Catecholamine Mechanisms Research Articles

Changes in brain catecholamine mechanisms following perinatal exposure to marihuana

Adult female rats received daily oral doses of a crude marihuana extract (CME; equivalent to 20 mg/kg Δ 9-THC) throughtout gestation and lactation. The offspring were sacrified at 10, 20, 40 or 60 days postpartum and tissue samples of cerebral cortex and striatum were dissected and assayed for α 1-adrenergic and D 2-dopaminergic receptors, respectively, and tyrosine hydroxylase activity. The body weight at birth and 10 days of age was reduced as was brain weight at 10 and 60 days of age in offspring exposed to CME. Perinatal exposure to CME reduced in the cerebral cortex was not altered at any age. Tyrosine hydroxylase activity was significantly decreased in the striatum of 20 and 40-day-old offspring exposed to CME. The results indicate that chronic perinatal exposure to CME can selectively alter the development of specific catecholamine mechanisms in rat brain.

Pulmonary edema and death induced by sinoaortic denervation in fastigial nucleus-lesioned rats

When adult male rats with lesions of the cerebellar fastigial nucleus were subjected to sinoaortic denervation and instrumented for aortic pressure recording, their elevated mean arterial pressure was found to rise no higher than that of rats with sinoaortic denervation alone; however all of the doubly operated rats died or became moribund within 4 days. Pulmonary edema and gastric ulcers were frequently seen. When the order of operations was reversed, all animals survived. The possible mechanism and involvement of other brain nuclei, catecholamines and vasopressin in these pathological changes is discussed.

Brain stem catecholamine mechanisms in tonic and reflex control of blood pressure.

Neurons of the lower brain stem maintain resting levels of arterial pressure (AP), mediate reflex responses from cardiopulmonary receptors, and are an important site of the hypotensive actions of alpha 2-adrenergic agonists. Details of the pathways and transmitters that mediate tonic and reflex control of AP are emerging. Afferent fibers of cardiopulmonary receptors in the ninth and tenth nerves terminate bilaterally in the nucleus of the tractus solitarius (NTS). Although some neurons contain substance P, the primary neurotransmitter appears to be the excitatory amino acid L-glutamate (L-glu). Neurons in rostral ventrolateral medulla, which most probably comprise the C1 group of epinephrine neurons, are also critical in AP control. C1 neurons project to innervate cholinergic preganglionic sympathetic neurons in the spinal cord. Stimulation of the C1 area electrically or with L-glu increases AP, while lesions or local injection of the inhibitory amino acid gamma-aminobutyric acid (GABA) lowers AP to levels comparable to spinal cord transection. Lesions of C1 neurons or their pathways abolish vasodepressor reflexes from baroreceptors and vagal afferents. In contrast, noradrenergic neurons of the caudal ventrolateral medulla, the A1 group, project rostrally to innervate, in part, vasopressin neurons of the hypothalamus. Stimulation of A1 neurons lowers AP, while lesions or GABA elevates it. We propose that C1 neurons comprise the so-called tonic vasomotor center of the brain stem and also mediate, via a projection from the NTS, the vasodepressor limb of baroreflexes. The NTS-C1 projection may be GABAergic.

The platelet-independent release of thromboxane A2 by Paf-acether from guinea-pig lungs involves mechanisms distinct from those for leukotriene.

