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PubMed1989

The role of tail skin temperature in the facilitation of the tail-flick reflex after spinal transection or interference with descending serotonergic neurotransmission.

We examined in mice whether tail skin temperatures and tail-flick reflexes were changed after spinal transection or intrathecal (i.th.) injection of the serotonin (5-HT) neurotoxin 5,6-dihydroxytryptamine (5,6-DHT) or the 5-HT receptor antagonist metergoline. Transection of the spinal cord reduced tail-flick latency (the time needed to evoke the tail-flick reflex by radiant heat) and increased tail skin temperature 15-21 days after surgery. Analysis of covariance showed that the effect of tail skin temperature on tail-flick latency was far more pronounced than the effect of spinal transection. Intrathecal injection of 5,6-DHT (5 or 10 micrograms mouse-1), which extensively reduced the spinal levels of 5-HT, reduced tail-flick latency and increased tail skin temperature 1-5 days after treatment. Similarly, tail-flick latency was shortened and tail skin temperature elevated 15 min after i.th. injection of metergoline (0.5 micrograms mouse-1). Analysis of covariance showed no significant effect of i.th. 5,6-DHT or i.th. metergoline on tail-flick latency. Tail skin temperature, on the other hand, had a highly significant effect on tail-flick latency. The results show that the facilitation of the tail-flick reflex in spinally transected mice and mice injected i.th. with 5,6-DHT or metergoline is mainly caused by increased tail skin temperature. The data do not indicate that descending 5-HT pathways tonically inhibit the tail-flick reflex.

5,6-Dihydroxytryptamine↗

PubMed1991

Lesions of bulbo-spinal serotonergic or noradrenergic pathways reduce nociception as measured by the formalin test.

Intrathecal administration of the neurotoxins 5,6-dihydroxytryptamine (5,6-DHT) and 6-hydroxydopamine (6-OHDA) in rats selectively lesioned the descending spinal serotonergic and noradrenergic pathways, respectively. Four days after neurotoxin administration the behaviour was evaluated in the formalin test. Several behavioural variables were recorded. The statistical analysis of the results was supplemented using a multivariate statistical method (partial least squares projection to latent variables, PLS) in addition to traditional analysis of variance. The described methods for recording and statistical analysis of behaviour appear to be useful in describing drug-induced differences in behavioural patterns in the formalin test. Both types of lesion reduced the pain-related behaviour in the formalin test (protection of the paw, biting and licking). The results indicate that the descending monoaminergic pathways are parts of a network which maintains adequate nociceptive responses to a chemical stimulus, or to stimuli lasting several minutes, as in the formalin test.

Animals↗

PubMed1980

Vasoactive intestinal polypeptide (VIP)-sensitive adenylate cyclase in rat brain: regional distribution and localization on hypothalamic neurons.

The regional distribution of the vasoactive intestinal polypeptide (VIP)-sensitive stimulation of adenylate cyclase activity was studied in homogenates or rat brain. The order of sensitivity of this peptide on enzyme activity was: olfactory bulb > hippocampus > thalamus > occipital cortex congruent to frontal cortex congruent to midbrain congruent to hypothalamus > striatum > cerebellum congruent to brain stem > spinal cord. With neurotoxin-induced lesions the possible location of VIP-sensitive adenylate cyclase within the anterior hypothalamus was investigated. Intrahypothalamic 6-hydroxydopamine blocked the stimulatory effect of VIP on hypothalmic adenylate cyclase, but neither kainic acid nor 5,7-dihydroxytryptamine lesions had any effect. Similarly, there was a 71% reduction in the sensitivity of VIP-sensitive adenylate cyclase activity in animals whose hypothalamic noradrenergic innervation had been interrupted by transection of the ascending dorsal and ventral bundles. Biochemical analyses of the lesions suggested that loss of VIP action on adenylate cyclase was associated with loss of hypothalamic noradrenaline-containing neurons. These results may give insight into those regions of rat brain where VIP may have a neurotransmitter role, and point to a possible noradrenergic localization of the VIP-sensitive adenylate cyclase within the hypothalamus.

5,7-Dihydroxytryptamine↗

PubMed1979

Selective response of rat peripheral sympathetic nervous system to various stimuli.

