Biomedical subjects

A T Tan

Publications and source records attributed to A T Tan.

66 records · Page 4Linked to original sources

PubMed1981

Alcohol feeding alters (3H)dopamine uptake into rat cortical and brain stem synaptosomes.

The uptake of (3H)dopamine into nerve endings (synaptosomes) isolated from cortex and brain stem of rats under various stages of ethanol intoxication were studied. Acute or chronic ethanol treatment inhibited the high affinity uptake of dopamine into both regions by about 30% when rats were still under ethanol. The inhibition in brain stem persisted even after 120 h of withdrawal from ethanol. In cortex, 16 h after acute treatment, the uptake was slightly (about 10%) elevated from that of control in contrast to chronic rats, which were 43 and 41% more than that of the control after withdrawal from ethanol for 48 and 120 h, respectively.

Administration, Oral↗

PubMed1979

Thyrotropin-releasing hormone selectively depresses glutamate excitation of cerebral cortical neurons.

The microiontophoretic application of thyrotropin-releasing hormone causes a selective reduction in neuronal excitation evoked by L-glutamate but not by acetylcholine in rat cerebral cortex. Thyrotropin-releasing hormone has no influence on the activity of acetylcholinesterase or on choline uptake and release from cerebral synaptosomes. This evidence for a selective interaction between a centrally acting peptide and an excitatory amino acid neurotransmitter may indicate a specific locus of thyrotropin-releasing hormone action at glutamate-activated receptor sites.

Acetylcholine↗

PubMed1978

Effect of opioid peptides on L-noradrenaline-stimulated cyclic AMP formation in homogenates of rat cerebral cortex and hypothalamus.

Morphine and the opioid peptides leucine-enkephalin (leu-enk), methionine-enkephalin (met-enk) and beta-endorphin had no effect on basal cyclic AMP levels in rat cerebral cortex and hypothalamus, but each inhibited noradrenaline (NA)-stimulated cyclic AMP formation in both brain regions. This inhibition was reversed by naloxone. Naloxone did not reverse phentolamine- or propranolol-induced inhibition of NA-stimulated cyclic AMP formation. The increase in cyclic AMP formation induced by NaF or MnCl2 was unaffected by met-enk or morphine. These data suggest that in rat cerebral cortex and hypothalamus opiates bind to opiate receptors and that the opiate-receptor complex interferes with noradrenergic receptor activity.

Animals↗

PubMed1977