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D P Cardinali

Publications and source records attributed to D P Cardinali.

At least 127 records · Page 7Linked to original sources
PubMed1990

Quantitative analysis of "synaptic" ribbon profiles in the pineal complex of male and female Pirbright-White guinea pigs.

Previous studies have pointed in the direction of sex differences as well as regional differences in the pineal gland of guinea pigs. In the present investigation these aspects were studied at the electron-microscopic level by quantitating different types of "synaptic" bodies, intrinsic to pinealocytes. The two major types of "synaptic" organelles, ribbons and spherules, did not exhibit regional or sex differences. "Synaptic" structures intermediate in appearance to ribbons and spherules were significantly larger in number in males in the distal region of the pineal gland, compared to females. As previous studies have shown that ribbon and spherule numbers undergo characteristic changes depending on the functional state of the pineal gland, it is concluded that, as far as the "synaptic" organelles are concerned, no clear-cut sex or regional differences appear to exist in the guinea pig pineal gland.

Animals↗
PubMed1990

GABA as a presumptive paracrine signal in the pineal gland. Evidence on an intrapineal GABAergic system.

GABA is present in the pineal gland of several mammals, where it is synthesized in situ as well as taken up from the circulation. This article reviews available information suggesting a local, physiological role of pineal GABA. Both the pinealocytes and the glial pineal cells have the capacity to take up GABA from the extracellular space. The GABA synthesizing enzyme glutamic decarboxylase (GAD) is detectable in the pineal gland; in the bovine pineal GAD exhibits "neuronal-like" properties. By employing a specific antibody against GABA, about 15% of pinealocytes gave a positive reaction in bovine pineal glands. After a depolarizing stimulus, GABA was released from bovine and rat pineal glands by both Ca2(+)-dependent and Ca2(+)-independent processes. By employing neuronal and glial GABA uptake inhibitors, most 3H-GABA release in bovine pineal gland could be attributed to a "neuronal" (presumably pinealocyte) compartment. Several components of the GABA type A receptor supramolecular complex (i.e., GABA binding sites, central-type benzodiazepine binding sites, Cl- ionophore), as well as a minor population of GABA type B receptor sites, were detected in bovine and human pineal glands. In the rat pineals, GABA is released by norepinephrine (NE) acting through alpha 1-adrenoceptors. Physiological concentrations of GABA, by its effect on type A receptor sites, impaired NE-induced melatonin release; by acting on GABA type B receptors, it decreased NE release. Another presumable presynaptic effect of GABA (i.e., to augment maximal velocity and to decrease affinity of NE uptake) was mediated by type A receptor sites. It is proposed that pre- and postsynaptic activity of GABA in the pineal does not differ from that found for GABA interneurons in local circuits of the brain.

Animals↗
PubMed1990

Regional differences in norepinephrine and dopamine concentration and effect on serotonin uptake and release in bovine pineal gland.

In order to analyze whether the bovine pineal gland is a homogeneous or a heterogeneous structure as far as monoamine content, the regional differences in norepinephrine (NE), dopamine (DA), serotonin (5HT), and 5-hydroxyindoleacetic acid (5HIAA) contents were assessed by high-pressure liquid chromatography. NE content was maximal in the proximal (close to the recessus pinealis) region and decreased in a rostral-caudal direction to achieve minimal values at the distal region. DA exhibited an opposite trend to NE, NE/DA ratios varying from 3.2 (proximal region) to 1.4 (distal region). Significantly lower NE content was found at the inferior as compared to the superior pineal region, and at the cortex as compared to the medulla. No significant differences were detected in DA concentration of these latter pineal regions, or in 5HT or 5HIAA concentration as a function of the region examined. 3H-5HT and 3H-NE uptake were maximal at the proximal zone in a rostral-caudal direction, at the superior as compared to the inferior region, and at the medulla as compared to the cortex. Unlabeled NE was equally effective to compete with 3H-5HT uptake in the several pineal regions studied. While NE increased maximally 3H-5HT release in a rostral-caudal direction, DA exhibited an opposite trend, displaying maximal 5HT release activity at the distal pineal region. DA and NE 5HT-releasing activity were greater in the pineal medulla than in the cortex, and did not exhibit differences in the superior as compared to the inferior pineal aspects. Excess (55 mM) K+ released 3H-5HT to a similar extent regardless of the pineal region examined.

