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J B Martin

Publications and source records attributed to J B Martin.

At least 307 records · Page 17Linked to original sources
PubMed1977

Properties of soluble somatostatin-binding protein.

A soluble somatostatin-binding protein was detected in the cytosol fractions of various rat, human and bovine tissues. Maximum binding occurred at pH8.0-8.5 and was Ca(2+)-dependent. The specific binding of somatostatin per 10mug of cytosol protein from 12 rat tissues ranged between 36 and 15%, and 3% for peripheral blood cells. There was also substantial binding in cytosol from human anterior pituitary and liver, and bovine anterior pituitary. The specific binding in rat and human plasma in the presence of EDTA was only 1%. Gel filtration suggested a molecular weight of approx. 80000 for the somatostatin-binding protein from several sources. Exposure of the binding protein to trypsin eliminates somatostatin-binding activity but ribonuclease and deoxyribonuclease have no effect. The binding protein is thermolabile, ethanol-precipitable, and not completely specific for somatostatin. Bound (125)I-labelled [Tyr(1)]somatostatin is not easily displaced by excess of unlabelled somatostatin. The effects of dithiothreitol and mercaptoethanol on the binding of (125)I-labelled [Tyr(1)]somatostatin to the binding protein suggests that binding involves two sequential steps, first loose binding, then disulphide linkage. Since semipurified somatostatin-binding protein causes a dose-related inhibition of the binding of (125)I-labelled [Tyr(1)]somatostatin in radioimmunoassays for somatostatin, estimates of somatostatin content of tissue extracts by radioimmunoassay in some cases may be spuriously high. It is not yet clear whether the binding protein is a true cytosol protein or an easily solubilized membrane protein.

Animals↗
PubMed1977

Pulsatile growth hormone, prolactin, and thyrotropin secretion in rats with hypothalamic deafferentation.

Fifteen minute sequential blood sampling of male rats via right atrial cannulae was used to examine the patterns of anterior pituitary hormone secretion following hypothalamic deafferentations. Growth hormone (rGH) profiles from rats with complete hypothalamic deafferentation (CC) showed persistence of episodic rGH secretion with greatly increased frequency and elevated trough values, but without apparent entrainment to the light-dark cycle. Anterior (AC) and posterior (PC) deafferentation had no effect on the normal 3 h periodicity of rGH secretory episodes, but light-dark entrainment was lost in AC rats. Prolactin (rPRL) secretion in CC rats remained at normal low baseline levels without secretory episodes, while in AC and PC rats, as in normal rats, bursts of rPRL secretion occurred, often temporally related to rGH bursts. Thyrotropin (rTSH) levels in CC rats were less variable, and lower than in normal rats, while rTSH secretory profiles appeared normal in AC and PC rats. These results suggest that the isolated medial basal hypothalamus (MBH) contains neural substrates for episodic rGH secretion, and to a lesser extent, for rTSH. It is hypothesized that excessive rGH secretion in CC rats results from surgery damaging the rhythmicity of the rGH releasing factor (GRF) michanism, so that both sustained secretion and more frequent bursts of GRF occur. An effective rPRL inhibitory mechanism remains intact within complete hypothalamic deafferentations, while episodic rPRL and rTSH secretion require intact lateral afferents to the MBH. Visual pathway connections to the MBH, which mediate light-dark cycle entrainment of episodic rGH secretion, appear to pass through the region of the anterior hypothalamic and suprachiasmatic nuclei.

Afferent Pathways↗
PubMed1977

Subcellular distribution of radioimmunoassayable somatostatin in rat brain.

A specific, sensitive and reproducible radioimmunoassay is described for measurement of somatostatin in brain tissue. The sensitivity of the assay is 10 pg/tube and recovery of synthetic somatostatin added to brain homogenates was 95.8 +/- 6.2%. Dilution of tissue extracts from various brain regions showed parallelism in standard curves with labelled somatostatin. Somatostatin is shown to be widespread in the central nervous system with highest concentrations in hypothalamus, particularly the median eminence. Subcellular preparations of medial basal hypothalamus, preoptic area and amygdala indicate that over 70% of somatostatin immunoreactivity is localized to the synaptosome fraction. Recovery of activity in the P2 pellet prior to separation on sucrose gradient is approximately 100%. It is hypothesized that somatostatin, in addition to being released into blood vessels of the median eminence, may also be liberated from nerve terminals in other brain regions.

Amygdala↗
PubMed1977

Physiologic secretion of growth hormone and prolactin in male and female rats.

Growth hormone and prolactin are secreted episodically in man and experimental animals. To investigate physiologic mechanisms of GH and PRL secretion, a series of experiments were performed in individual, unanaesthetized male and female rats. GH secretion in the male rat is characterized by intermittent surges that occur approximately every 3 h and are entrained to the light-dark cycle. Peaks reach 200--400 ng/ml and troughs are unmeasurable. PRL is secreted in more frequent episodes with a pattern distinct from GH. In the female rat, GH surges occur more frequently--approximately once each hour. PRL levels are low (less than 15 ng/ml) except on the afternoon of pro-oestrous when they surge to levels of 100--300 ng/ml. Prolactin rises 4--6 h before delivery. Levels decline rapidly at the onset of parturition and surge with each episode of suckling in the post-partum period. Growth hormone and corticosterone rise during delivery and remain elevated for several hours after delivery. Reinstitution of suckling after removal of pups causes an immediate rise in PRL and GH. The PRL response is sustained for 3--4 h, whereas the GH response is brief with return to baseline within 1 h. The time courses of the two responses are clearly independent. Stress in the male rat causes a rapid rise in PRL and suppression in GH. The PRL surge to stress is brief with return to baseline by 1 h. GH pulses are suppressed for up to 5 h after stress. These studies indicate that separate neuroendocrine control mechanisms exist for regulation of the episodic release of GH and PRL in the rat.

Animals↗
PubMed1977

Evidence for a role of alpha-adrenergic mechanisms in regulation of episodic growth hormone secretion in the rat.

The role of catecholamines in regulation of episodic GH secretion was investigated in the male rat. Administration of alpha-methyl-p-tyrosine (alpha-MT; 250 mg/kg ip) caused significant suppression of GH bursts and resulted in marked elevation of plasma PRL. Intravenous administration of apomorphine (.03 and .1 mg/kg) had no effect on decreased GH levels, whereas clonidine (150 micrograms/kg) restored GH secretion. Apomorphine significantly reduced PRL levels in alpha-MT-treated rats whereas, clonidine resulted in a further increase in PRL.

Animals↗
PubMed1977

Pulsatile growth hormone and prolactin: effects of (+) butaclamol, a dopamine receptor blocking agent.

Growth hormone (rGH) and prolactin (rPRL) secretory profiles were obtained before and after treatment with a dopamine receptor blocking agent, (+) butaclamol, in 10 male rats chronically implanted with right atrial cannulae. Mean rGH plasma concentrations, determined by planimetry, were reduced (202 +/- 20 ng/ml vs. 135 +/- 20ng/ml, P less than .01), but the basic configuration and periodicity of rGH secretory bursts were unaltered. Mean rPRL plasma concentrations were elevated (11.1 +/- 2.1 ng/ml vs 65.5 +/- 8.1 ng/ml, P less than .0005), but rPRL episodic secretion was still apparent. It is concluded that dopaminergic neurons have a minor role in facilitating episodic rGH secretion. Furthermore, persisting episodic rPRL secretion in rats administered a dopamine antagonist suggests that rPRL feedback inhibition does not inactivitate the neural mechanism generating episodic rPRL secretion.

Animals↗