PubMed Health⌕ Search

Biomedical subjects

J J Reid

Publications and source records attributed to J J Reid.

At least 19 recordsLinked to original sources
PubMed1996

The aldose reductase inhibitor sorbinil does not prevent the impairment in nitric oxide-mediated neurotransmission in anococcygeus muscle from diabetic rats.

This study investigated whether increased polyol pathway activity could contribute to alterations in nitrergic neurotransmission in anococcygeus muscles from 8-week diabetic rats. In the presence of guanethidine (10-30 microM) and clonidine (0.01-0.05 microM), relaxations obtained to nitrergic nerve stimulation (0.5-5 Hz, 10-s train), to sodium nitroprusside (5-500 nM) and to nitric oxide (0.1-3 microM) were significantly reduced in muscles from diabetic rats compared to responses from control rats. Treatment of diabetic rats with the aldose reductase inhibitor sorbinil (42 mg/kg per day via feed for 8 weeks) did not affect impaired reactivity to nitrergic nerve stimulation, sodium nitroprusside or nitric oxide. The results suggest increased polyol pathway activity does not contribute to the alterations in nitrergic neurotransmission in anococcygeus muscles from diabetic rats.

Aldehyde Reductase↗
PubMed1996

HSP binding and mitochondrial localization of p53 protein in human HT1080 and mouse C3H10T1/2 cell lines.

In normal cells, the tumor suppressor actions of p53 protein are mediated by specific DNA binding and protein-protein interactions within the nucleus. Mutant p53 proteins, however, often assume an aberrant conformation devoid of tumor suppressor activity and newly capable of binding to the cognate or inducible HSP70. Recent reports from our laboratory and others show that additional unknown proteins may also complex with mutant p53. In this study, we characterize p53:HSP complexes and their subcellular location in the transformed cell lines, human HT1080 and murine C3H10T1/2, which both contain aberrant p53 conformers. Immunoprecipitation and SDS-PAGE of p53 from whole cell lysates revealed the additional presence of a broad 70 kDa band and a 90 kDa band in both lines, while p53 isolated from nuclear lysates was free from other proteins. 2D-PAGE was used to isolate and identify HSP members from cytoplasmic and nuclear lysates by immunoprecipitation, Western blotting and protein sequencing. Anti-p53 immune complexes from cytoplasmic lysates contained not only HSC70 but also GRP75, GRP78 and a weakly basic 90 kDa protein, which may be related to HSP90. The inducible form of HSP70 was not complexed to p53 protein, even though expressed in these cells. Analysis of anti-HSP70, anti-GRP75 and anti-HSP90 immune complexes suggests that HSP members exist as performed complexes in the cytoplasm, but not the nucleus. The presence of the mitochondrial and endoplasmic reticular chaperones, GRP75 and GRP78, in p53:HSP complexes suggested that p53 might be found in these cytoplasmic organelles which was confirmed in mitochondria by biochemical and immunoelectron microscopic evidence. These studies suggest that newly identified members of p53:HSP complexes represent components of a chaperone program which affects the subcellular distribution of p53 protein in these transformed lines.

Amino Acid Sequence↗
PubMed1995

Hydroxocobalamin and haemoglobin differentiate between exogenous and neuronal nitric oxide in the rat gastric fundus.

In longitudinal strips of rat gastric fundus, hydroxocobalamin (30 microM) significantly reduced relaxations to sodium nitroprusside (100 nM), nitric oxide (NO; 5 microM) and S-nitrosocysteine (3 microM), whereas responses to non-adrenergic, non-cholinergic (NANC) nerve stimulation were only slightly reduced. The stimulation-induced relaxations were markedly reduced by the NO synthase inhibitor NG-nitro-L-arginine (100 microM). Hydroxocobalamin (30 microM) enhanced relaxations to S-nitrosoglutathione (1 and 3 microM), and had no effect on responses to vasoactive intestinal polypeptide (1 nM). Haemoglobin (10 microM) significantly reduced relaxations to sodium nitroprusside, NO, S-nitrosocysteine and S-nitrosoglutathione, but did not affect responses to NANC nerve stimulation or vasoactive intestinal polypeptide. The results suggest that hydroxocobalamin and haemoglobin can differentiate between exogenous and neuronally released NO, and that the transmitter released from nitrergic nerves in the rat gastric fundus is not free NO or the nitrosothiols, S-nitrosocysteine and S-nitrosoglutathione.

