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Biomedical subjects

P Slater

Publications and source records attributed to P Slater.

At least 73 records · Page 4Linked to original sources
PubMed1986

Autoradiographic analysis of D-[3H]aspartate binding in human basal ganglia.

The binding of D-[3H]aspartate to sections of human basal ganglia was measured autoradiographically. Highest binding was observed in the cerebral cortex, nucleus accumbens, caudate nucleus and putamen. The level of binding in the globus pallidus was low. D-[3H]Aspartate binding had a similar distribution to the high-affinity [3H]glutamate uptake sites and may be a useful marker for glutamate-aspartate terminals in human brain.

Aged↗
PubMed1986

Reduced high-affinity glutamate uptake sites in the brains of patients with Huntington's disease.

The binding of D-[3H]aspartic acid to the high-affinity glutamate uptake system was studied in membrane preparations of postmortem brains from controls and Huntington's disease (HD) subjects. The groups were matched for age and postmortem delay. A large (60-72%) and significant reduction in D-[3H]aspartate binding was observed in both the caudate nucleus and putamen, but not in the frontal cortex of the HD brains. The loss of striatal D-[3H]aspartate binding may reflect a loss of the high-affinity glutamate uptake system contained on the terminals of corticostriatal afferents. In contrast, the binding of [3H]paroxetine to the serotonin uptake system was marginally increased in the caudate nucleus and unchanged in the putamen. It is suggested that the reduction of high-affinity glutamate uptake sites may contribute to the production of the striatal lesion in HD.

Aged↗
PubMed1986

The association of [3H]D-aspartate binding and high-affinity glutamate uptake in the human brain.

The binding of [3H]D-aspartate ([3H]D-Asp) to human cerebellum homogenate was compared with the uptake of [3H]glutamate ([3H]Glu) by homogenates prepared from rapidly frozen human cerebral cortex. There was a close correlation between the potencies of a range of drugs for inhibiting the binding of [3H]D-Asp and the uptake of [3H]L-Glu. Compounds selective for postsynaptic Glu receptors were inactive. The findings are consistent with the labelling of high-affinity Glu uptake sites by [3H]D-Asp, which may be a valuable ligand for studying excitatory amino acid terminals in human brain.

Aspartic Acid↗
PubMed1986

The effects of opioids in the periaqueductal grey region of rat brain on hind-limb muscle tone.

A mechanical apparatus was used to measure hind limb resistance to flexion in rats injected with opioid peptides in the brain periaqueductal grey region (PAG). (D-Ala2, D-Leu5) enkephalin (delta agonist) and dynorphin1-8 and ethylketocyclazocine (kappa agonists) had no effects on hind limb tone. The mu agonist (D-Ala2, MePhe4, Gly-ol5) enkephalin induced limb rigidity when injected into the PAG. beta-Endorphin caused a dose-related limb rigidity that persisted for up to 2h. beta-Endorphin rigidity was prevented by pretreatment of rats with the serotonin depletor 5,7-dihydroxytryptamine. It is concluded that mu receptors and serotonin mechanisms in the PAG can mediate opiate rigidity.

Animals↗
PubMed1986

Autoradiographic distribution of dynorphin1-9 binding sites in primate brain.

The autoradiographic distribution of kappa opioid binding sites was evaluated in sections of monkey brain using the selective ligand [3H]dynorphin1-9. Kappa receptors were highly concentrated in the deep layers of the cerebral cortex, the substantia nigra, the hippocampus and the dentate gyrus. Lower levels were seen in the outer cortical layers, the caudate nucleus, the claustrum, parts of the amygdala and the cerebellum. These data are discussed in relation to the distribution in brain of the endogenous kappa-ligand.

Animals↗
PubMed1986

A semi-quantitative atlas of 5-hydroxytryptamine-1 receptors in the primate brain.

The regional distribution of 5-hydroxytryptamine-1 receptors in the primate brain was studied by semi-quantitative autoradiographic analysis of tritiated ligand binding. Areas showing the highest density of 5-hydroxytryptamine-1 receptors (greater than 200 fmol [3H]5-hydroxytryptamine bound per mg tissue), included the cerebral cortex (laminae I-II), claustrum, posterior cell group of the basal nucleus of Meynert, the infracommissural part of the globus pallidus, cortical amygdaloid nucleus, hippocampal formation (CA1-subiculum region, the anterior CA2, CA3 and CA4 regions and the molecular layer of the dentate gyrus), thalamic nuclei (parafascicular, parataenial, paraventricular and superior central lateral nuclei), substantia nigra pars reticulata, dorsal raphe nucleus and choroid plexus. The distribution of 5-hydroxytryptamine-1 receptors is compared to the distribution of both 5-hydroxytryptamine receptors and terminal fields of serotonergic projections as previously described in subprimates.

Amygdala↗
PubMed1986

Binding sites for [3H]glutamate and [3H]aspartate in human cerebellum.

