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Biomedical subjects

P B May

Publications and source records attributed to P B May.

At least 19 recordsLinked to original sources
PubMed2001

Ventricular enlargement in adults with profound mental retardation who demonstrate violent/destructive behaviors.

The authors determined brain ventricular size (ventricular brain ratio [VBR]) in 39 ambulatory adult mentally retarded individuals who did or did not require psychotropic medication for violent/destructive behavior. The mean VBR of mentally retarded patients who required psychotropic medication was significantly greater than the VBR of those who did not require such medication.

Adolescent↗
PubMed1992

Blockade of hippocampal long-term potentiation by saccharin.

Population spikes, population excitatory postsynaptic potentials and intracellular excitatory postsynaptic potentials were recorded in the CA1 area of guinea-pig hippocampal slices in response to low frequency stimulation of the stratum radiatum. Tetanic stimulation of the same afferents during an application of saccharin (10 mM, 10 min) failed to induced a long-term potentiation of the population spike, population excitatory postsynaptic potential and intracellularly recorded excitatory postsynaptic potential. A post-tetanic application of saccharin did not prevent long-term potentiation of the population spike from developing. Saccharin did not change the input resistance, the membrane potential or the ability to induce action potentials in the CA1 neurons. The slope of the intracellular excitatory postsynaptic potentials recorded in normal medium, in normal medium containing 2-amino-5-phosphonovalerate, or in Mg(2+)-free medium containing 6-cyano-7-nitroquinoxaline-2,3-dione was not significantly altered by saccharin. The depolarizations of CAI neurons produced by superfusion of N-methyl-D-aspartate or during a brief tetanic stimulation of the stratum radiation were also not altered by the drug. It therefore appears that saccharin blocks the induction of long-term potentiation by a mechanism that does not involve a blockade of N-methyl-D-aspartate receptors. Application of fluid samples collected from rabbit neocortical surface during a tetanic stimulation of the neocortex caused neurite growth in PC-12 cells, suggesting that growth-related substances were present in the collected samples. If these samples were superfused onto hippocampal slices, long-term potentiation developed. If however, the samples were co-applied with saccharin, neither neurite growth in PC-12 cells nor long-term potentiation in hippocampal slices was observed, raising the possibility that growth-related substances are involved in long-term potentiation.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1988

Substances released during tetanic stimulation of rabbit neocortex induce neurite growth in PC-12 cells and long-term potentiation in guinea pig hippocampus.

Samples collected from rabbit neocortical surface during a tetanic stimulation of the neocortex induced neurite growth in PC-12 cells in culture and synaptic long-term potentiation (LTP) in guinea pig hippocampal slices. If these samples were preheated and cooled, or if they were collected in the absence of a tetanic stimulation of the rabbit neocrotex, they did not induce neurite growth in PC-12 cells or LTP in the guinea pig hippocampus. These results suggest that neurite-inducing factors are released during tetanic stimulations and that these substances are involved in LTP.

Action Potentials↗
PubMed1988

Manganese can inhibit or potentiate contractile responses in mesenteric portal vein.

The effects of a number of agents believed to interfere with Ca were examined on contraction induced by noradrenaline (NA) or K in rat mesenteric portal veins. The organic calcium antagonists nifedipine, verapamil, methoxyverapamil, and felodipine slowly produced maximum inhibitory effects, nifedipine being fastest with a T1/2 of 20 min. In contrast, the inhibitory effects of Mn were immediate but disappeared on continued exposure of the tissue to Mn. After removal of Mn from the bath fluid, an above normal contraction was produced by K or NA. Measurement of Mn by atomic absorption spectrometry showed that the concentrations of EDTA-resistant Mn increased in parallel with the loss of inhibitory effects of Mn. This is consistent with an external inhibitory effect of Mn but a potentiating effect of Mn once it reaches an EDTA-inaccessible site. The potentiating effect of Mn was not seen with other ions such as Cd, Ni, Co, Mg, and La, which produced only inhibition of responses to NA or K. Contractile responses to Ba were examined in the absence of external Ca and it was found that the responses decreased with time. The presence of Mn not only prevented the loss of contractility but produced a marked increase in the response to Ba. Relaxation rates were also studied and it was found that Mn speeds the relaxation of contractures produced by NA or Ba as long as Mn is present in the bath fluid, but Mn slows relaxation when it is present (presumably) intracellularly. Mn does not alter relaxation rates of K contractures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

The involvement of nonspiking cells in long-term potentiation of synaptic transmission in the hippocampus.

In guinea pig hippocampal slices, stimulation of stratum radiatum during depolarization (with intracellular current injections) of nonspiking cells (presumed to be glia) in the apical dendritic area of CA1 pyramidal neurons resulted in a subsequent long-term potential of intracellularly recorded excitatory postsynaptic potentials as well as extracellularly recorded population spikes in the CA1 area. Tetanic stimulation of stratum radiatum resulted in a subsequent prolonged depolarization of the presumed glial cells, and this depolarization was smaller when the tetanus was given during the presence of 2-amino-5-phosphonovalerate or when the slices were exposed to Ca2+-free medium containing Mn2+ and Mg2+. These results suggest that glial depolarization is involved as one of the steps in generating long-term potentiation.

Action Potentials↗
PubMed1987

Temporal requirements of associative short-term potentiation in CA1 neurons of rat hippocampus.

Temporal separation and juxtaposition of stimulations for the induction of associative short-term potentiation in the rat hippocampus were examined. A series of stimulations of stratum radiatum during brief tetanic stimulations of stratum oriens resulted in a short-term potentiation (of about 3 min duration) of stratum radiatum-induced CA1 population excitatory postsynaptic potential. Potentiation was evident when the stratum radiatum stimulus preceded the onset of the conditioning tetanus by no more than 50 ms, or followed by no more than 80 ms. These parameters closely resemble those found for associative long-term potentiation, suggesting the possibility of shared mechanisms for the induction of these two forms of potentiation.