Intra-arterial injections of platelet-activating factor (Paf-acether, 10-300 ng) to the perfused guinea-pig lung induced a dose-related bronchoconstriction, followed by contraction of the rat aorta superfused with the lung effluent, indicating the release of thromboxane A2 (TXA2) activity. These effects were matched with injections of bradykinin (Bk) at 100-1000 ng, leukotriene C4(LTC4) at 10-300 ng or arachidonic acid (AA) at 30-300 micrograms. Repeated doses of Paf-acether led to a specific desensitization of the release of TXA2, under conditions where Bk, LTC4 and arachidonic acid retained their ability to release TXA2. Bronchoconstriction and the release of TXA2 induced by Paf-acether were suppressed when the lungs were perfused with acetylsalicylic acid, but not with salicylic acid. The phospholipase A2 inhibitor, p-bromophenacyl bromide suppressed the release of TXA2 by Bk, but did not interfere with its formation from AA, nor with its release with Paf-acether and LTC4. The lipoxygenase inhibitor, nordihydroguaiaretic acid, inhibited to a similar extent the release of TXA2 by Bk, LTC4 and Paf-acether but also reduced directly the formation of TXA2 from arachidonic acid, invalidating its use as a specific antilipoxygenase agent. The leukotriene C4/D4 antagonist, FPL 55712, suppressed the TXA2 releasing effects of LTC4, and was completely inactive against Paf-acether, Bk or arachidonic acid. The aerosol of Paf-acether was tested in the anaesthetized guinea-pig and resulted in bronchoconstriction, unaccompanied by thrombocytopenia. Unlike bronchoconstriction induced by intravenous Paf-acether, which is refractory to cyclo-oxygenase inhibitors, the effects of the aerosol were suppressed by aspirin. Platelet depletion, which blocks the intravenous effects of Paf-acether, failed to interfere with those of the aerosol. Paf-acether induced a marked contraction of the superfused guinea-pig isolated parenchyma lung strip, which was followed by total and irreversible desensitization to itself. The contractile effect was not inhibited by aspirin or indomethacin, atropine, mepyramine, methysergide, phenoxybenzamine or propranolol, indicating that cyclo-oxygenase products, cholinergic stimuli, histamine, 5-hydroxytryptamine and catecholamine mechanisms are not involved. Our results indicate that Paf-acether interacts with pulmonary sites distinct from those for Bk, LTC4 or AA, since no cross-desensitization between Paf-acether and the other agonists was noted, p-bromophenacyl bromide inhibited Bk only and FPL 55712 inhibited only LTC4. The phospholipase A2 involved with the release of the arachidonate needed for the formation of TXA2 by Paf-acether or LTC4-stimulated lungs may differ from the enzyme accounting for its formation by Bk. The cellular sites with which Paf-acether interacts may also be distinct and less readily accessible to p-bromophenacyl bromide.

Electrophysiological and catecholamine mechanisms of negative feedback in hypothalamic regulation of the male gonads

Electrophysiological and catecholamine mechanisms of negative feedback in hypothalamic regulation of the male gonads

Catecholamine mechanisms in the stimulation of mouse locomotor activity by nitrous oxide and morphine

Nitrous oxide, like morphine, produces a significant increase in mouse locomotor activity. This stimulation of locomotor activity is antagonized by the narcotic antagonist naloxone (10 mg/kg). The catecholamine synthesis inhibitor α-methyl-p-tyrosine (300 mg/kg) also significantly reduced the nitrous oxide stimulation of mouse locomotor activity. Administration of naloxone (10 mg/kg) to mice previously treated with α-methyl-p-tyrosine resulted in a further decrease in nitrous oxide stimulated activity levels. Haloperidol (0.08–0.64 mg/kg), a potent dopamine receptor antagonist, dose dependently reduced the activity stimulation resulting from exposure to nitrous oxide. Administration of haloperidol (0.08 mg/kg) in conjunction with naloxone (10 mg/kg) further reduced the nitrous oxide effect. In view of the fact that morphine's activity stimulating effects are reduced by α-methyl-p-tyrosine and haloperidol, the results reported here suggest additional similarities in the pharmacology of morphine and nitrous oxide. The stimulation of mouse locomotor activity produced by nitrous oxide appears to be mediated by both endogenous opioid and catecholamines.

Catecholamine mechanisms in medio-basal hypothalamus influence prolactin but not growth hormone secretion

Medio-basal hypothalamic (MBH) catecholamine mechanisms in the regulation of prolactin and growth hormone (GH) secretion were investigated in unanesthetized rats with chronic indwelling venous cannulae and bilateral MBH directed intracerebral guide cannulae. MBH injections of the catecholamine-specific neurotoxin 6-hydroxydopamine (6-OHDA; 2 μg based in 0.5 μl 0.9% saline) had no effect upon basal prolactin or GH secretion. Examination of catecholamine fluorescence indicated that MBH 6-OHDA treatment produced widespread disruption of MBH catecholamine afferents but did not destroy tuberoinfundibular dopamine neurons of the arcuate nucleus, nor median eminence catecholamine structures. MBH injections (0.5 μl, 0.032 M solutions) of dopamine, noradrenaline or adrenaline all produced statistically significant increases in plasma prolactin levels. The potency of these 3 catecholamines in evoking prolactin release differed markedly, adrenaline having the greatest effect. MBH catecholamine injections had no effect upon plasma GH levels compared to saline injected controls. The present data suggest that MBH catecholamine afferents are unimportant in the regulation of basal patterns of GH or prolactin secretion. As MBH catecholamine injections stimulate prolactin release this region may contain a prolactin-facilitatory catecholamine mechanism which is capable of generating prolactin surges in response to certain environmental or endogenous stimuli.