Analysis of Variance↗
PubMed1990

Time-dependent effect of melatonin on actin mRNA levels and incorporation of 35S-methionine into actin and proteins by the rat hypothalamus.

The synthesis of the cytoskeletal protein actin exhibits, in the rat hypothalamus, a diurnal variation with maxima during morning hours. The objective of the present study was to assess whether melatonin injection could affect the in vitro incorporation of 35S-methionine into actin, as well as the levels of actin mRNA, in the hypothalamus of adult male rats treated either acutely or chronically with the hormone at 10:00 or 18:00. Injection of 100 micrograms/kg of melatonin for ten days at either time induced a significant depression in the incorporation of 35S-methionine into a 43 kDa protein with the electrophoretic mobility of actin. The specific activity of total soluble proteins after labeled methionine incubations decreased only after evening melatonin administration (100 micrograms/kg, ten days). Hypothalamic actin mRNA levels, quantitated by dot-blot analysis, decreased only after the injection of 100 micrograms/kg melatonin for ten days at 10:00. Neither a 10-micrograms/kg dose of melatonin, nor a single injection of 100 micrograms/kg melatonin, caused any significant change in the parameters examined. Melatonin (100 micrograms/kg for ten days) did not modify hypothalamic somatostatin or H-Ras mRNA concentration. These results suggest the existence of an inhibitory effect of melatonin on hypothalamic actin synthesis.

Actins↗
PubMed1990

Increase in adrenocorticotropin release during wallerian degeneration of peripheral sympathetic neurons after superior cervical ganglionectomy of rats.

The changes in adrenocorticotropin (ACTH) release before, during and after sympathetic nerve degeneration following superior cervical ganglionectomy (SCGx) were examined in male rats. A 12-fold increase of circulating ACTH was found in both SCGx and sham-operated rats 6 h after surgery. In sham-operated rats, plasma ACTH decreased by about half 16-22 h after surgery, whereas in SCGx rats it remained at a high concentration from 16 to 54 h after surgery, attaining basal values by 120 h post-SCGx. In SCGx rats, MBH corticotropin-releasing hormone (CRH) content decreased significantly from 16 to 54 h after surgery, while in controls it remained unmodified. Significantly smaller arginine vasopressin (AVP) contents were found in MBH of SCGx rats as compared to sham-operated controls, 16-54 h after surgery. In rats exposed to ether or immobilization stress 22 h after SCGx, plasma ACTH levels were significantly higher than in controls; however, since unstressed ACTH levels were about twice as high in SCGx rats, the percent increase of ACTH was smaller in the SCGx group. A decreased response of plasma ACTH to ether or immobilization stress was found in rats 7 days after SCGx. In rats subjected to a simultaneous adrenalectomy (Adx) and SCGx or sham-SCGx, plasma ACTH levels increased to a similar extent in both groups. ACTH increase after Adx was accompanied by decreases in MBH CRH, and absence of significant changes in MBH AVP contents. Rats subjected to pinealectomy (Px) or sham-Px 1 week earlier and killed 22 h earlier exhibited similar responses in plasma ACTH and MBH CRH to SCGx regardless of pineal intactness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1990

Inhibition of human platelet aggregation and thromboxane-B2 production by melatonin: evidence for a diurnal variation.

The effects of melatonin on platelet aggregation and thromboxane-B2 (TxB2) production induced by 1-4 x 10(-6) M adenosine diphosphate (ADP) or 0.6 x 10(-3) M arachidonic acid (AA) were assessed in platelet-rich plasma (PRP). Micromolar concentrations of melatonin inhibited in a dose-dependent way ADP-induced platelet aggregation with individual inhibitions 40% or more at 10(-6)-10(-5) M. A significant depression of AA-induced platelet aggregation was observed only at 10(-5)-10(-4) M melatonin. Morning (0830 h)-evening (1800 h) studies of ADP-induced platelet aggregation in seven normal men showed a higher sensitivity at 1800 h when analyzed as a global inhibitory effect of melatonin (P less than 0.01). Moreover, only during the evening hours did melatonin induce reversible aggregation, an index of inhibition of the platelet secretory process elicited by ADP exposure. No diurnal variability in melatonin inhibition of AA-induced aggregation was detected. TxB2 production elicited by AA in the evening was inhibited significantly in a concentration-related manner by a 2-min preincubation with 10(-9)-10(-5) M melatonin, while during the morning hours the inhibition was significant only at 10(-6) M or higher melatonin concentrations. In the case of ADP, the inhibition of TxB2 release attained significance at 10(-5)-M (0830 h) or 10(-6)-M concentrations (1800 h). In the presence of either stimulatory agent, melatonin depression of TxB2 generation was about 2-fold greater at 1800 h than at 0830 h. The diurnal changes in melatonin effect on TxB2 production were also observed in thrombin-stimulated washed platelets. The present data indicate the existence of circadian variations in platelet responsiveness to melatonin in humans.