The binding of [3H]aspartate and [3H]glutamate to membranes prepared from frozen human cerebellar cortex was studied. The binding sites differed in their relative proportions, their inhibition by amino acids and analogues, and by the effects of cations. A proportion (about 30%) of [3H]glutamate binding was to sites similar to those labelled by [3H]aspartate. An additional component of [3H]glutamate binding (about 50%) was displaced by quisqualate and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid, and may represent a "quisqualate-preferring" receptor. Neither N-methyl-D-aspartic acid-sensitive nor DL-2-amino-4-phosphonobutyric acid-sensitive [3H]glutamate binding was detected.

Aspartic Acid↗
PubMed1986

The hypothermic action of carbachol in the rat brain periaqueductal grey area may involve neurotensin.

Neurotensin (NT) and carbachol both caused hypothermia when injected into the periaqueductal grey area (PAG) of rat brain. Atropine prevented carbachol- but not NT-induced hypothermia. NT-induced hypothermia was unaffected by various neurotransmitter agonists and antagonists in the PAG. Both NT antibodies and thyrotrophin releasing hormone prevented carbachol hypothermia. It is concluded that the hypothermic action of carbachol in the PAG is mediated via endogenous NT.

Animals↗
PubMed1985

A lesioning and 2-deoxyglucose study of the hyperactivity produced by an intra-accumbens dopamine agonist.

Lesioning and 2-deoxyglucose (2-DG) autoradiographic studies were applied to the hyperactivity induced in rats by intra-accumbens treatment with the dopamine agonist 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydro-naphthalene (ADTN). Lesions made in substantia innominata and rostro-ventral globus pallidus both attenuated the hyperactivity although no consistent changes in 2-DG uptake were recorded in these areas. Compared to normal rats, hyperactive rats showed greatly increased glucose utilization in the subthalamic nucleus and lateral habenula. Lesioning the subthalamic nucleus greatly reduced the hyperactivity, whereas a lateral habenula lesion was ineffective. Hyperactivity was associated with a discrete, bilateral area of increased 2-DG uptake in the reticular formation which corresponded to the description of the deep mesencephalic nucleus (DMN). Lesions made in the DMN greatly attenuated the hyperactivity response. The DMN may be a locomotor region in the rat.

Animals↗
PubMed1983

Antinociceptive effects of thyrotrophin-releasing hormone and its analogues in the rat periaqueductal grey region.

Thyrotrophin-releasing hormone (TRH) and its analogues were injected into the periaqueductal grey (PAG) area of brain in conscious rats and the response time (tail-flick) to a thermal stimulus was recorded. TRH and some of the analogues had an antinociceptive action which, in the case of TRH, was prevented by naltrexone. TRH may interact with endogenous opioid systems in the PAG.

Analgesics↗
PubMed1983

Effects of lesions in some basal ganglia nuclei and efferent projections on tremorine-induced limb rigidity in rats.

A mechanical apparatus was used to measure in rats the effects of some unilateral basal ganglia lesions on the hind-limb rigidity produced by the cholinomimetic compound, tremorine. A globus pallidus lesion reduced the resting tone and greatly increased rigidity in the contralateral leg. Lesions in the entopeduncular, subthalamic, and accumbens nuclei had no effects on rigidity, although the entopeduncular nucleus lesion reduced resting limb tone. The role of the globus pallidus in rigidity is significant in relation to work in which striatal lesions abolished tremorine-induced rigidity. Some brain regions that receive basal ganglia efferent fibers received a lesion unilaterally. Lesions in the substantia nigra, red nucleus, or pedunculopontine nucleus had no effect on tremorine-induced rigidity. A habenular lesion significantly reduced rigidity in both hind legs. Very pronounced reductions in rigidity occurred after midbrain lesions involving the central periaqueductal grey region and the superior colliculus. The basal ganglia output pathways that may mediate tremorine rigidity are discussed, together with the possibility that the superior colliculus, which has many muscarinic receptors, may be influenced directly by tremorine.

Animals↗
PubMed1983

Body temperature effects of opioids administered into the periaqueductal grey area of rat brain.

The ability of opioids to influence rectal temperature after injection into the periaqueductal grey region (PAG) of rat brain was investigated. Both morphine and beta-endorphin caused a dose-dependent increase in rectal temperature of up to 2 degrees C. By using selective ligands of the subclasses of opiate receptor such as [D-Ala2,D-Leu5]enkephalin for delta-receptors and ethylketocyclazocine, dynorphin(1-17) and dynorphin(1-8) for kappa-receptors, it was possible to show that neither the delta- nor the kappa-opiate receptor was involved in the hyperthermic response. However, [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAGO), a mu-receptor ligand, did produce a dose-dependent hyperthermia. The ability of naltrexone, an opiate receptor antagonist, to reverse the hyperthermia induced by beta-endorphin and DAGO suggests that the opioid-stimulated increase in body temperature via the PAG is mediated through the mu-opiate receptor. Since the application of opioids to the PAG produces a hyperthermic response, it is possible that this brain site may have a role in the peptidergic control of body temperature.

Animals↗