Analysis of Variance↗
PubMed1995

Endothelin-1 and the regulation of vascular tone.

1. In 1988, Yanagisawa et al. reported the presence of a potent peptide from the supernatant of porcine endothelial cells. This was later named endothelin-1 (ET-1) and was found to belong to a new family of vasoconstrictor peptides. There are at least three isoforms of endothelin: ET-1, endothelin-2 and endothelin-3. 2. ET-1 is produced from a larger precursor molecule by endothelin converting enzyme (ECE); there may be a number of ECE but the most physiologically relevant appears to be a membrane-bound neutral metalloprotease. The endothelin precursor is produced on demand and is regulated at the mRNA level. 3. Two subtypes of mammalian endothelin receptors have been cloned and sequenced: ETA receptors which mediate vasoconstriction and ETB receptors which mediate both vasoconstriction and vasodilatation. However, functional studies have indicated that other subtypes of endothelin receptors may exist. 4. ET-1 has a wide range of biological actions apart from its direct effects on vascular tone, including constriction of non-vascular smooth muscle, cardiac effects, mitogenesis and stimulation of the release of hormones such as atrial natriuretic peptide and prostacyclin. At low concentrations which have no direct vasoconstrictor action, ET-1 potentiates the effect of other vasoconstrictor agonists. 5. The precise role of ET-1 in health and disease is not well defined at present; however, there are indications that it may have a role in the pathogenesis of some cardiovascular disease states, including subarachnoid haemorrhage, renal ischaemia and certain types of hypertension.

Amino Acid Sequence↗
PubMed1995

Effect of diabetes and elevated glucose on nitric oxide-mediated neurotransmission in rat anococcygeus muscle.

1. Nitric oxide (NO)-mediated neurotransmission is impaired in anococcygeus muscle from 8-week streptozotocin-induced diabetic rats. This study investigated the effects of insulin treatment, and the duration of diabetes on this impairment. In addition, the effect of in vitro exposure to elevated glucose has been investigated on NO-mediated relaxations, in muscles from untreated rats. 2. Relaxant responses to field stimulation (0.5-5 Hz, 10s train), sodium nitroprusside (SNP; 5 and 10 nM) and NO (1 and 3 microM) were significantly impaired in anococcygeus muscles from 8-week diabetic rats, compared to responses from control rats. Insulin treatment (5 u Lente day-1, s.c.) of diabetic rats prevented the development of this impairment. 3. Consistent with findings in 8-week diabetic rats, relaxation induced by field stimulation, SNP and NO were attenuated in tissues from 2-week and 4-week diabetic rats compared to corresponding control responses, whereas relaxations to papaverine (3 and 10 microM) were not reduced. In contrast, diabetes of 3-days duration did not affect relaxations to field stimulation, SNP or NO. 4. Incubation of anococcygeus muscles from untreated rats in medium containing elevated glucose (44.1 mM) for 6 h, significantly impaired relaxations to field stimulation compared to responses obtained after normal glucose (11.1 mM) incubation. Relaxations to SNP and to NO were not affected by 6 h exposure to elevated glucose. Similarly, incubation in hyperosmolar solutions containing mannose or sucrose for 6 h, impaired relaxations to field stimulation, but not to SNP or NO. 5. The results indicate that the diabetes-induced impairment of NO-mediated neurotransmission in the rat anococcygeus muscle develops between 3 days and 2 weeks after the induction of diabetes with streptozotocin. Prevention of the impairment by insulin treatment suggests that it is specific for the diabetic state. In addition, the impairment may be related to hyperglycaemia and the consequent rise in osmolarity, since in vitro exposure to high glucose as well as to other hyperosmolar media impaired NO-mediated relaxations to field stimulation.

Analysis of Variance↗
PubMed1995

Effect of diabetes on relaxations to non-adrenergic, non-cholinergic nerve stimulation in longitudinal muscle of the rat gastric fundus.