1. We utilized the induction of tyrosine hydroxylase, a catecholamine-synthesizing enzyme, in sympathetic ganglia and adrenal medullae to explore the central and peripheral mechanisms through which choline, various environmental stresses, and drugs that alter blood pressure or central neurotransmission affect various portions of the sympathetic nervous system. Animals received each treatment chronically, and enzyme activity was measured in the superior cervical, stellate, and coeliac ganglia and in the adrenal medullae.2. Choline administration increased tyrosine hydroxylase activity in all four tissues, probably by increasing the release of acetylcholine from preganglionic sympathetic neurones that synapse on catecholamine-producing ganglion and chromaffin cells; carbachol and nicotine had similar effects.3. Insulin enhanced tyrosine hydroxylase activity primarily in the coeliac ganglion and the adrenal medullae, but not in the superior cervical ganglia.4. Reserpine and phenoxybenzamine increased the activity of the enzyme in all four tissues.5. Prolonged exposure to a cold environment increased enzyme activity in all four tissues, but especially in the stellate and coeliac ganglia; forced swimming affected tyrosine hydroxylase only in these two ganglia.6. Several drugs known to modify central neurotransmission were found to increase tyrosine hydroxylase activity in some portions of the sympathetic nervous system but not in others. 5,7-Dihydroxytryptamine, which destroys terminals of serotoninergic neurones, enhanced enzyme activity in all four tissues, but primarily in the coeliac ganglion and adrenal medullae. ET-495 (a dopaminergic agonist), D-amphetamine, and morphine induced tyrosine hydroxylase activity in the adrenal medullae and the coeliac ganglion, but not in the superior cervical ganglia. Oxotremorine, a centrally acting muscarinic agonist, increased tyrosine hydroxylase activity only in the adrenal medullae; its effect was not blocked by methylatropine, a peripheral muscarinic blocker.7. These data indicate that specific neurones in the central nervous system, which utilize specific neurotransmitters and which are differentially affected by drugs and environmental inputs, selectively influence the outflows through the various zones of the sympathetic nervous system.

5,7-Dihydroxytryptamine↗

PubMed1979

Metabolic, respiratory, vasomotor and body temperature responses to beta-endorphin and morphine in rabbits.

1. The effects of beta-endorphin and morphine on thermoregulatory responses of unanaesthetized rabbits to different ambient temperatures (Ta) of 2, 22 and 32 degrees C were assessed. 2. Intraventricular administration of either beta-endorphin or morphine produced dose-dependent hypothermia at 2 and 22 degrees C Ta. At 2 degrees C Ta the hypothermia was brought about solely by a decrease in metabolic heat production. At 22 degrees C Ta the hypothermia was due to a decrease in metabolism and an increase in peripheral blood flow. However, at 32 degrees C Ta, there were no changes in rectal temperature in response to either beta-endorphin or morphine application. 3. Hypothermic effects of the administration of beta-endorphin or morphine were greatly antagonized by pretreatment of animals with either an opiate antagonist naloxone or a serotonin depletor 5,6-dihydroxytryptamine. 4. These findings indicate that the hypothermic responses to beta-endorphin or morphine in rabbits may be mediated through central serotonergic mechanisms. The hypothermia was due to a decrease in heat production and/or an increase in heat loss.

5,6-Dihydroxytryptamine↗

PubMed1987

Release of substance P from the cat spinal cord.