Dopaminergic properties of nomifensine

Nomifensine and a proposed dihydroxy metabolite produced stimulation of motor behavior in mice with nomifensine being more potent. Weak cage-climbing behavior (stereotypy) was also produced. The stimulatory effects were greater in mice in which dopamine receptor sensitivity was increased by long-term haloperidol. Both of the analogs were potent inhibitors of dopamine and norepinephrine uptake in vitro with nomifensine approximately 3 times more potent than the metabolite. In contrast, the two analogs had weak affinity for the post-synaptic dopamine receptor (as measured by displacement of ligand binding in vitro) with dihydroxynomifensine approximately 6 times more potent than nomifensine. These results suggest that the behavioral effects of nomifensine are largely dependent on presynaptic catecholamine mechanisms but that weak direct dopamine agonist properties do exist, particularly in vivo where the drug may be metabolized to a more active form.

Hypertension, bradycardia, and pulmonary edema in the conscious rabbit after brainstem lesions coinciding with the A1 group of catecholamine neurons.

HomeCirculation ResearchVol. 49, No. 4Hypertension, bradycardia, and pulmonary edema in the conscious rabbit after brainstem lesions coinciding with the A1 group of catecholamine neurons. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessAbstractPDF/EPUBHypertension, bradycardia, and pulmonary edema in the conscious rabbit after brainstem lesions coinciding with the A1 group of catecholamine neurons. W W Blessing, M J West and J Chalmers W W BlessingW W Blessing Search for more papers by this author , M J WestM J West Search for more papers by this author and J ChalmersJ Chalmers Search for more papers by this author Originally published1 Oct 1981https://doi.org/10.1161/01.RES.49.4.949Circulation Research. 1981;49:949–958 Previous Back to top Next FiguresReferencesRelatedDetailsCited ByOkuda B, Tachibana H, Sugita M and Maeda Y (1993) Bilateral internuclear ophthalmoplegia, ataxia, and tremor from a midbrain infarction., Stroke, 24:3, (481-482), Online publication date: 1-Mar-1993.Giroud M, Gras P, Dumas R and Becker F (1993) Spontaneous vertebral artery dissection initially revealed by a pain in one upper arm., Stroke, 24:3, (480-481), Online publication date: 1-Mar-1993.Malik A (1985) Mechanisms of neurogenic pulmonary edema., Circulation Research, 57:1, (1-18), Online publication date: 1-Jul-1985.Reis D, Granata A, Joh T, Ross C, Ruggiero D and Park D (1984) Brain stem catecholamine mechanisms in tonic and reflex control of blood pressure., Hypertension, 6:5_pt_2, (II7), Online publication date: 1-Sep-1984.West M, Blessing W and Chalmers J (1981) Arterial baroreceptor reflex function in the conscious rabbit after brainstem lesions coinciding with the A1 group of catecholamine neurons., Circulation Research, 49:4, (959-970), Online publication date: 1-Oct-1981. October 1, 1981Vol 49, Issue 4Article InformationMetrics Copyright © 1981 by American Heart Associationhttps://doi.org/10.1161/01.RES.49.4.949 Originally publishedOctober 1, 1981 PDF download Advertisement

Effects of estradiol and progesterone on catecholamine turnover rates in discrete hypothalamic regions in ovariectomized rats.

Norepinephrine (NE) and dopamine (DA) activities were measured in several discrete brain areas (medial preoptic nucleus, suprachiasmatic nucleus, median eminence, and arcuate nucleus) in ovariectomized (OVX) and OVX steroidtreated rats. We wished to determine whether catecholamine (CA) mechanisms are involved in estradiol (E2)-induced LH surges and if amplification of such surges by progesterone (P)affects these CA systems. Animals were OVX, and 1 week later (day 0), groups were treated with Silastic capsules containing oilor an E2 solution (150 μg/ml in sesame oil). At 0900 h on day 2, E2-treated animals received Silastic capsules containing oil or P (50 mg/ml in oil). This steroid treatment results in physiologicalserum concentrations of both steroids. CA concentrations were determined by radioenzymatic assay in animals killed at 1000 or 1500 h on day 2 and in animals which were sacrificed 2 h after receiving a-methyl paratyrosine (400 mg/kg) at 1000 or 1500 h. Serum LH, FSH, PRL, E2, and P concentratio...

