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K L Voss

Publications and source records attributed to K L Voss.

6 recordsLinked to original sources
PubMed1994

Impaired spatial memory in aged rats is associated with alterations in inositol phospholipid metabolism.

WE have investigated changes in inositol phospholipid turnover and membrane arachidonic acid concentration in the dentate gyrus and frontal cortex of animals aged 3-6 months, 14 months or 22 months which were trained in the Morris water maze. Ageing was associated with poorer performances in the behavioural test, characterized by increased variability in retention and acquisition amongst individuals, a decrease in membrane arachidonic acid concentration and increased unstimulated inositol phospholipid metabolism in synaptosomes prepared from frontal cortex and dentate gyrus. Arachidonic acid stimulated inositol phospholipid metabolism in synaptosomes, but in the older groups, stimulation was associated with good performance in the Morris water maze. In slices prepared from frontal cortex, responsiveness of inositol phospholipid metabolism to glutamate was also age- and performance-dependent. The findings highlight a correlation between age, inositol phospholipid metabolism and performance in the Morris water maze.

Aging↗
PubMed1994

Membrane arachidonic acid concentration correlates with age and induction of long-term potentiation in the dentate gyrus in the rat.

We examined the induction and maintenance of long-term potentiation (LTP) in vivo in the dentate gyrus of 4-month-old and 22-month-old urethane-anaesthetized rats. High-frequency stimulation of the perforant path induced an immediate increase in the slope of the population excitatory postsynaptic potential (EPSP), which was sustained in the 4-month-old animals for the duration of the experiment (45 min post-tetanus). In the 22-month-old group, the mean slope of the population EPSP decreased almost to baseline by the end of the experiment. Examination of the individual records indicated that LTP was sustained for the duration of the experiment in half of the 22-month-old animals, while in the others only post-tetanic potentiation was observed. Membrane arachidonic acid concentration was reduced in aged compared with young animals and was lowest in the subgroup of aged animals which failed to sustain LTP. Potassium-stimulated, calcium-dependent release of glutamate was also decreased in aged compared with young animals, but LTP was associated with an increase in glutamate release in the 4-month-old group and 22-month-old subgroup in which LTP was successfully sustained; no change was observed in the 22-month-old group in which LTP was not sustained. The results indicate a correlation between membrane arachidonic acid concentration, glutamate release and ability to sustain LTP in aged animals.

Aging↗
PubMed1994

Increase in synaptic vesicle proteins accompanies long-term potentiation in the dentate gyrus.

Maintenance of long-term potentiation in synapses formed by the perforant path on to granule cells of the dentate gyrus is accompanied by a sustained increase in the extracellular concentration of glutamate, the presumed transmitter at this excitatory hippocampal pathway. Quantal analysis indicates that, at least in the first hour of induction, this reflects an increase in transmitter release rather than a decrease in glutamate uptake, while biochemical studies have suggested that the increase in release persists for several hours. Morphological studies have described early but persistent increases in the spine number and area. Increases in the number of segmented/perforated synapses persisting for at least 1 h after induction of long-term potentiation, have also been reported. These morphological changes suggest both presynaptic and postsynaptic modifications. Increases in synaptic vesicle number and distribution lasting for at least 1 h specifically indicate presynaptic changes. To explore further the role of the presynaptic terminal in long-term potentiation, we have investigated changes in three synaptic vesicle proteins, synapsin, synaptotagmin and synaptophysin, in control tissue and in tissue prepared from potentiated dentate gyrus 45 min and 3 h after induction of long-term potentiation. We found that there was an increase in the concentration of the three proteins 3 h after induction of long-term potentiation. No such increase was observed 45 min after induction or in tissue prepared from animals in which an intraventricular injection of the N-methyl-D-aspartate receptor antagonist, D(-)-2-amino-5-phosphonopentanoic acid, blocked induction of long-term potentiation.

2-Amino-5-phosphonovalerate↗
PubMed1991

Presynaptic changes in long-term potentiation: elevated synaptosomal calcium concentration and basal phosphoinositide turnover in dentate gyrus.

In this report, two changes that occur in the presynaptic terminal following induction of long-term potentiation in the dentate gyrus are examined, and the results demonstrate that the same changes are stimulated by the putative retrograde messenger arachidonic acid. First, there is an increase in the concentration of intracellular calcium in synaptosomes prepared from potentiated tissue compared with control tissue. This effect on intracellular calcium concentration was mimicked in control tissue by treatment of synaptosomes with either arachidonic acid or inositol 1,4,5-trisphosphate in a dose-dependent but nonadditive manner. Second, there is an increase in phosphoinositide turnover in synaptosomes prepared from potentiated tissue compared with control tissue, and this change can also be mimicked in control tissue by exposure of synaptosomes to arachidonic acid. These findings are consistent with the hypothesis that the increase in glutamate release associated with long-term potentiation may be stimulated by arachidonic acid, as a result of an increase in intrasynaptosomal calcium concentration, perhaps occurring as a result of arachidonate-stimulated phosphoinositide metabolism.

Animals↗
PubMed1990

Arachidonic acid increases inositol phospholipid metabolism and glutamate release in synaptosomes prepared from hippocampal tissue.

We have been interested in the possibility that arachidonic acid or one of its 12-lipoxygenase metabolites may function as a retrograde messenger in long-term potentiation (LTP) in the dentate gyrus of the hippocampus. One criterion required of a retrograde messenger is that it stimulates presynaptic changes. Here, two possible presynaptic actions of arachidonic acid and its 12-lipoxygenase metabolites, 12-hydroxyeicosatetraenoic acid (HETE) and 12-hydroperoxyeicosatetraenoic acid (HPETE), are examined. We report that arachidonic acid, HETE, and HPETE significantly increase both K(+)-stimulated release of [3H]glutamate and [3H]inositol labelling of inositol phosphates in synaptosomes, whereas other biologically important fatty acids (oleic, palmitic, and stearic) failed to induce a similar response. The findings of these experiments are consistent with the hypothesis that arachidonic acid, HETE, or HPETE may play the role of a retrograde messenger in LTP.

Animals↗