1. The present experiments examine the physiology and pharmacology of the release of substance P-like immunoreactivity (SP-l.i.), from the spinal cord in the halothane-anaesthetized, artificially ventilated cat. 2. Resting release of SP-l.i. was 36 +/- 4 fmol/30 min (mean +/- S.E.; n = 106). Bilateral stimulation of the sciatic nerves at intensities which evoked activity in fibres conducting at A beta conduction velocities (greater than 40 m/s), resulted in no change in blood pressure, pupil diameter or release of SP-l.i. Stimulation intensities which activate fibres conducting at velocities less than 2 m/s resulted in increased blood pressure, miosis and elevated release of SP-l.i. (278 +/- 16% of control). 3. The relationship between nerve-stimulation frequency and release was monotonic up to approximately 20 Hz. Higher stimulation frequencies did not increase the amounts of SP-l.i. released. At 200 Hz there was a reduction. 4. Capsaicin (0.1 mM) increased the release of SP-l.i. from the spinal cord and resulted in an acute desensitization to subsequent nerve stimulation. This acute effect was not accompanied by a reduction in spinal levels of SP-l.i. measured 2 h after stimulation. 5. Cold block of the cervical spinal cord resulted in an increase in the amounts of SP-l.i. released by nerve stimulation. 6. Pre-treatment with intrathecal 5,6-dihydroxytryptamine (300 micrograms) 7 days prior to the experiment caused a reduction in the dorsal and ventral horn stores of SP-l.i., but had no effect on the release of SP-l.i. evoked by nerve stimulation. Similar pre-treatment with intrathecal capsaicin (300 micrograms) resulted in depletion of SP-l.i. in the dorsal but not in the ventral horn of the spinal cord and diminished the release of SP-l.i. evoked by nerve stimulation. 7. Intense thermal stimulation of the flank resulted in small (20-35%), but reliable increases in the release of SP-l.i. above control. 8. Putative agonists for the opioid mu-receptor (morphine, 10-100 microM; sufentanil, 1 microM), and for the delta-receptor (D-Ala2-D-Leu5-enkephalin, 1-10 microM; D-Pen2-D-Pen5-enkephalin, 10 microM), but not the kappa-receptor (U50488H, 100-1000 microM), produced a dose-dependent, naloxone-reversible reduction of the evoked, but not of the resting release of SP-l.i. (-)-Naloxone, but not (+)-naloxone, resulted in a significant increase in evoked but not resting SP-l.i. release.(ABSTRACT TRUNCATED AT 400 WORDS)

5,6-Dihydroxytryptamine↗

PubMed1995

Tachykininergic slow depolarization of motoneurones evoked by descending fibres in the neonatal rat spinal cord.

1. In the isolated spinal cord of the neonatal rat, repetitive electrical stimulation of the upper cervical region elicited a prolonged depolarization of lumbar motoneurones (L3-5) lasting 1-2 min, which was recorded extracellularly from ventral roots, or intracellularly. 2. This depolarizing response was markedly depressed by the excitatory amino acid receptor antagonists D-(-)-2-amino-5-phosphonovaleric acid (D-APV, 30 microM) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM). The remaining response was further depressed by a 5-hydroxytryptamine (5-HT) receptor antagonist, ketanserin (3 microM). 3. In the presence of these antagonists, a small part of the depolarizing response of slow time course remained, and this response was partially blocked by the tachykinin NK1 receptor antagonists GR71251 (0.3-5 microM) and RP67580 (0.3-1 microM). In contrast, RP68651 (0.3-1 microM), the inactive enantiomer of RP67580, had no effect on the depolarizing response. 4. The slow depolarizing response in the presence of D-APV, CNQX and ketanserin was markedly potentiated by a peptidase inhibitor, thiorphan (1 microM). 5. This descending fibre-evoked slow depolarization became smaller after prolonged treatment (5-7 h) with 5,7-dihydroxytryptamine (10 microM), a neurotoxin for 5-HT neurones. Under such conditions, the effects of thiorphan and GR71251 on the slow depolarization were virtually absent. 6. Under the action of D-APV, CNQX and ketanserin, applications of tachykinins, substance P and neurokinin A produced depolarizing responses of lumbar motoneurones, and the responses were depressed by GR71251 and potentiated by thiorphan. 7. These results suggest that tachykinins contained in serotonergic fibres serve as neurotransmitters mediating the descending fibre-evoked slow excitatory postsynaptic potentials in motoneurones.

5,7-Dihydroxytryptamine↗

PubMed2005

(+/-)-3,4-Methylenedioxymethamphetamine administration to rats does not decrease levels of the serotonin transporter protein or alter its distribution between endosomes and the plasma membrane.