1. The effect of 8-week streptozotocin-induced diabetes has been examined on relaxations to non-adrenergic, non-cholinergic (NANC) nerve stimulation in longitudinal strips of rat gastric fundus. 2. In the presence of noradrenergic and cholinergic blockade and raised tissue tone, electrical field stimulation (0.5-4 Hz, 30 s trains) induced frequency-dependent relaxations that were significantly smaller in gastric fundus strips from diabetic rats than in strips from control rats. 3. NG-nitro-L-arginine methyl ester (NAME, 100 microM) significantly reduced NANC relaxations in muscle strips from both control and diabetic rats, but the reduction was greater in muscle strips from diabetic rats than in those from control rats at frequencies of 2 and 4 Hz. alpha-Chymotrypsin (1 u ml-1) slightly reduced relaxations to nerve stimulation in muscle strips from both control and diabetic rats. 4. The duration of NANC nerve relaxations (1-4 Hz, 30 s trains) was smaller in muscle strips from diabetic rats than in those from control rats. The duration of NANC relaxations was reduced by alpha-chymotrypsin (1 u ml-1) in muscle strips from control rats but not in muscle strips from diabetic rats. 5. Relaxations to both nitric oxide (NO; 1-30 microM) and vasoactive intestinal polypeptide (VIP; 0.1-30 microM) were concentration-dependent and did not differ between muscle strips from control and diabetic rats. 6. The results suggest that streptozotocin-induced diabetes impairs relaxations to NANC nerve stimulation in the rat gastric fundus, which are largely mediated by NO and to a lesser extent by VIP. The impairment appears to occur at the prejunctional level, as smooth muscle reactivity to NO and VIP is not altered.

Adrenergic Fibers↗
PubMed1995

Sexual dimorphism in copackaging of luteinizing hormone-releasing hormone and galanin into neurosecretory vesicles of hypophysiotrophic neurons: estrogen dependency.

Hypophysiotrophic neurons projecting to hypophyseal portal vessels in the median eminence of the hypothalamus maintain the operation of the master gland, the pituitary, by secreting releasing and release-inhibiting hormones into the bloodstream. LHRH, synthesized in neurons of the rat prosencephalon, is one of the key substances that governs the anterior pituitary-gonadal axis. Recently, it has been shown that the peptide galanin (GAL) is coproduced in a subpopulation of LHRH neurons and is a potent modulator of central processes regulating reproduction. A better understanding of the secretory mechanisms involved in pulsatile hormone release from LHRH axons of the median eminence requires exploration of the organelle domain that displays the cosynthesized peptides in terminal boutons. This study shows that LHRH- and GAL-immunoreactive axons overlap heavily in the lateral part of the median eminence. Double fluorescent labeling revealed colocalization of the peptides at the level of single axon terminals. By means of dual colloidal gold immunolabeling, LHRH and GAL were detected in the same secretory vesicles at the ultrastructural level. The incidence of colocalizing vesicles was high in the female (45%) and low in the male (3%) rat. Ovariectomy resulted in a dramatic decline in the number of LHRH/GAL-coexpressing vesicles (23%), which was reversed (55%) by the administration of estradiol. The observations indicate a sex-related difference in the packaging of LHRH and GAL and suggest that the events are estrogen dependent. Furthermore, the simultaneous release of GAL and LHRH from the colocalizing vesicles provides a mechanism that might ensure the potentiating effect of GAL on LHRH by synchronizing events at the receptor sites in the anterior pituitary.

Animals↗
PubMed1994

Changes in the responsiveness to endothelin-1 in isolated atria from diabetic rats.

This study investigates the influence of diabetes on the cardiac responsiveness to endothelin-1. The effects of endothelin-1 on rate and force of contraction were examined in isolated right and left atria, respectively, obtained from either streptozotocin (65 mg/kg)-treated rats (diabetic) or vehicle (0.02 M citric acid)-treated rats (control). The positive chronotropic and inotropic effects of endothelin-1 did not change in atria from diabetic rats at 2 and 4 weeks, but were reduced at 8 and 12 weeks. The positive chronotropic response to noradrenaline, but not to sympathetic nerve stimulation, was also reduced in 12-week diabetic rats. Endothelin-1 caused a decrease in the positive chronotropic and inotropic responses to sympathetic nerve stimulation and to noradrenaline; these inhibitory effects of endothelin-1 were not altered in 2-, 4-, 8- or 12-week diabetic rats. The study demonstrates that atrial responses to endothelin-1 and to noradrenaline are reduced by streptozotocin-induced diabetes, but the alteration depends on the duration of diabetes.