Animals↗
PubMed1983

Nodular adrenal hyperplasia with elevated adrenocorticotropic hormone levels.

Micronodular adrenal hyperplasia is an uncommon adrenal disorder characterized by failure of urinary corticosteroid excretion to be suppressed by high-dose dexamethasone therapy. Thus, micronodular adrenal hyperplasia demonstrates dexamethasone suppressibility that resembles primary adrenal neoplasia. However, since some cases have been reported to have measurable plasma adrenocorticotropic hormone (ACTH) levels, it is unclear whether this disorder arises primarily in the pituitary-hypothalamic region or in the adrenal gland. Our patient had clinical features of Cushing's syndrome and elevated urinary corticosteroid excretion that did not suppress with even high doses of dexamethasone; however, ACTH levels were elevated and were suppressible with high-dose dexamethasone therapy. At operation, enlarged adrenal glands with multiple micronodules were found. This case is compatible with the hypothesis that hypothalamic-pituitary hyperfunction precedes the development of micronodular adrenal disease in some cases.

Adrenal Glands↗
PubMed1979

Elevated prolactin levels in bronchogenic carcinoma.

The frequency and significance of hyperprolactinemia was studied in 21 consecutive, untreated male patients with bronchogenic carcinoma. Seven patients (33%) were found to have elevated serum prolactin (hPRL) levels. No correlation was demonstrated between increased hPRL levels, tissue histology, or tumor burden. L-dopa suppression and/or TRH stimulation tests were obtained in three untreated patients with hyperprolactinemia. The results of these tests were considered normal suggesting hypothalamic control.

Adenocarcinoma↗
PubMed1979

Enkephalins and pituitary hormone release: modification of responsiveness to LHRH.

An intraperitoneal injection of leucine-enkephalin into rats stimulates gonadotropin and prolactin release. To elucidate the mechanism of this releasing property of leucine-enkephalin, rat hemipituitaries were incubated with either enkephalin alone or enkephalin in combination with OHRH. Enkephalin alone had no effect on LH or prolactin release in vitro but potentiated the LH response to LHRH. Neither leucine-enkephalin nor LHRH alone had an effect on GH release; however, when combined, a GH response to LHRH occurred. These results suggest that leucine-enkephalin can modify the pituitary responsiveness to certain hypothalamic releasing hormones by a direct pituitary action.

Animals↗
PubMed1978

Hypoglycemia-induced prolactin release.

Recent advances in neurosurgical techniques have made it possible to remove pituitary adenomata with minimal morbidity and mortality. These developments have focused attention on early recognition of pituitary tumors, before the onset of visual disturbances or endocrine dysfunction. We have studied the prolactin response to insulin-induced hypoglycemia as an aid in the evaluation of patients with hypothalamic and pituitary disease. Regular insulin 0.1 units/kg was administered intravenously to normal subjects, to patients with pituitary tumors, and to patients with idiopathic galactorrhea. While the normal subjects regularly showed a prolactin response to hypoglycemia, this was observed infrequently in the other groups. It is possible that prolactin nonresponsiveness to insulin hypoglycemia may reflect nonspecific pituitary damage or may represent an abnormality specific to patients with galactorrhea. Our data suggest that the prolactin response to insulin hypoglycemia is a sensitive index of hypothalamic-pituitary dysfunction.

Adult↗
PubMed1977

Initial evaluation and management of patients with suspected pituitary tumors.

While pituitary tumors are not as rare as was once thought, it is difficult to assess how many are of clinical significance. Trans-sphenoidal pituitary exploration is a technique which can be performed with low operative morbidity and mortality, and when instituted early can prevent subsequent visual and endocrine impairment from an expanding lesion. Thus early recognition has increased importance.

Acromegaly↗
PubMed1975

In vitro pituitary responsiveness to gonadotropin-releasing hormone (LH-RH) in intact and castrated male and female rats.

The in vitro response of pituitaries isolated from both normal and 18-21 day post-castration male and female intact rats to incremental doses of synthetic gonadotropin-releasing hormone (LH-RH) has been investigated. Intact male pituitaries released luteinizing hormone (LH) maximally at the smallest dose of LH-RH (0.1 ng/ml) whereas intact female pituitaries released LH in a dose-response fashion. FSH release from intact male pituitaries was considerably greater than that from intact female pituitaries. As with LH, intact male pituitaries appeared maximally stimulated at 0.1 ng/ml of LH-RH. Intact female pituitaries did not release FSH until a 10 ng/ml dose of LH-RH was used. Male and female castrate pituitaries were more susceptible to LH-RH-induced LH and FSH release than were their intact counterparts, although this was more pronounced with regard to LH release. In addition castrate male pituitaries were more sensitive to lower doses of LH-RH than were castrate female pituitaries, this being most pronounced regarding LH release. Castrate female pituitaries released less FSH at the 100 ng/ml dose than at the 10 ng/ml dose, possibly indicating inhibition at these higher doses. In addition, pituitary extraction and serum from normal and castrate male and female rats were examined for LH and FSH content. LH content of castrated rat pituitaries of both sexes was considerably greater than that of their intact counterparts, as expected. However, castrate male pituitaries contained significantly less FSH than intact male pituitaries, whereas the opposite was true for the female groups. Serum LH and FSH levels were increased in the castrate groups with no difference between sexes. Serum from intact males contained considerably more FSH than did the serum from intact females.

Animals↗