Adult↗
PubMed1990

Diurnal variation in melatonin effect on adenosine triphosphate and serotonin release by human platelets.

The effect of the pineal hormone melatonin on adenosine diphosphate-induced human platelet aggregation and adenosine triphosphate release was assessed in platelet-rich plasma obtained from normal volunteers at 08.30 and 20.30 h. In 10(-7)-10(-5) mol/l concentrations melatonin inhibited ADP-induced platelet aggregation only in the evening (p less than 0.05). ADP-induced ATP release, an index of platelet secretory processes, showed a generally greater, dose-dependent inhibition after adding melatonin (10(-9)-10(-5)mol/l) at 20.30 h as compared with 08.30 h. The inhibitory activity of melatonin (10(-9)-10(-5) mol/l) on [3H]serotonin release elicited by thrombin in washed human platelets obtained from normal volunteers was dose-dependent; the effect was generally greater at 20.30 h. The activity of the potent platelet anti-aggregating agent prostacyclin did not exhibit diurnal differences with respect to impairing ADP-induced platelet-rich plasma aggregation. These results indicate the existence of a diurnal variation of sensitivity to melatonin in human platelets.

Adenosine Diphosphate↗
PubMed1989

Release and effect of gamma-aminobutyric acid (GABA) on rat pineal melatonin production in vitro.

1. 3H-gamma-Aminobutyric acid (GABA) release elicited by a depolarizing K+ stimulus or by noradrenergic transmitter was examined in rat pineals in vitro. 2. The release of 3H-GABA was detectable at a 20 mM K+ concentration in medium and increased steadily up to 80 mM K+. 3. In a Ca2+-free medium 3H-GABA release elicited by 30 mM K+, but not that elicited by 50 mM K+, became blunted. 4. Norepinephrine (NE; 10(-6)-10(-4) M) stimulated 3H-GABA release from rat pineal explants in a dose-dependent manner. 5. The activity of 10(-5) M NE on pineal GABA release was suppressed by equimolecular amounts of prazosin or phentolamine (alpha 1- and alpha 1/alpha 2-adrenoceptor blockers, respectively) and was unaffected by propranolol (beta-adrenoceptor blocker). 6. The alpha 1-adrenoceptor agonist phenylephrine (10(-7)-10(-5) M) and the beta-adrenoceptor agonist isoproterenol (10(-5) M) mimicked the GABA releasing activity of NE, while 10(-7) M isoproterenol failed to affect it; the alpha 2-adrenoceptor agonist clonidine (10(-7)-10(-5) M) did not modify 3H-GABA release. 7. The addition of 10(-4) M GABA or of the GABA transaminase inhibitor gamma-acetylenic GABA or aminooxyacetic acid inhibited the melatonin content and/or release to the medium in rat pineal organotypic cultures. 8. GABA at concentrations of 10(-5) M or greater partially inhibited the NE-induced increase in melatonin production by pineal explants. 9. The depressant effect of GABA on melatonin production was inhibited by the GABA type A receptor antagonist bicuculline; bicuculline alone increased the pineal melatonin content. Baclofen, a GABA type B receptor agonist, did not affect the pineal melatonin content or release. 10. The decrease in serotonin (5-HT) content of rat pineal explants brought about by NE was not modified by GABA; GABA by itself increased 5-HT levels. 11. These results indicate that (a) GABA is released from rat pineals by a depolarizing stimulus of K+ through a mechanism which is partially Ca2+ dependent; (b) NE releases rat pineal GABA via interaction with alpha 1-adrenoceptors; (c) GABA inhibits melatonin production in vitro via interaction with GABA type A receptor sites; and (d) GABA's effect on NE-induced melatonin release does not correlate with the lack of effect on the NE-induced decrease in pineal 5-HT content.

