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Biomedical subjects

G R Siggins

Publications and source records attributed to G R Siggins.

120 records · Page 7Linked to original sources
PubMed1969

Prostaglandins E1 and E2 antagonize norepinephrine effects on cerebellar purkinje cells: microelectrophoretic study.

In microelectrophoretic experiments, prostaglandins E(1) and E(2) antagonize the reduction in discharge rate of cerebellar Purkinje cells produced by norepinephrine. Slowing of discharge evoked by 3',5'-adenosine monophosphate or gamma aminobutyric acid is not antagonized. These data provide the first indication that endogenous prostaglandins may physiologically function to modulate central noradrenergic junctions.

Action Potentials↗
PubMed1969

Cyclic adenosine monophosphate: possible mediator for norepinephrine effects on cerebellar Purkinje cells.

Microelectrophoretic application of norepinephrine or cyclic adenosine monophosphate reduces the discharge frequency of Purkinje cells in the rat cerebellum. In contrast, other nucleotides accelerate the discharge rate of most units. Parenterally administered theophylline, which inhibits the hydrolysis of cyclic adenosine monophosphate enhances the effects of norepinephrine and cyclic adenosine monophosphate. Therefore, norepinephrine may be able to regulate Purkinje cells functionally by metabolic stimulation of cyclic adenosine monophosphate synthesis.

Action Potentials↗
PubMedDate not supplied

Central neurons are depressed by iontophoretic and micropressure application of ethanol and tetrahydropapaveroline.

In an attempt to circumvent the complexities of systemically administered ethanol and tetrahydroisoquinolines (TIQs), iontophoresis and micropressure application were used to test these agents in single rat neurons. Alcohol applied by either method depressed cerebellar Purkinje cells in a concentration-dependent, non-specific, local anesthetic-like manner. Tests of tetrahydropapaveroline.HCl (THP) on neurons from three brain areas also showed depression of spontaneous discharge, although, in contrast to ethanol, little or no local anesthetic-like action was observed, and at equivalent ejection currents or pressures, the THP depressions appeared to be more pronounced. The underlying mechanisms for these responses are unknown.

Animals↗
PubMedDate not supplied

Cyclic nucleotides in the development of alcohol tolerance and dependence: a commentary.

This paper aims to outline some of the caveats inherent in studies on first and second messengers in the central nervous system as related to tolerance and dependence. Analysis of systems based on measures of first and second messengers may be an over-simplification, since the actual molecular consequences of neurotransmission might result in a multilevel cascade of many sequential messages including protein kinase activation and protein phosphorylation and/or dephosphorylation.

Adenylyl Cyclases↗
PubMedDate not supplied

Electrophysiological action of ethanol at the cellular level.

To examine how ethanol interferes with brain function on the global levels of brain activity reflected by event-related potentials, we summarize here our recent efforts to characterize the acute cellular effects of ethanol. Four regions of the rodent brain (cerebellum, hippocampus, locus coeruleus and inferior olive) have so far been examined. The effects of acute parenteral ethanol on specific identifiable neurons within these 4 regions are highly consistent, dose-related, and spontaneously reversible. Furthermore, different patterns of response are seen in each responsive region, ranging from general increased firing in inferior olive to generally depressed synaptic transmission in hippocampus, and with more subtle effects within the cerebellum and within the locus ceruleus. This survey of consistent but differing patterns of responsiveness to ethanol at specific time points after acute exposure, suggests that the global effects of ethanol must be composed of several distinct effects both within and across many cellular systems.

Animals↗