Abstract
Since D. O. Hebb (1949) inaugurated the search for cellular mechanisms underlying brain function and behavioral plasticity, many strategies and model systems have been employed. One fruitful strategy has been the search for specific chemical transmitters able to modulate firing patterns of neurons in specific pathways for long periods of time. A promising model system has arisen from the discovery that brief, high-frequency stimulation of afferent pathways in the hippocampus leads to long-lasting enhancements of neuronal excitability whose persistence approach that of conditioned behavior (Bliss and Gardner-Medwin, 1973; Douglas and Goddard, 1975). The enhancement of evoked potentials after one such tetanus has been termed long-term potentiation (LTP; Bliss and Lømo, 1973; Schwartzkroin and Wester, 1975; Alger and Teyler, 1976), and repeated application of such stimulation yields the seizure state known as kindled epilepsy (Goddard et al., 1969). In both cases, the location of such long-lasting plasticity in a brain structure implicated in memory processes (Milner, 1972; Berger, 1984), its production by brief (a few seconds) stimulation within the physiological range (10–400 Hz), and the long duration of the changes (months in vivo) all led to extreme interest in their underlying mechanisms (Swanson et al., 1982).
This chapter is dedicated to the memory of Gary L. Stanton.
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References
Alger, B. E., and Teyler, T. J., 1976, Long-term and short-term plasticity in the CA1, CA3, and dentate regions of the hippocampal slice, Brain Res. 110: 463–480.
Berger, T. W., 1984, Long-term potentiation of hippocampal synaptic transmission affects rate of behavioral learning, Science 224: 627–630.
Bliss, T. V. P., and Gardner-Medwin, A. R., 1973, Long-lasting potentiation of synaptic transmission in the dentate area of the unanaesthetized rabbit following stimulation of the perforant path, J. Physiol. (Lond.) 232: 357–374.
Bliss, T. V. P., and Lmo, T., 1973, Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path, J. Physiol. (Lond.) 232: 331–356.
Bliss, T. V. P., Goddard, G. V., and Riives, M., 1983, Reduction of long-term potentiation in the dentate gyros of the rat following selective depletion of monoamines, J. Physiol. (Gond.) 334: 475–491.
Collingridge, G. L., Kehl, S. J., and McLennan, H., 1983, Excitatory amino acids in synaptic transmission in the Schaffer collateral—commissural pathway of the rat hippocampus, J. Physiol. (Lond.) 334: 33–46.
Crow, T. J., and Wendlandt, S., 1976, Impaired acquisition of a passive avoidance response after lesions induced in the locus coeruleus by 6-OH-dopamine, Nature (Land.) 259: 42–44.
Douglas, R. M., and Goddard, G. V., 1975, Long-term potentiation of the perforant path—granule cell synapse in the rat hippocampus, Brain Res. 86: 205–215.
Everitt, B. J., Robbins, T. W., Gaskin, M., and Fray, P. J., 1983, The effects of lesions to ascending noradrenergic neurons on discrimination learning and performance in the rat, Neuroscience 10: 397–410.
Fricke, R. A., and Prince, D. A., 1984, Electrophysiology of dentate gyros granule cells, J. Neurophysiol. 51: 195–209.
Goddard, G. V., McIntyre, D. C., and Leech, C. K., 1969, A permanent change in brain function resulting from daily electrical stimulation, Exp. Neurol. 25: 295–300.
Haas, H. L., and Konnerth, A., 1983, Histamine and noradrenaline decrease-calcium-activated potassium conductance in hippocampal pyramidal cells, Nature (Land.) 302: 432–434.
Harris, E. W., Ganong, A. H. and Cotman, C. W., 1984, Long-term potentiation in the hippocampus involves activation of N-methyl-D-aspartate receptors, Brain Res. 323: 132–137.
Hebb, D. O., 1949, The Organization of Behavior, John Wiley and Sons, New York.
Heinemann, U., Lux, H. D., and Gutnick, M. J., 1977, Extracellular free calcium and potassium during paroxysmal activity in the cerebral cortex of the cat, Exp. Brain Res. 27: 237–243.
Herron, C. E., Lester, R. A. J., Coan, E. J., and Collingridge, G. L., 1985, Intracellular demonstration of an N-methyl-D-aspartate receptor mediated component of synaptic transmission in the rat hippocampus, Neurosci. Lett. 60: 19–23.
Hotson, J. R., Prince, D. A., and Schwartzkroin, P. A., 1979, Anomalous rectification in hippocampal neurons, J. Neurophysiol. 42: 889–895.
Langmoen, I. A., Segal, M., and Andersen, P., 1981, Mechanisms of norepinephrine actions on hippocampal pyramidal cells in vitro, Brain Res. 208: 349–362.
Lux, H. D., and Heinemann, U., 1982, Consequences of calcium-electrogenesis for the generation of paroxysmal depolarization shift, in: Epilepsy and Motor System ( E. J. Speckmann and H. Elger, eds.), Urban and Schwarzenberg, Munich, pp. 101–119.
Madison, D. V., and Nicoll, R. A., 1982, Noradrenaline blocks accommodation of pyramidal cell discharge in the hippocampus, Nature (Lond.) 299: 636–638.