We showed that the serotonin (5-HT) neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) reduces brain tissue 5-HT, decreases expression of 5-HT transporter (SERT) protein, and increases expression of glial fibrillary acidic protein (GFAP). In contrast, doses of (+/-)-3,4-methylenedioxymethamphetamine (MDMA) that decrease brain tissue 5-HT fail to alter expression of SERT or GFAP. Using a new and highly sensitive anti-SERT antibody, we determined whether MDMA alters the subcellular distribution of SERT protein by measuring SERT expression in endosomes and plasma membranes 2 weeks after MDMA administration. Rat brain tissues (caudate, cortex, and hippocampus) were collected 3 days and 2 weeks after MDMA (7.5 mg/kg i.p., every 2 h x 3 doses) or 5,7-DHT (150 microg/rat i.c.v.) administration. Representative results from cortex are as follows. At both 3 days and 2 weeks postinjection, MDMA decreased tissue 5-HT (65%) and had no effect on GFAP expression. MDMA increased heat shock protein 32 (HSP32; a marker for microglial activation) expression (30%) at 3 days, but not 2 weeks. MDMA did not alter SERT expression at either time point and did not alter SERT levels in either endosomes or plasma membranes (2 weeks). 5,7-DHT decreased tissue 5-HT (80%), increased HSP32 expression at both time points (about 50%), and increased GFAP expression at 2 weeks (40%). 5,7-DHT decreased SERT expression (33%) at 2 weeks, but not at 3 days. These findings indicate that a dosing regimen of MDMA that depletes brain 5-HT does not alter SERT protein expression or the distribution of SERT between endosomes and the plasma membrane and does not produce detectable evidence for neurotoxicity.

5,7-Dihydroxytryptamine↗

PubMed1986

Morphological identification of serotonin-accumulating neurons in the living retina.

Neurons that accumulate the transmitter serotonin have been identified in the living retina by being labeled with 5,7-dihydroxytryptamine (5,7-HT), an autofluorescent serotonin analog. Iontophoretic injection of Lucifer yellow into the labeled cells under microscopic control revealed that the serotonin-accumulating neurons in rabbit retina constitute two morphological types of amacrine cells, termed S1 and S2, whose distal dendrites are stratified at the inner margin of the inner plexiform layer. The dendritic overlap of the S1 type is extraordinarily large: each point on the retina is covered by the fields of 550 to 900 S1 amacrines, and 6 to 8 meters of their dendrites are packed into each square millimeter of retina. Such a pervasive neuropil may provide an effective substrate for diffuse transmitter release, as proposed for serotonergic fibers elsewhere in the central nervous system.

5,7-Dihydroxytryptamine↗

PubMed1984

Facilitated sexual behavior reversed and serotonin restored by raphe nuclei transplanted into denervated hypothalamus.

Fetal raphe cells transplanted into the hypothalamus reversed facilitation of feminine sexual behavior in rats with brain lesions induced by 5,7-dihydroxytryptamine. Immunocytochemical and chemical analyses of serotonin indicate that reinnervation of the ventromedial nucleus of the hypothalamus by the transplants is associated with behavioral recovery. The findings suggest that transplanted fetal tissue can exert functional regulation over an innate, complex, hormone-dependent behavior in adult rats.

5,7-Dihydroxytryptamine↗

PubMed1982

Different synaptic location of mianserin and imipramine binding sites.

The high-affinity binding sites for mianserin and imipramine appear to be locate in different neurons of rat brain. Studies in which lesions were produced with 5,7-dihydroxytryptamine and other studies in which the 5-hydroxytryptamine content was decreased with p-chlorophenylalanine indicate that some of the imipramine binding sites are on serotonin axon terminals and others are on nonserotonergic synapses. The sites that bind mianserin are on postsynaptic serotonin sites as well as on synapses of other neuronal systems.

5,7-Dihydroxytryptamine↗

PubMed1979

Effects of apomorphine on thermoregulatory responses of rats to different ambient temperatures.

