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.

[1]  C. Barnes,et al.  Acetyl-l-carnitine: Behavioral, electrophysiological, and neurochemical effects , 1993, Neurobiology of Aging.

[2]  M. Miras-Portugal,et al.  Positive feedback of glutamate exocytosis by metabotropic presynaptic receptor stimulation , 1992, Nature.

[3]  Wen-Hwa Lee,et al.  Abrogation by c-myc of Gl phase arrest induced by RB protein but not by p53 , 1992, Nature.

[4]  K. Stratford,et al.  Presynaptic release probability influences the locus of long-term potentiation , 1992, Nature.

[5]  R. Nicoll,et al.  Long-term potentiation is associated with increases in quantal content and quantal amplitude , 1992, Nature.

[6]  D. Ingram,et al.  Reduced density of NMDA receptors and increased sensitivity to dizocilpine-induced learning impairment in aged rats , 1992, Brain Research.

[7]  M. Lynch,et al.  Increase in arachidonic acid concentration in a postsynaptic membrane fraction following the induction of long-term potentiation in the dentate gyrus , 1991, Neuroscience.

[8]  Leyla deToledo-Morrell,et al.  Induction of long-term potentiation is associated with an increase in the number of axospinous synapses with segmented postsynaptic densities , 1991, Brain Research.

[9]  R. Malinow Transmission between pairs of hippocampal slice neurons: quantal levels, oscillations, and LTP. , 1991, Science.

[10]  T. Bliss,et al.  Is arachidonic acid a retrograde messenger in long-term potentiation? , 1991, Biochemical Society Transactions.

[11]  D. Mckenna,et al.  Age-related changes in the synaptic plasticity of rat superior cervical ganglia , 1991, Brain Research.

[12]  J. McNamara,et al.  Decreased density, but not number, N-methyl-D-aspartate, glycine and phencyclidine binding sites in hippocampus of senescent rats , 1990, Brain Research.

[13]  C. Stevens,et al.  Presynaptic mechanism for long-term potentiation in the hippocampus , 1990, Nature.

[14]  M. Krug,et al.  Spinules in axospinous synapses of the rat dentate gyrus: changes in density following long-term potentiation , 1990, Brain Research.

[15]  R. Tsien,et al.  Presynaptic enhancement shown by whole-cell recordings of long-term potentiation in hippocampal slices , 1990, Nature.

[16]  M. Lynch,et al.  Arachidonic Acid Increases Inositol Phospholipid Metabolism and Glutamate Release in Synaptosomes Prepared from Hippocampal Tissue , 1990, Journal of neurochemistry.

[17]  W. F. Hopkins,et al.  Presynaptic ultrastructural correlates of long-term potentiation in the CA1 subfield of the hippocampus , 1990, Brain Research.

[18]  T. Bliss,et al.  Arachidonic acid induces a long-term activity-dependent enhancement of synaptic transmission in the hippocampus , 1989, Nature.

[19]  M. Er̀rington,et al.  The increase in [3H]glutamate release associated with long-term potentiation in the dentate gyrus is blocked by commissural stimulation , 1989, Neuroscience Letters.

[20]  A. Gaiti The Aging Brain: A Normal Phenomenon with Not‐So‐Normal Arachidonic Acid Metabolism a , 1989 .

[21]  T. Bliss,et al.  NMDA receptors - their role in long-term potentiation , 1987, Trends in Neurosciences.

[22]  P. Landfield,et al.  Redistribution of synaptic vesicles during long-term potentiation in the hippocampus , 1987, Brain Research.

[23]  F. Morrell,et al.  Aged rats need a preserved complement of perforated axospinous synapses per hippocampal neuron to maintain good spatial memory , 1986, Brain Research.

[24]  T. Bliss,et al.  Correlation between long‐term potentiation and release of endogenous amino acids from dentate gyrus of anaesthetized rats. , 1986, The Journal of physiology.

[25]  H. Miwa,et al.  Assay of free and total fatty acids (as 2-nitrophenylhydrazides) by high performance liquid chromatography. , 1986, Clinica chimica acta; international journal of clinical chemistry.

[26]  M. Lynch,et al.  Long-term potentiation is associated with an Increase in calcium-dependent, potassium-stimulated release of [14C]glutamate from hippocampal slices: an Ex Vivo study in the rat , 1986, Brain Research.

[27]  R. Baker,et al.  The subcellular distribution of free fatty acids released during post-decapitative ischemia in rat cerebral cortex. , 1985, Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire.

[28]  F. Morrell,et al.  Electrophysiological Markers of Aging and Memory Loss in Rats a , 1985, Annals of the New York Academy of Sciences.

[29]  D. Kendall,et al.  Inositol Phospholipid Hydrolysis in Rat Cerebral Cortical Slices: I. Receptor Characterisation , 1984, Journal of neurochemistry.

[30]  T. Bliss,et al.  Long-term potentiation of the perforant path in vivo is associated with increased glutamate release , 1982, Nature.

[31]  D. Bowen,et al.  Protection of Neocortical Tissue Prisms from Freeze‐Thaw Injury by Dimethyl Sulphoxide , 1981, Journal of neurochemistry.

[32]  D. Deykin,et al.  The activation of phosphatidylinositol-hydrolyzing phospholipase A2 during prostaglandin synthesis in transformed mouse BALB/3T3 cells. , 1981, The Journal of biological chemistry.

[33]  C. Barnes Memory deficits associated with senescence: a neurophysiological and behavioral study in the rat. , 1979, Journal of comparative and physiological psychology.

[34]  J. D. McGaugh,et al.  Impaired synaptic potentiation processes in the hippocampus of aged, memory-deficient rats , 1978, Brain Research.

[35]  T. Bliss,et al.  Long‐lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path , 1973, The Journal of physiology.

[36]  Oliver H. Lowry,et al.  Protein measurement with the Folin phenol reagent. , 1951, The Journal of biological chemistry.

[37]  B. McNaughton,et al.  Long‐term enhancement of CA1 synaptic transmission is due to increased quantal size, not quantal content , 1991, Hippocampus.

[38]  C A Barnes,et al.  Effects of aging on the dynamics of information processing and synaptic weight changes in the mammalian hippocampus. , 1990, Progress in brain research.

[39]  G. V. Aprikyan,et al.  Release of neurotransmitter amino acids from rat brain synaptosomes and its regulation in aging. , 1988, Gerontology.

[40]  Bruce L. McNaughton,et al.  An age comparison of the rates of acquisition and forgetting of spatial information in relation to long-term enhancement of hippocampal synapses. , 1985, Behavioral neuroscience.