only 40%. However, the electrically evoked noradrenaline release from perfused hearts was completely blocked at 100-300 microM gallopamil. When neurohypophyses were homogenized and fractionated at room temperature only 13% of the total vasopressin was found in the soluble fraction and Gd3+ did not further reduce this fraction. When unstimulated hearts were homogenized and fractionated at room temperature the fraction of soluble dopamine beta-hydroxylase was reduced by 40% compared to the experiments at 0-4 degrees C.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Release and metabolism of [3H]dopamine in the neurointermediate lobe of the rat pituitary gland.

Neurointermediate lobes of the rat pituitary gland were incubated with [3H]dopamine in the presence of desipramine and then superfused with radioactivity-free medium. The outflow of tritium was studied and in most experiments [3H]dopamine and its metabolites were separated by column chromatography. After 60-70 min of superfusion, the spontaneous rate of tritium outflow was 1.2%/min. The spontaneously released radioactivity consisted of 52% O-methylated and deaminated metabolites, 28% 3,4-dihydroxyphenylacetic acid, 18% dopamine and 2% 3-methoxytyramine. In the presence of pargyline (10 microM) the spontaneous rate of total tritium outflow decreased by 46%, that of the O-methylated and deaminated metabolites by 72% and that of 3,4-dihydroxyphenylacetic acid by 79%. The spontaneous rate of outflow of dopamine was unchanged and that of 3-methoxytyramine increased 3-fold. Further addition of nomifensine (10 microM) doubled the rate of outflow of dopamine and 3-methoxytyramine, but had no effect on the other metabolites. Electrical stimulation of the pituitary stalk (0.2 ms, 80 V, 3 Hz, 2 min) caused a tritium release of 8.5% of the tissue tritium. The evoked tritium release was only partially dependent on the extracellular calcium and not affected by tetrodotoxin. In contrast, vasopressin release evoked by stimuli of the same strength was completely calcium-dependent and blocked by tetrodotoxin. After modification of the stimulation conditions (1 ms, 10 V, 10 Hz, 2 min) the evoked tritium release was 4.1% of the tissue tritium. This tritium release was reduced by 73% in the presence of tetrodotoxin. The total evoked tritium release was decreased by 30% in the presence of pargyline and increased by 150% after further addition of nomifensine. Under the latter conditions, tetrodotoxin reduced the evoked tritium release by 67%, but nearly all of the tetrodotoxin-resistant tritium release could be identified as dopamine metabolites. Thus, the electrical stimulation appears to liberate some [3H]dopamine metabolites from an extraneuronal compartment. In conclusion, oxidative deamination and O-methylation are important pathways of the catabolism of dopamine in the neurointermediate lobe of the pituitary gland. After labelling of the transmitter stores with [3H]dopamine, the total tritium release is a poor indicator of [3H]dopamine release from the nerve terminals. Only the isolated [3H]dopamine fraction appears to reflect the release of neuronal [3H]dopamine.

Animals↗
PubMed1985

Gadolinium ions inhibit exocytotic vasopressin release from the rat neurohypophysis.

Single rat neurointermediate lobes (n.i.l.s) were fixed by their stalks to a platinum wire clip electrode and incubated in oxygenated Krebs-HEPES medium. Vasopressin release int the medium was determined by radioimmunoassay. Vasopressin secretion was increased by different stimuli and the effects of gadolinium (Gd3+) were tested. Electrical stimulation (15 Hz, three times 1 min with 1 min intervals) increased vasopressin release in a calcium-dependent manner. Gd3+ (10 microM to 3 mM) inhibited the evoked release of vasopressin in a concentration-dependent fashion; at 3 mM the inhibition was 98%. The inhibitory effect of Gd3+ up to 300 microM was antagonized by increasing the calcium concentration in the medium up to 6 mM. The effects of 1 and 3 mM-Gd3+ were unaffected by increasing the calcium concentration. Exposure of n.i.l.s to depolarizing concentrations of potassium (high K+, 60 mM, 30 min) increased the vasopressin release more than 33-fold. The elevated vasopressin release remained constant during six consecutive 5 min periods. In the initial 5 min period 300 microM-Gd3+ reduced the evoked vasopressin release by 80% but during the last 5 min period only by 30%. At 3 mM-Gd3+ vasopressin release was completely blocked during the whole time of incubation with high K+. Vasopressin release induced by exposure of n.i.l.s to cold (4 degrees C, 20 min) was completely inhibited by 3 mM-Gd3+, but reduced by only 25% in the presence of 300 microM-Gd3+. Vasopressin release induced by incubation of n.i.l.s with the ionophore X-537A (lasalocid) (10 microM, 30 min) was reduced by 90% in the presence of 300 microM-Gd3+ and completely prevented by 3 mM-Gd3+. 300 microM-Gd3+, added to the incubation medium, had no significant effect on the vasopressin release from crude synaptosomal preparations evoked by high K+. However, when 300 microM-Gd3+ was already present during the tissue homogenization, the evoked vasopressin release from the synaptosomes was completely blocked. It is concluded that Gd3+ inhibits exocytotic vasopressin release at two different sites. First, Gd3+ may block voltage-regulated calcium channels. Secondly, Gd3+ may inhibit the exocytotic release mechanism by an intracellular site of action. It is speculated that contractile proteins may be the intracellular target for Gd3+.

