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Biomedical subjects

H Pollard

Publications and source records attributed to H Pollard.

At least 37 records · Page 2Linked to original sources
PubMed1987

Major localization of aminopeptidase M in rat brain microvessels.

The localization of two enkephalin-hydrolysing aminopeptidases i.e. aminopeptidase M (aminopeptidase N, EC 3.4.11.2) relatively insensitive to puromycin (Ki = 78 microM), and a puromycin-sensitive aminopeptidase (Ki = 1 microM) was studied in rat brain. The two aminopeptidases were differentially identified and/or localized using polyclonal anti-aminopeptidase M antibodies displaying anticatalytic activity and the inhibitors puromycin, bestatin and amastatin. Microvessels represent a major localization of cerebral aminopeptidase M as shown by the intense immunostaining of their walls in sections from various regions as well as in a fraction isolated from cerebral cortex homogenates by a sieving procedure. As compared to the starting homogenate, aminopeptidase M activity was enriched about twenty fold in this microvascular fraction. Aminopeptidase M was identified in this fraction by comparing the inhibitory potencies of antibodies and peptidase inhibitors towards the hydrolysis of [tyrosyl-3,5-3H, Met5]enkephalin to those found for the purified enzyme. A rather high aminopeptidase M activity was also localized in choroid plexuses. Following differential and gradient centrifugation analysis of cerebral cortex homogenates, aminopeptidase M activity was also enriched (by five to six fold) in fractions containing synaptic membranes. No significant soluble aminopeptidase M activity could be detected. These data suggest a dual localization of cerebral aminopeptidase M in microvessels and synaptic membranes consistent with its roles in preventing the access of circulating peptides to brain as well as in inactivating neuropeptides released from cerebral neurones. In comparison, puromycin-sensitive aminopeptidase activity, which is about 100 fold higher than aminopeptidase M activity in brain, was relatively low in microvessels and non-detectable in fractions enriched in synaptic membranes, being almost entirely restricted to soluble fractions.

Aminopeptidases↗
PubMed1985

Monoclonal antibody against L-histidine decarboxylase for localization of histaminergic cells.

The immunochemical and immunohistochemical properties of a monoclonal antibody (Mab HI 113-12) developed in mice against a partially purified preparation of rat gastric L-histidine decarboxylase (HD) were studied. The Mab recognised the HD activity from the antigen and from crude tissue extracts with a high histamine (HA)-synthesizing capacity (stomach, hypothalamus, striatum, mastocytoma). In contrast, neither a bacterial HD nor other decarboxylases (glutamic and DOPA decarboxylases) were immunoprecipitated. In preliminary immunohistochemical studies, staining of the cytoplasm of mastocytoma as well as of hypothalamic neurons, particularly magnocellular ones in the mamillary region, were observed. The latter presumably correspond to the cells of origin of a long ascending histaminergic pathway.

Animals↗
PubMed1976

Dual localization of histamine in an ascending neuronal pathway and in non-neuronal cells evidenced by lesions in the lateral hypothalamic area.

The effects of lesions placed in the lateral hypothalamic area, i.e., interrupting the MFB (as evidenced by a 65% decrease in cortical noradrenaline and serotonin) suggest a pluricompartmentation of brain histamine (HA). The existence of an ascending histaminergic system is indicated by the reductions in l-histidine decarboxylase (H.D.) activity, in [3H]histamine synthesis and in HA content, in the cortex of lesioned rats. Moreover, the decrease in H.D. activity was restricted to the regions rostral to the lesion, without modification caudally. The time-course of the alterations in H.D. activity and in HA content is compatible with a process of anterograde degeneration. In subcellular fractionation studies, the reduction in cortical HA content was found to be mainly confined to the P2 fraction, which contains the synaptosomes. Although the widespread ipsilateral distribution of HA synthesizing terminals resembles that of monoaminergic ones, the absence of reduction in H.D. activity after selective destruction of catecholaminergic and serotoninergic neurons, by 6-hydroxydopamine or 5,6-dihydroxytryptamine respectively, renders likely the existence of specific HA-containing neurons. That the release of the amine from these neurons might be related to the nerve impulse flow is suggested by the transient effects of the lesions which preceded the degenerative process (elevated endogenous HA level and slowed rate of [3H]HA synthesis). In addition, the discrepancy between the reduction in H.D. activity and in HA level after the lesions could be explained by the presence of the amine in another neuronal system and/or in non-neuronal cells, not affected by the lesion. This additional compartment is characterized by a high HA content and a low H.D. activity and could therefore be localized in mast-cells. The respective sizes of these two compartments, estimated by several methods, appear to be approximately the same.

5-Hydroxytryptophan↗
PubMed1976

Neurochemical evidence for histamine acting as a transmitter in mammalian brain.

HA, besides its function in immune processes, is probably a neurotransmitter in mammalian brain. It is synthesized by a specific decarboxylase localized in the cytoplasm of nerve endings. It is stored in synaptic vesicles. Its release might depend on nerve-impulse flow; specific receptors to this amine have been evidenced both electrophysiologically and by the activation of cyclic AMP formation. Lesion studies indicate that histamine-containing neurons might constitute an ascending bundle arising from the brainstem and widely projecting into the whole telencephalon. This disposition, together with neuropharmacological data, suggests that histaminergic neurons, like the monoaminergic ones, might be involved in the control of arousal mechanisms, an idea consistent with the observed fluctuations of the endogenous amine content during the day-night cycle. On the other hand, the investigation of the effect of stress situations on the turnover of HA in brain leads to the conclusion that histaminergic neurons are specifically affected.

Animals↗