Animals↗
PubMed1994

Nitric oxide-mediated neurotransmission is attenuated in the anococcygeus muscle from diabetic rats.

The effect of STZ-induced diabetes of 8-weeks duration was examined on nitric oxide-mediated neurotransmission in the rat anococcygeus muscle. In the presence of noradrenergic blockade and raised tissue tone, relaxant response to nerve stimulation (0.5-5 Hz, for 10 s), sodium nitroprusside (5 and 10 nmol/l) and nitric oxide (1 and 3 mumol/l) were significantly reduced in anococcygeus muscles from diabetic rats compared to responses from control rats (p < 0.05). In contrast, relaxations to papaverine (3 and 10 mumol/l) were not reduced in tissues from diabetic rats. The nitric oxide synthesis inhibitor NOLA (100 mumol/l) abolished relaxant responses to nerve stimulation but had no effect on responses to any of the relaxant agents used. Exposure to NOLA at 10 mumol/l reduced stimulation-induced relaxations; this reduction was significantly greater in tissues from the diabetic group than from the control group (p < 0.05), probably as a consequence of the smaller relaxant responses in muscles from diabetic rats. Contractile responses to nerve stimulation (1-10 Hz, for 10 s), but not noradrenaline (0.03-30 mumol/l), were significantly greater in anococcygeus muscles from diabetic rats than from control rats (p < 0.05). NOLA (100 mumol/l) significantly enhanced stimulation-induced contractions (p < 0.05), however the enhancement was significantly less in tissues from diabetic rats (p < 0.05). The results suggest that STZ-induced diabetes impairs smooth muscle reactivity to nitric oxide in the rat anococcygeus muscle.

Animals↗
PubMed1994

Effect of aminoguanidine on the impaired nitric oxide-mediated neurotransmission in anococcygeus muscle from diabetic rats.

The contribution of advanced glycation end-product (AGE) formation to alterations in nitrergic neurotransmission caused by 8-week streptozotocin-induced diabetes has been examined in the rat anococcygeus muscle. Relaxant responses to nitrergic nerve stimulation (0.5-5 Hz, 10-sec train), to nitric oxide (NO; 0.1-3 microM), to the NO donor, sodium nitroprusside (SNP; 5-500 nM), and to the cell-permeable analogue of cyclic guanosine monophosphate (cGMP), 8-bromo-cGMP (15 and 30 microM), were significantly smaller in muscles from diabetic rats than from control rats. Pretreatment with aminoguanidine hemisulphate (1 milligram drinking water) to inhibit AGE formation, did not alter the relaxant responses to nitrergic nerve stimulation, NO or SNP in tissues from control rats, or responses to NO or SNP in tissues from diabetic rats, however relaxations to nitrergic nerve stimulation were further reduced in tissues from diabetic rats. In anococcygeus muscles from untreated animals, a 20-min exposure to aminoguanidine (1 mM) in vitro had no effect on relaxations to nitrergic nerve stimulation. The results suggest that diabetes impairs nitrergic transmission in the rat anococcygeus at least partly through alterations in the cGMP-relaxation pathway. The impaired neurotransmission does not appear to be related to the formation of AGEs.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1994

Sympathomimetic actions of methylenedioxymethamphetamine in rat and rabbit isolated cardiovascular tissues.

The aim of this study was to investigate the actions of methylenedioxymethamphetamine (MDMA) in several isolated cardiovascular tissues. In spontaneously beating rat atria, concentration-dependent positive chronotropic responses to MDMA and amphetamine were blocked by the neuronal-uptake inhibitor desipramine (1 microM) and the beta-adrenoceptor antagonist propranolol (1 microM). In atria incubated with [3H]noradrenaline to label transmitter stores, 10 microM MDMA and 1 microM amphetamine increased the resting outflow of radioactivity, while 1 microM desipramine had no effect on resting outflow. The MDMA- and amphetamine-induced release of radioactivity were blocked by 1 microM desipramine. MDMA, amphetamine and desipramine each enhanced the electrical stimulation-induced (2 Hz, 30-s train) release of radioactivity; the enhancing effects of MDMA and amphetamine were blocked by 1 microM desipramine. In rat isolated perfused hearts, MDMA (1 and 10 microM) increased heart rate by a similar amount to the increase caused by noradrenaline (10 and 50 nM). MDMA also induced dysrhythmias in 7 out of 11 rat isolated perfused heart preparations. In rabbit isolated perfused and superfused ear arteries preloaded with [3H]noradrenaline, MDMA increased the resting release of radioactivity by 230 +/- 18% (n = 6) of control resting release; the increase was accompanied by a rise in perfusion pressure of 17 +/- 7 mmHg (n = 6). MDMA also facilitated the vasoconstrictor responses to noradrenaline (3-9 ng) and perivascular nerve stimulation (1-5 Hz, 10-s train). MDMA-induced vasoconstriction and the facilitation of vasoconstrictor responses to noradrenaline and electrical stimulation were blocked by 1 microM desipramine.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamine↗
PubMed1993