Abnormal catecholamine mechanisms in hypothalamic-pituitary disorders

Patients with growth hormone or prolactin-secreting pituitary tumors failed to show normal plasma catecholamine (especially norepinephrine) responses to oral bromocriptine. These patients had normal basal plasma catecholamine concentrations. Patients with anorexia nervosa had low basal levels of dopamine, norepinephrine, and epinephrine. These data are consistent with disordered catecholamine metabolism in patients with these neuroendocrine disorders.

The catecholamine mechanisms of prostaglandin E1-induced hypothermia in rats.

Intraperitoneal administration of prostaglandin E1 (PGE1) produced a hypothermia in rats at room temperatue (22 degrees C). The hypothermia in response to PGE1 was due to cutaneous vasodilatation and decreased metabolic heat production. Depletion of brain 5-hydroxytryptamine (with 5,6-dihydroxytryptamine and p-chlorophenylalanine) did not alter the PGE1-induced hypothermia. However, depletion of bran catecholamines (with 6-hydroxydopamine) and blockade of central catecholaminergic receptors (with phentolamine and propranolol) both greatly reduced the PGE1-induced hypothermia. The data indicate that PGE1 lowers body temperature in rats by acting on the central catecholaminergic systems.

Effects of Dopamine Agonists and Antagonists in Tourette's Disease

The actions of haloperidol, dextroamphetamine sulfate, levamfetamine succinate, apomorphine, and piribedil were studied in two patients with Giles de la Tourette's disease in an attempt to clarify the catecholamine mechanisms involved in this condition. Both dextroamphetamine and levamfetamine increased the severity of the symptoms; dextroamphetamine was more potent. Haloperidol controlled the symptoms and also antagonized the effect of dextroamphetamine. Apomorphine injections reduced the severity of symptoms, even in the presence of dextroamphetamine. We conclude that dopamine rather than norepinephrine is the principal catecholamine responsible for the symptoms. The effect of apomorphine may be understood through its action on postulated presynaptic inhibitory dopamine receptors, or other presynaptic mechanisms of action.

Brain biochemical and behavioral changes in 4 weeks old rats after neonatal oxygen deprivation

The acquisition of a conditioned avoidance response (CAR) and the effects on monoamine neurotransmittor synthesis was investigated in 28 days old rats after neonatal oxygen deprivation (100% N 2 for 20 min or 6% O 2-94% N 2 for 4.5 hr). The rats subjected to 6% O 2-94% N 2 for 4.5 hr at 1 day of age were markedly inferior in the CAR acquisition than the control group. The animals subjected to 20 min neonatal anoxia did not differ in avoidance responding compared to controls. Tyrosine hydroxylase and tryptophan hydroxylase activity was studied in vivo in whole brain at 28 days of age by measuring the accumulation of dihydroxyphenylalanine (DOPA) and 5-hydroxytryptophan (5-HTP) respectively after inhibition of aromatic L-amino acid decarboxylase with NSD 1015. An inhibition of tyrosine hydroxylase and tryptophan hydroxylase activity was found after neonatal exposure to 6% O 2-94% N 2 for 4.5 hr while the rats exposed to 100% N 2 for 20 min did not differ from controls. The precursor amino acids tyrosine and tryptophan and the levels of the endogenous monoamines dopamine (DA), noradrenaline (NA) and 5-hydroxytryptamine (5-HT) did not differ from controls in any of the groups. It is suggested that the observed behavioral deficits after prolonged hypoxia may be due to an impaired development of central catecholamine mechanisms.

Changes in the sensitivity of dopamine receptors in the nucleus accumbens and in the striatum induced by chronic ethanol administration.

Rats of the Sprague-Dawley strain were maintained on ad libitum food and a forced-intake regimen of ethanol for up to 270 days. Bilateral application of dapamine (DA) into the nucleus accumbens of both chronic ethanol rats and rats undergoing withdrawal produced a pronounced increase in coordinated locomotor activity which was 8--10 times higher than that of untreated water control rats. This phenomenon was first observed after 5 months of ethanol treatment and lasted for about 4 weeks after cessation of the treatment. It is concluded that prolonged ethanol administration produces an increased sensitivity of the DA-receptors in the nucleus accumbens and further supports the contention that central catecholamine mechanisms are involved in the mediation of the withdrawal syndrome observed after chronic treatment with ethanol.