Animals↗
PubMed1989

GABA and its neural regulation in rat brown adipose tissue.

By using a radioreceptor assay GABA was detectable in rat interscapular brown adipose tissue (IBAT), the levels being 1% those of CNS and 10-fold those of peripheral plasma. Injection of the glutamic acid decarboxylase (GAD) inhibitor 3-mercaptopropionic acid lowered IBAT GABA levels by about half while injection of the GABA transaminase inhibitor gamma-acetylenic GABA increased them by 230%. Rats kept at 4 degrees C for 14 days exhibited IBAT GABA levels that were about half those found at 22 degrees C. Accumulation of IBAT GABA after gamma-acetylenic GABA increased by 2-fold in cold-exposed rats. Sympathetic denervation of IBAT prevented the effect of the cold environment on GABA content and impaired that on GABA accumulation. GAD activity was detectable in IBAT homogenates and isolated brown adipocytes. Exposure of rats to cold increased Vmax of GAD without modifying its Km, regardless of intactness of innervation. In binding studies with 3H-GABA as a ligand, two types of sites were uncovered of KD = 14 and 146 nM, respectively. In the presence of 2.5 mM Ca2+ bicuculline and baclofen were 57 and 46% as effective as GABA to displace 3H-GABA from IBAT binding sites. The results indicate existence, possible synthesis and type A and B receptors of GABA in rat IBAT.

Adipose Tissue↗
PubMed1989

gamma Aminobutyric acid uptake, release, and effect on 36Cl--influx in bovine pineal gland.

Two apparent affinities for Na+-dependent, 3H-GABA uptake were found in bovine pineal fragments in vitro i.e., a high affinity uptake (Km = 37 +/- 5 microM) and a low affinity uptake (Km = 435 +/- 50 microM). GABA or the neuronal and glial GABA uptake inhibitor nipecotic acid was significantly more effective than the inhibitor of the GABA glial uptake beta-alanine to decrease pineal 3H-GABA uptake. High K+ concentration release 3H-GABA in superfused bovine pineals, no differences in 3H-GABA release among fragments taken from medial, proximal or distal pineal regions being apparent. Superfusion of pineal fragments in the absence of Ca2+ but in the presence of EGTA, Mg2+ or verapamil decreased significantly 3H-GABA release induced by K+. In every case a Ca2+-independent pineal GABA release was found. Preincubation with GABA or nipecotic acid, but not with beta-alanine, blunted subsequent 3H-GABA release. GABA increased 36Cl--influx in pineal homogenates, an effect blocked by picrotoxin. Incubation of pineal homogenates in the presence of aminooxyacetic acid decreased Vmax of glutamic acid decarboxylase, without modifying its Km. These results are compatible with a transmitter or modulator role of GABA in bovine pineal gland.

Alanine↗
PubMed1989

Serotonin release mechanisms in bovine pineal gland: stimulation by norepinephrine and dopamine.

An assessment of serotonin (5HT) release was made in bovine pineal gland. Bovine pineal fragments took up [3H]5HT by a Na+-dependent process exhibiting two apparent Km, i.e. a high affinity uptake system (Km = 220 nM) and a low affinity uptake system (Km = 197 microM). A significant release of [3H]5HT was elicited by increasing K+ concentrations in the medium (20-80 mM). Exposure of bovine pineal fragments to varying doses of catecholaminergic agonists indicated that a significant [3H]5HT release was elicited at the following threshold concentrations: 10(-6) M norepinephrine (NE), 10(-7) M dopamine (DA), 10(-6) phenylephrine and 10(-6) M isoproterenol. By employing specific receptor agonists and antagonists, the 5HT release activity of adrenergic agonists was found to be mediated by alpha 1-adrenoceptors, while that of DA by D2-dopaminergic receptors. 5HT release elicited by NE or DA, as well as that by 30 mM K+, was Ca2+-dependent. Both NE and DA increase 45Ca2+ uptake in a dispersed cell preparation of bovine pineal glands. As in the case of 5HT release, the effect of NE and DA on calcium uptake was mediated by alpha 1-adrenoceptors and D2-dopaminergic receptors, respectively. These results indicate that both NE and DA control 5HT release in bovine pineal gland.