Light and electron microscopic immunocytochemical localization of PKC delta immunoreactivity in the rat central nervous system.

Protein kinase C (PKC) is one of the major cellular signal transduction systems. Since at least nine different PKC isoenzymes have been described, the purpose of the present studies was to identify the regional, cellular, and subcellular distributions of PKC delta in the rat central nervous system (CNS) by light and electron microscopic immunocytochemistry. We have found that PKC delta immunoreactivity is present in all major subdivisions of the rat CNS. Within each of the subdivisions, PKC delta immunoreactivity is localized to perikarya that monitor sensory and motor functions. More specifically, PKC delta is found in the olfactory bulb, cerebral cortex, lateral septum, thalamus, vestibular and cochlear nuclei, inferior olive, nucleus of the solitary tract, cerebellum, and superficial layers of the dorsal horn in the spinal cord. In most cases, the distribution of this isoenzyme is distinct from that of the conventional isoforms. Within the CNS, PKC delta is localized primarily in neurons; however, neurons of the same type are not uniformly labeled. This is most evident in the cerebellum, where alternating columns of Purkinje cells are immunostained. While PKC delta is prominent in perikarya, occasional immunostaining is seen in dendrites, fibers or axons, and nerve terminal. Electron microscopic analysis of the posterolateral nucleus of the thalamus reveals that the cell nucleus, the rough endoplasmic reticulum, and the plasma membrane are all immunopositive. Since each of the PKC subspecies may have different substrate, lipid, and other co-factor requirements, the regional, cellular, and subcellular distribution of each of these isoforms should help to define their functional environments.

Animals↗
PubMed1993

Interactions of methylenedioxymethamphetamine with monoamine transmitter release mechanisms in rat brain slices.

This study investigates the effects of methylenedioxymethamphetamine (MDMA) and amphetamine on monoamine release from rat superfused brain slices in both the presence and absence of vesicular stores of transmitter. MDMA caused the release of radioactivity from slices incubated with [3H]5-hydroxytryptamine, [3H]noradrenaline or [3H]dopamine with EC50 values of 1.9 mumol/l (95% confidence limits 1.5-2.3 mumol/l), 4.5 mumol/l (2.3-8.7 mumol/l), and greater than 30 mumol/l, respectively. In contrast, amphetamine (0.1-300 mumol/l) was more effective in releasing radioactivity from slices incubated with [3H]dopamine than [3H]noradrenaline or [3H]5-hydroxytryptamine. When Ca2+ was excluded from the superfusion fluid, the MDMA-induced release of radioactivity from slices incubated with [3H]dopamine was unaltered, but that from slices incubated with [3H]noradrenaline or [3H]5-hydroxytryptamine was enhanced. MDMA (10 mumol/l) facilitated the stimulation-induced (5 Hz, 1 min) outflow of radioactivity from slices incubated with [3H]noradrenaline or [3H]5-hydroxytryptamine to 7.5-fold and 2.1-fold of control values, respectively, but had no effect on that from slices incubated with [3H]dopamine. Amphetamine (1 mumol/l) increased the stimulation-induced outflow from slices incubated with [3H]noradrenaline, but not that from slices incubated with [3H]5-hydroxytryptamine or [3H]dopamine. Inhibition of monoamine oxidase by a 30-min incubation with pargyline (100 mumol/l) enhanced the releasing action of MDMA on all three monoamines. Pargyline (100 mumol/l) also enhanced the facilitation caused by MDMA, of the stimulation-induced outflow of radioactivity from slices incubated with [3H]noradrenaline, [3H]5-hydroxytryptamine or [3H]dopamine. In some experiments, slices were obtained from reserpinised rats (2.5 mg/kg s.c. 24 h prior) and pre-exposed for 30 min to the monoamine oxidase inhibitor parglyine (100 mumol/l). Under these conditions, electrical stimulation evoked a small residual stimulation-induced outflow of radioactivity from slices incubated with [3H]noradrenaline, and failed to evoke an outflow of radioactivity from slices incubated with [3H]5-hydroxytryptamine or [3H]dopamine. However, a Ca(2+)-dependent stimulation-induced outflow of radioactivity was evoked in the presence of either MDMA (10 mumol/l) or amphetamine (1 mumol/l) from slices incubated with either [3H]dopamine or [3H]noradrenaline, but not from slices incubated with [3H]5-hydroxytryptamine. The stimulation-induced outflow of radioactivity from slices incubated with [3H]noradrenaline was enhanced in the presence of desipramine (1 mumol/l), however this enhancement was less than that caused by 10 mumol/l MDMA or 1 mumol/l amphetamine. The Ca(2+)-dependent response to electrical stimulation in the presence of MDMA from slices incubated with [3H]noradrenaline was greatly reduced when rats were pretreated with a higher dose of reserpine (10 mg/kg s.c.).(ABSTRACT TRUNCATED AT 400 WORDS)