Either systemic or central administration of apomorphine produced dose-related decreases in rectal temperature at ambient temperatures (Ta) of 8 and 22 degrees C in rats. At Ta = 8 degrees C, the hypothermia was brought about by a decrease in metabolic rate (M). At Ta = 22 degrees C, the hypothermia was due to an increase in mean skin temperature, an increase in respiratory evaporative heat loss (Eres) and a decrease in M. This increased mean skin temperature was due to increased tail and foot skin temperatures. However, at Ta = 29 degrees C, apomorphine produced increased rectal temperatures due to increased M and decreased Eres. Moreover, the apomorphine-induced hypothermia or hyperthermia was antagonized by either haloperidol or 6-hydroxydopamine, but not by 5,6-dihydroxytryptamine. The data indicate that apomorphine acts on dopamine neurons within brain, with both pre- and post-synaptic sites of action, to influence body temperature.

5,6-Dihydroxytryptamine↗

PubMed1979

The role of the cholinergic system in the central control of thermoregulation in rats.

Systemic and central administration of methacholine (a synthetic choline derivative) both produced dose-dependent decreases in rectal temperature in rats at all the ambient temperatures studied. Both at room temperature (22 degrees C) and in the cold (8 degrees C), the hypothermia in response to methacholine application was brought about by both a decrease in metabolic heat production and an increase in cutaneous circulation. In the heat (29 degrees C), the hypothermia was due solely to an increase in respiratory evaporative heat loss. Furthermore, the methacholine-induced hypothermia was antagonized by central pretreatment of atropine (a selective blocker of cholinergic receptors), but not by the central administration of either 6-hydroxydopamine (a relative depletor of catecholaminergic nerve fibers) or 5,6-dihydroxytryptamine (predominately a serotonin depletor). The data indicate that activation of the cholinergic receptors within brain with methacholine decreases heat production and (or) increases heat loss which leads to hypothermia in rats.

5,6-Dihydroxytryptamine↗

PubMed1980

Angiotensin II inhibits both heat production and heat loss mechanisms in the rat.

The effects of intracerebroventricular injections of angiotensin II on thermoregulatory responses of conscious rats to ambient temperatures (Ta) of 8, 22, and 30 degrees C were assessed. Administration of angiotensin II produced dose-dependent hypothermia in rats at both Ta 8 and 22 degrees C. The hypothermia in response to angiotensin II was due to decreased metabolic heat production. In addition, angiotensin II produced cutaneous vasoconstriction at Ta 8-22 degrees C. However, at Ta 30 degrees C angiotensin II produced no change in rectal temperature or other thermoregulatory responses. Furthermore, the hypothermia induced by angiotension II was antagonized by pretreatment with 6-hydroxytryptamine (a selective catecholamine neurotoxin) and propranolol (a selective beta-adrenergic antagonist) but not either 5,6-dihydroxytryptamine (a selective serotonin neurotoxin), atropine (a cholinergic antagonist), or phentolamine (a selective alpha-adrenergic antagonist). The data indicate that angiotension II inhibits both heat production and heat loss mechanisms which lead to an alteration in body temperature, probably via the activation of central adrenergic receptors.

5,6-Dihydroxytryptamine↗

PubMed1982

Adrenomedullary secretory response to midbrain stimulation in rat: effects of depletion of brain catecholamines or serotonin.

Electrical stimulation of the periaqueductal gray substance (PAG) of the rostral midbrain of the rat produced biphasic or monophasic pressor responses depending on the duration of the stimulus train. Marked increases in plasma noradrenaline (NA) and adrenaline (A) levels accompanied the pressor responses, indicating the participation of the adrenal medulla. Depletion of central catecholamines (CA) by intraventricular administration of 6-hydroxydopamine (6-OHDA) did not affect the primary vasomotor component but markedly depleted adrenal CA levels and attenuated the adrenomedullary component of the response to brain stimulation. The intraperitoneal administration of p-chlorophenylalanine (pCPA) not only depleted brain serotonin (5-HT) levels but also reduced brain CA levels significantly. The adrenaline (A) levels were reduced in the adrenal glands of these rats and the adrenal secretory response to brain stimulation was attenuated. In contrast, the selective destruction of central 5-HT neurons by intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) in rats pretreated with desmethylimipramine (DMI) did not influence either the pressor nor the plasma CA responses to brain stimulation. Furthermore, the adrenal glands of these rats were normal. The results suggest that: (i) the central catecholaminergic neurons play an important role in the regulation of the adrenal glands but are not essential for the activation of the sympathetic vasoconstrictor fiber system: (ii) the pressor and plasma CA responses to PAG stimulation are not dependent on the central serotonergic system.