Animals↗
PubMed1989

Estrous cycle delay and inhibition of gonadotropin and prolactin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats.

The changes in the activity of the pituitary-gonadal axis during sympathetic nerve degeneration after superior cervical ganglionectomy (SCGx) were examined in female rats. In a first experiment SCGx performed at 24.00 h of diestrus II, 17 h in advance to the critical period for gonadotropin and prolactin (PRL) release, caused a delay of 1 day or more in estrous cyclicity, while SCGx at 24.00 h on estrus did not modify the estrous cycle. In a second experiment ovariectomized rats injected subcutaneously with estradiol-progesterone or vehicle were subjected to SCGx 17 h before the expected maxima in luteinizing hormone (LH), follicle-stimulating hormone (FSH), and PRL serum levels. A significant decrease of serum gonadotropin and PRL concentration was found in SCGx, steroid-treated rats. In a third experiment groups of rats injected with estradiol-progesterone and killed at 15.00, 16.00, 17.00, or 18.00 h at or around the time of maximal FSH, LH, and PRL release were used. SCGx performed 17 h before killing caused a generally depressive effect of LH, FSH, and PRL release. In a fourth experiment ovariectomized rats were subjected to pinealectomy and, 1 week later, to estradiol-progesterone treatment and SCGx as in experiment 2. Pinealectomy did not modify the depression of steroid-induced LH, FSH, and PRL release found during wallerian degeneration of sympathetic nerves after SCGx. In a fifth experiment the effect of alpha 1- and/or beta-adrenoceptor blockade on SCGx-induced inhibition of hormone release was assessed in estradiol-progesterone treated, spayed rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of adenosine on melatonin and norepinephrine release in rat pineal explants.

To study adenosine effect on melatonin production, rat pineal explants were incubated for 6 h with 10(-4) M adenosine or 2-chloroadenosine in the presence or absence of 5 x 10(-5) M norepinephrine (NE). Melatonin content in pineal gland and medium was measured by RIA. Both adenosine and 2-chloroadenosine increased melatonin production rate by 3-4-fold, and augmented NE stimulation by 30-40%. Addition of adenosine deaminase prior to NE reduced stimulated melatonin release by 40-46%. 2-Chloroadenosine counteracted the inhibition of NE response given by adenosine deaminase. Either adenosine or its A1 receptor agonist cyclohexyl adenosine (CHA) decreased by 20-22% 3H-transmitter release induced by a K+ depolarizing stimulus in rat pineal incubated with 3H-NE. These results suggest that adenosine affects both pre- and postsynaptic pineal mechanisms.

2-Chloroadenosine↗
PubMed1988

24 hour changes in catecholamine content of rat thyroid and submaxillary glands.

The occurrence of diurnal rhythmicity in tissue norepinephrine (NE), epinephrine (E) and dopamine (DA) levels of rat thyroid and submaxillary glands was assessed in animals killed at eight time intervals during a 24 hour period. In both tissues significant peak values of NE content were found at the third hour of dark onset (at 23:00 h). Additionally a minimum of NE content of thyroid gland was apparent in rats killed at the fifth hour of photophase (at 11:00 h). As in the case of NE, peak values of E content were found during the scotophase in both tissues examined. In contrast, DA levels exhibited no diurnal rhythmicity in the rat thyroid gland, and an early rise at the beginning of the photophase in the submaxillary glands. These results support an activation of the sympathetic nervous system innervating the thyroid and submaxillary glands at the beginning of the scotophase. Tissue DA levels do not resemble the activity of peripheral sympathetic nerves in the tissues examined.

Animals↗
PubMed1988

Benzodiazepine binding sites in rat interscapular brown adipose tissue: effect of cold environment, denervation and endocrine ablations.