3,4-Methylenedioxyamphetamine↗
PubMed1993

Endothelin-1 may be a physiologic modulator of vasoconstriction in rat kidney.

The effect of endothelin-1 (ET-1), in concentrations well below threshold and near physiologic levels, has been examined on vasoconstrictor responses to perivascular nerve stimulation and norepinephrine in rat isolated kidney, perfused through the renal artery with physiologic salt solution. A 60-min exposure to ET-1 (1, 10, and 100 pM) had little or no effect on the basal perfusion pressure but enhanced responses to nerve stimulation (4 Hz, 10-s train) by 123 +/- 12% (n = 6), 125 +/- 8% (n = 6), and 226 +/- 49% (n = 7) of the control response, respectively. Responses to nerve stimulation were consistent in the absence of ET-1. Vasoconstrictor responses induced by norepinephrine (30-300 pmol) increased with time in control experiments, but the increase was markedly greater in the presence of 10 and 100 pM ET-1. The vasoconstrictor responses caused by nerve stimulation and norepinephrine were greatly increased by the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (NOLA, 100 microM). In the presence of NOLA, ET-1 (1 pM) enhanced the responses to nerve stimulation (1-8 Hz, 10-s trains) by a significantly greater amount than in the absence of NOLA, suggesting that the enhancement by ET-1 is suppressed by NO release. The responses to norepinephrine (3-100 pmol) were also enhanced by 1 pM ET-1 in the presence of NOLA. The data suggest that ET-1 in physiologically relevant concentrations may have a role in the modulation of vascular reactivity in the renal circulation.

Amino Acid Oxidoreductases↗
PubMed1993

Galanin-immunoreactive axons innervate somatostatin-synthesizing neurons in the anterior periventricular nucleus of the rat.

The anterior periventricular nucleus (PeN) regulates GH secretion by synthesizing and releasing somatotropin release-inhibiting factor (SRIF) into the portal circulation. This territory of the diencephalon is heavily innervated by axons of galanin (GAL)-immunoreactive (IR) neurons. The connections between GAL-IR fibers and hypophysiotropic SRIF neurons were studied by means of immunocytochemical double labeling at the light and electron microscopic levels. Retrograde axonal labeling with Fluoro-Gold revealed the anterior PeN as the main site of hypophysiotropic SRIF-synthesizing neurons. These cells were densely surrounded by GALergic axons that made contacts with their cell bodies and dendrites. At the ultrastructural level, diaminobenzidine-labeled SRIF neurons received synapsing GAL-IR axons marked with silver-gold particles. Both axo-somatic and axo-dendritic forms of connections were observed. These morphochemical data revealed an interaction between GAL- and SRIF-synthesizing neurons in the anterior PeN. Furthermore, the presence of synaptic connections between these neuronal systems suggests a role for GAL in the control of SRIF secretion and, in turn, in the regulation of GH release.

Animals↗