Neural uptake of catecholamines and their molecular structures: a histopharmacologic study.

Using ultrastructural and histofluorescence methods, we investigated the uptake mechanism of catecholamines by the nerve terminals in the cutaneous smooth muscles of stump-tailed macaques (Macaca arctoides). This in vivo approach ultilized the observed cytotoxic effects of 6-hydroxydopamine on these catecholamine-containing terminals and the protective effects of simultaneous treatment with catecholamines (dopamine, norepinephrine, and epinephrine), their 3-0-methylated derivatives (metanephrine and normetanephrine), and catechol acids (3,4-dihydroxymandelic acid and 2, 4, 5-trihydroxymandelic acid). Both catecholamines and 3-0-methylated derivatives protected these nerve terminals from destruction by 6-hydroxydopamine, but catechol acids did not. However, the 3-0-methylated derivatives were less effective than the catecholamines. The degree of protection afforded by these amines depended largely on their concentration. Only catecholamines intensified the electron density of the intravesicular mass or the fluorescence in the nerve terminals; therefore, 3-0-methylated derivatives may inhibit 6-hydroxydopamine uptake at axoplasmic membrane sites, but not inside the axon. These observations led to the discovery that these are two sites for the catecholamine uptake process. One site is the axoplasmic membrane. The terminals are protected by catecholamines and their 3-0-methylated derivatives from 6-hydroxydopamine uptake and thus destruction. The other site is the intraaxonal compartments. Here competitive binding between the vesicular protein and both 6-hydroxydopamine and the catecholamines plays a main role.

The effect of chronic ethanol treatment on behaviour and central monoamines in the rat.

Rats weaned at 16 days of age were treated with various ethanol concentrations (8--24% w/v) for 270 days. The effect of the chronic ethanol treatment on the growth rate, the diurnal pattern of drinking, the open field activity, and the conditioned avoidance acquisition and retention of the rats were studied. Termination of the chronic ethanol administration caused two types of withdrawal syndromes. The first, an acute withdrawal syndrome was observed within 12 h after the discontinuation of the ethanol treatment and was characterized by extreme hyperexcitability. The second, a delayed withdrawal syndrome was characterized by a more coordinated behavioural stimulation and developed first after about 3 days after the discontinuation of the ethanol treatment. Biochemically, the latter withdrawal syndrome was accompanied by an increased rate of tyrosine hydroxylation (measured as the accumulation of dopa after inhibition of aromatic amino acid decarboxylase) in the striatum and dopamine-rich limbic structures. No differences in the accumulation of 5-hydroxytryptophan were observed. Furthermore, there was an increased level of dopamine concomitant with a decreased level of noradrenaline in the limbic areas during ongoing ethanol treatment. On the 4th day after withdrawal of ethanol the endogenous levels of dopamine and noradrenaline were statistically significantly reduced in the limbic structures. The data of the present study indicate that chronic ethanol administration induces various kinds of behavioural changes and that these changes at least partially are mediated via central catecholamine mechanisms.

Catecholamine mechanisms in the canine and feline lung

Catecholamine mechanisms in the canine and feline lung

Catecholamine Mechanisms in the Canine and Feline Lung

Catecholamine Mechanisms in the Canine and Feline Lung

Heart infarction-like effect induced by natural catecholamines in vitro

Isolated rat hearts were perfused using retrograde technique under constant perfusion pressure or under constant coronary flow. The addition of L-epinephrine or L-nor-epinephrine (1 microgram per ml) into the perfusion medium for one hour caused visible and irreversible morphological changes. They became apparent usually after 4 hours of perfusion in the form of small, pale, opaque spots of streaks gradually enlarging on the surface or on the transverse section of myocardium. Light microscope and electron microscope examination showed the disintegration process analogous to myocardial infarction but lacking the infiltration with blood elements. The structural changes were preceeded by increased release of lactate dehydrogenase into the effluent, the most characteristic metabolic change a accompanying myocardial injury. Although the underlying mechanism of cardiotoxic action catecholamines remains to be clarified, several factors under consideration could be eliminated like hyperlipidemia, thrombogenic process or reduced total coronary inflow rate.