Animals↗
PubMed1985

The dopaminergic innervation of the intermediate lobe and of the neural lobe of the pituitary gland.

The intermediate and the neural lobe of the pituitary gland are innervated by two, virtually independent, groups of dopaminergic neurons which, until recently, were considered as a uniform system and referred to as the "tubero-hypophyseal dopamine system". Some aspects of the separate physiological functions of these neurons in the intermediate and in the neural lobe, of their microanatomy and biochemistry as well as of dopamine release from their terminals are discussed in this review.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Regional differences in the effect of pargyline on dopamine concentrations in the rat hypophysis.

Dopamine concentrations were estimated in different regions of the infundibular-pituitary system of the rat. The highest values were found in the pituitary stalk where they are comparable to the concentrations in the striatum, and higher than in the median eminence. In the anterior lobe the dopamine (DA) concentrations of the upper pole (10% of the lobe tissue) were 2-5 times higher than in the rest of the lobe. Anterior lobe DA was significantly higher in rats about 6 months old than in rats about 3 months old. After inhibition of MAO, the DA concentrations in the isolated neural lobe (NL) were more than doubled. In contrast there was no increase in the DA concentrations of the intermediate lobe, an observation which is in agreement with our previous finding that DA synthesis in the intermediate lobe after electrical stimulation of the pituitary stalk is much slower than in the neural lobe. Pargyline treatment caused an increase in the DA concentrations in the anterior lobe by about 150%. This rise (together with a DA increase in the stalk-infundibulum) may be related to the decrease in circulating prolactin which occurs in pargyline treated rats.

Aging↗
PubMed1983

Dopamine release and synthesis in the neurointermediate lobe of the rat hypophysis in vitro after electrical stimulation of the pituitary stalk.

The isolated neurointermediate lobe of the rat hypophysis was incubated in Krebs solution and the stalk was electrically stimulated. The endogenous dopamine (DA) released into the medium was estimated by HPLC with electrochemical detection. Stimulation with biphasic pulses (1 ms, 10 Hz) in the presence of pargyline elicited a mean DA output of 200 fg X pulse-1. This release was calcium-dependent but was only partially inhibited by tetrodotoxin (TTX) (1 microM), effects typical for direct electrical depolarization of the nerve endings. Reducing the duration of the electric pulses to 0.2 ms (15 Hz) caused a reduction in DA output to about 40 fg X pulse-1 which was completely blocked by TTX indicating that it was evoked by propagated action potentials. DA overflow was enhanced when the action potential was prolonged with tetraethylammonium (TEA) or when DA uptake was inhibited with GBR 12921. Evidence for a calcium-dependent increase in DA synthesis in electrically stimulated NILs has been obtained when monoamine oxidase was inhibited and TEA or GBR 12921 was present in the Krebs solution. The present results complete the requirements for the DA in the NIL to be classified as a neurotransmitter substance. The NIL-pituitary stalk preparation is a useful model for studying regulatory mechanisms in dopaminergic nerve terminals.

Animals↗
PubMed1983

Uptake of [3H]dopamine into dopaminergic and noradrenergic neurones of the isolated neurointermediate lobe of the rat hypophysis. Effects of desipramine and nomifensine.

The isolated neurointermediate lobe (NIL) of the rat hypophysis accumulates [3H]dopamine from the incubation medium. Column chromatographic analysis showed that 92% of the tissue radioactivity was contained in the catecholamine fraction. [3H]Dopamine represented 70% and [3H]noradrenaline 30% of the [3H]catecholamines. Desipramine (1 microM) prevented the formation of [3H]noradrenaline without affecting the storage of [3H]dopamine. Nomifensine (10 microM) blocked the storage of [3H]dopamine and [3H]noradrenaline. Thus, in the NIL, [3H]dopamine is taken up into dopaminergic and noradrenergic neurones. In the latter, [3H]dopamine is converted to [3H]noradrenaline, indicating a significant dopamine beta-hydroxylase activity in the NIL tissue. A selective labeling of the dopamine stores with [3H]dopamine can be achieved in the presence of desipramine.

Animals↗