5,7-Dihydroxytryptamine↗

PubMed1985

Relationship between levels and uptake of serotonin and high affinity [3H]imipramine recognition sites in the rat brain.

High affinity [3H]imipramine binding, endogenous levels of serotonin and noradrenaline, and serotonin uptake were determined in brain regions of rats with selective destruction of serotonergic neurons by 5,7-dihydroxytryptamine (5,7-DHT), of adrenergic neurons by 6-hydroxydopamine (6-OHDA), and of rats treated with reserpine. Neonatal treatment with 5,7-DHT resulted in a significant decrease of both serotonin levels and density (Bmax) of high affinity [3H]imipramine binding sites in the hippocampus. In contrast, an elevation of serotonin levels and an increase in Bmax of [3H]imipramine binding were noted in the pons--medulla region. No changes were observed in the noradrenaline content in either of these regions. Intracerebral 6-OHDA lesion produced a drastic suppression of noradrenaline levels in cerebral cortex but failed to alter the binding affinity (KD) or density (Bmax) of [3H]imipramine recognition sites. A single injection of reserpine (2.5 mg/kg) resulted in marked depletion of both serotonin (by 57%) and noradrenaline (by 86%) content and serotonin uptake (by 87%) in the cerebral cortex but had no significant influence of the parameters of high affinity [3H]imipramine binding in this brain region. The results suggest that high affinity [3H]imipramine binding in the brain is directly related to the integrity of serotonergic neurons but not to the magnitude of the uptake or the endogenous levels of the transmitter, and is not affected by damage to noradrenergic neurons or by low levels of noradrenaline.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Effects of Shan-dou-gen (Euchresta formosana) on metabolic, respiratory and vasomotor activities as well as body temperature in rats.

The effects of the Chinese herb Shan-dou-gen, Euchresta formosana, on metabolic, respiratory and vasomotor activities as well as body temperature were assessed in conscious rats at various ambient temperatures. Systemic administration of Shan-dou-gen produced a dose-dependent hypothermia in rats at room temperature (22 degrees C) and below. The hypothermia in response to Shan-dou-gen was brought about by both cutaneous vasodilatation and decreased metabolic heat production. There were no changes in respiratory evaporative heat loss. However, in the heat (30 degrees C), administration of Shan-dou-gen produced no changes in rectal temperature or other thermoregulatory variables. Furthermore, the hypothermia induced by Shan-dou-gen was greatly antagonized by pretreatment of animals with 5,6-dihydroxytryptamine (predominantly a depletor of central serotonin nerve fiber), but not with 6-hydroxydopamine (a relative depletor of central catecholamine nerve fiber). It appears that the hypothermic effects of Shan-dou-gen may be mediated through serotonin release within the brain.

Animals↗

PubMed1995

Brain serotonin depletion attenuates diabetogenic effects of streptozotocin.

The diabetogenic effects of streptozotocin (STZ) were studied on blood glucose, plasma insulin, feeding and drinking, body weight, islet morphology, and hypothalamic serotonin (5-HT) release in vehicle-pretreated rats and in rats pretreated with either intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT; a 5-HT nerve fiber depletor), intraperitoneal injection of p-chlorophenylalanine (PCPA; a tryptophan hydroxylase inhibitor), or intraperitoneal injection of p-chloroamphetamine (PCA; a neurotoxin for 5-HT nerve fiber). At four days after STZ administration, vehicle-treated rats displayed hyperglycemia, polydipsia, polyphagia, decreased plasma insulin level, derangement of islet morphology (few insulin cells, accumulation of glucagon cells), and elevated 5-HT release in the hypothalamus. The above diabetogenic effects of STZ were attenuated by brain serotonin depletion induced by 5,7-DHT, PCPA, or PCA. Furthermore, the STZ-induced hyperglycemia or derangement of islet morphology was attenuated by peripheral sympathectomy or adrenalectomy. It is concluded that brain serotonin depletion attenuates diabetogenic effects of STZ by reducing sympathetic efferent activity in rats.

5,7-Dihydroxytryptamine↗