3H-Flunitrazepam (FNZP) binding was examined in a crude membrane fraction obtained from rat interscapular brown adipose tissue (IBAT). A single population of binding sites was apparent with dissociation constant (KD) = 0.47 +/- 0.04 microM and maximal number of binding sites (Bmax) = 31 +/- 5 pmol.mg prot-1. From the activity of several benzodiazepine (BZP) analogs to compete for the binding, the peripheral nature of FNZP binding was tentatively established. Similar BZP binding sites were detectable in isolated IBAT mitochondria. Exposure of rats to 4 degrees C for 15 days decreased Bmax significantly without affecting KD. Cold-induced decrease in Bmax of BZP binding was prevented by surgical IBAT denervation. Denervation prevented or impaired the increased activity of the mitochondrial markers succinate dehydrogenase and malate dehydrogenase in IBAT of cold-exposed rats, but did not affect monoamine oxidase activity. Hypophysectomy of rats decreased significantly both KD and Bmax of IBAT BZP binding. Thyroidectomy, adrenalectomy or ovariectomy did not affect IBAT BZP binding parameters. The BZP analogs diazepam, clonazepan and Ro 5-4864 decreased significantly guanosine 5'-diphosphate binding (GDP) in IBAT mitochondria while co-incubation of Ro 5-4964 or clonazepam with the peripheral type BZP antagonist PK 11195 did not modify BZP activity on GDP binding. Our results indicate that BZP binding in rat IBAT may belong to the peripheral type, is decreased by a cold environment through activation of peripheral sympathetic nerves and is affected by hypophysectomy. BZP and GDP binding in IBAT mitochondria seem not to be functionally related.

Adipose Tissue↗
PubMed1988

Effect of superior cervical ganglionectomy on insulin release by murine pancreas slices.

The effect of superior cervical ganglionectomy (SCGx) on basal and glucose-stimulated insulin release in vitro was examined in pancreas slices of BALB/c mice subjected to surgery 14-96 h earlier. Fourteen or 20 h after SCGx a significant increase of insulin response to 11 mM glucose was detectable, while 96 h after SCGx a depression in response was found. Perifused pancreas slices obtained from mice subjected to SCGx 7 days earlier showed a decreased in vitro insulin response to glucose during both phases of insulin secretion. In sham-operated mice, injection of the beta-adrenoceptor blocker propranolol or of the cholinergic muscarinic antagonist atropine decreased basal and glucose-stimulated insulin release, while the alpha-adrenoceptor blocker phenoxybenzamine did not affect it significantly. In mice subjected to SCGx 14 h earlier, propranolol treatment decreased basal insulin release and impaired the release elicited by glucose to values similar to those found in controls, phenoxybenzamine injection increased the basal and amplified the enhanced glucose-stimulated insulin release, and atropine injection, although unable to affect basal insulin release, impaired partially the amplification of response detectable after surgery. Our results support the existence of significant effects of SCG neurons on insulin release in mice.

Animals↗
PubMed1988

Effect of inferior laryngeal nerve section on thyroid function in rats.

To examine the role of thyroid parasympathetic innervation in organ's function, rats subjected to inferior laryngeal nerve (ILN) section were employed. This procedure decreased thyroid [3H]choline uptake by about half. Bilaterally ILN-sectioned rats treated with methylmercaptoimidazole for 4 days exhibited a significant impairment of the methylmercaptoimidazole-induced goitrogenic response. Unilateral ILN section resulted in further atrophy of the ipsilateral thyroid lobe in hypophysectomized rats. One week after ILN section a significant decrease of serum T4 and an increase of serum TSH were observed. Bilateral ILN section generally decreased circulating T4 for up to 28 days after surgery, while a unilateral ILN section caused a transient T4 decrease for 1 week after surgery. Compensatory thyroid growth in rats subjected to unilateral thyroidectomy (hemi Tx) and ILN section performed ipsilaterally to the remaining lobe, was significantly smaller than that of rats subjected to hemi Tx alone. Hemi Tx depressed serum T4 and increased serum TSH levels significantly. These hormonal changes were prevented by unilateral superior cervical ganglionectomy (SCGx), but were unaffected by ILN section. The combination of SCGx and ILN section negated the facilitating effect of SCGx on thyroid secretion and impaired the increase in compensatory thyroid growth brought about by thyroid sympathetic denervation. Thyroid mitotic index studies in hemi Tx rats receiving ILN section, SCGx, or a combination of both indicated that the increase in the number of follicular mitosis caused by hemi Tx was significantly impaired by ILN section and was significantly increased by SCGx. SCGx potentiation of thyroid follicular mitotic activity was partially prevented by concomitant ILN section. These results support a significant role of thyroid sympathetic and parasympathetic innervation in the control of organ's growth and secretory activity.

Animals↗