Mason, S. T., and Iversen, S. D., 1977, Effects of selective noradrenaline loss on behavioral inhibition in the rat, J. Comp. Physiol. Psychol. 91: 165–173.
McIntyre, D. C., and Edson, N., 1982, Effect of norepinephrine depletion on dorsal hippocampus kindling in rats, Exp. Neurol. 77: 700–704.
Milner, B., 1972, Disorders of learning and memory after temporal lobe lesions in man, Clin. Neurosurg. 19: 421–446.
Mody, I., and Heinemann, U., 1987, NMDA receptors of dentate gyms granule cells participate in synaptic transmission following kindling, Nature (Land.) 326: 701–704.
Mody, I., Lambert, J. D. C., and Heinemann, U., 1987, Low extracellular magnesium induces epileptiform activity and spreading depression in rat hippocampal slices, J. Neurophysiol. 57: 869–888.
Mueller A. L., Hoffer, B. J., and Dunwiddie, T. V., 1981, Noradrenergic responses in rat hippocampus: Evidence for mediation by a and ß receptors in the in vitro slice, Brain Res. 214: 113–126.
Neuman, R. S., and Harley, C. W., 1983, Long-lasting potentiation of the dentate gyms population spike by norepinephrine, Brain Res. 273: 162–165.
Peterson, D. W., Collins, J. F., and Bradford, H. F., 1984, Anticonvulsant action of amino acid antagonists against kindled hippocampal seizures, Brain Res. 311: 176–180.
Puil, E., and Werman, R., 1981, Internal cesium ions block various K conductances in spinal motoneurons, Can. J. Physiol. Pharmacol. 59: 1280–1284.
Schwartzkroin, P. A., and Wester, K., 1975, Long-lasting facilitation of a synaptic potential following tetanization in the in vitro hippocampal slice, Brain Res. 89: 107–119.
Segal, M., 1982, Norepinephrine modulates reactivity of hippocampal cells to chemical stimulation in vitro, Exp. Neurol. 77: 86–93.
Segal, M., and Bloom, F. E., 1974, The action of norepinephrine in the rat hippocampus. I. Iontophoretic studies, Brain Res. 77: 79–97.
Stanton, P. K., and Heinemann, U., 1986, Norepinephrine enhances stimulus-evoked Ca’- ` and K+ concentration changes in dentate granule cell layer, Neurosci. Lett. 67: 233–238.
Stanton, P. K., Jones, R. S. G., Mody, I., and Heinemann, U., 1987, Epileptiform activity induced by lowering extracellular [Mg2+] in combined hippocampal—entorhinal cortex slices: Modulation by receptors for norepinephrine and N-methyl-D-aspartate, Epilepsy Res. 1: 53–62.
Stanton, P. K., and Sarvey, J. M., 1985a, Depletion of norepinephrine, but not serotonin, reduces long-term potentiation in the dentate of rat hippocampal slices, J. Neurosci. 5: 2169–2176.
Stanton, P. K., and Sarvey, J. M., 1985b, The effect of high-frequency electrical stimulation and norepinephrine on cyclic AMP levels in normal versus norepinephrine-depleted rat hippocampal slices, Brain Res. 358: 343–348.
Stanton, P. K., and Sarvey, J. M., 1985c, Blockade of norepinephrine-induced long-lasting potentiation in the hippocampal dentate gyms by an inhibitor of protein synthesis, Brain Res. 361: 276–283.
Stein, L., Beluzzi, J. D., and Wise, C. D., 1975, Memory enhancement by central administration of norepinephrine, Brain Res. 84: 329–335.
Swanson, L. W., Teyler, T. J., and Thompson, R. F., 1982, Hippocampal long-term potentiation: Mechanisms and implications for memory, Neurosci. Res. Prog. Bull. 20: 612–769.
Wadman, W. J., Heinemann, U., Konnerth, A., and Neuhaus, S., 1985, Hippocampal slices of kindled rats reveal calcium involvement in epileptogenesis, Exp. Brain Res. 57: 404–407.
Walther, H., Lambert, J. D. C., Jones, R. S. G., Heinemann, U., and Hamon, B., 1986, Epileptiform activity in combined slices of the hippocampus, subiculum and entorhinal cortex during perfusion of low magnesium medium, Neurosci. Lett. 69: 156–161.
Wigstrom, H., and Gustafsson, B., 1984, A possible correlate of the postsynaptic condition for long-lasting potentiation in the guinea pig hippocampus in vitro, Neurosci. Lett. 44: 327–332.
Zornetzer, S. F., 1984, Brain substrates of senescent memory decline, in: Neuropsychology of Memory, Guilford, New York, pp. 588–600.
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Stanton, P.K., Heinemann, U. (1988). Mechanisms of Noradrenergic Modulation of Dentate Gyrus Long-Term Plasticity. In: Woody, C.D., Alkon, D.L., McGaugh, J.L. (eds) Cellular Mechanisms of Conditioning and Behavioral Plasticity. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9610-0_9
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DOI: https://doi.org/10.1007/978-1-4757-9610-0_9
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