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Relevant bibliographies by topics / Ischemia, paired pulse facilitation, hippocampus

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Journal articles

Academic literature on the topic 'Ischemia, paired pulse facilitation, hippocampus'

Author: Grafiati

Published: 10 March 2023

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Journal articles on the topic "Ischemia, paired pulse facilitation, hippocampus"

1

Tanaka, E., S. Yasumoto, G. Hattori, S. Niiyama, S. Matsuyama, and H. Higashi. "Mechanisms Underlying the Depression of Evoked Fast EPSCs Following In Vitro Ischemia in Rat Hippocampal CA1 Neurons." Journal of Neurophysiology 86, no. 3 (2001): 1095–103. http://dx.doi.org/10.1152/jn.2001.86.3.1095.

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The mechanisms underlying the depression of evoked fast excitatory postsynaptic currents (EPSCs) following superfusion with medium deprived of oxygen and glucose (in vitro ischemia) for a 4-min period in hippocampal CA1 neurons were investigated in rat brain slices. The amplitude of evoked fast EPSCs decreased by 85 ± 7% of the control 4 min after the onset of in vitro ischemia. In contrast, the exogenous glutamate-induced inward currents were augmented, while the spontaneous miniature EPSCs obtained in the presence of tetrodotoxin (TTX, 1 μM) did not change in amplitude during in vitro ischem

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2

Nathan, T., and J. D. Lambert. "Depression of the fast IPSP underlies paired-pulse facilitation in area CA1 of the rat hippocampus." Journal of Neurophysiology 66, no. 5 (1991): 1704–15. http://dx.doi.org/10.1152/jn.1991.66.5.1704.

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1. Intracellular recordings from CA1 pyramidal neurons in the rat hippocampal slice have been used to study synaptic transmission after maximal orthodromic stimulation of the Schaffer collateral-commissural fibers. Paired-pulse stimulation was used to investigate how the first (conditioning) stimulation influenced the response to the second (test) stimulation. 2. When the test stimulation was delivered up to approximately 4 s after the conditioning stimulation, the late phase of the excitatory postsynaptic synaptic potential (EPSP) was increased (“late-phase facilitation”) whereas the fast (f-

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3

Buonomano, Dean V., and Michael M. Merzenich. "Net Interaction Between Different Forms of Short-Term Synaptic Plasticity and Slow-IPSPs in the Hippocampus and Auditory Cortex." Journal of Neurophysiology 80, no. 4 (1998): 1765–74. http://dx.doi.org/10.1152/jn.1998.80.4.1765.

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Buonomano, Dean V. and Michael M. Merzenich. Net interaction between different forms of short-term synaptic plasticity and slow-IPSPs in the hippocampus and auditory cortex. J. Neurophysiol. 80: 1765–1774, 1998. Paired-pulse plasticity is typically used to study the mechanisms underlying synaptic transmission and modulation. An important question relates to whether, under physiological conditions in which various opposing synaptic properties are acting in parallel, the net effect is facilitatory or depressive, that is, whether cells further or closer to threshold. For example, does the net sum

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4

Saviane, Chiara, Leonid P. Savtchenko, Giacomo Raffaelli, Leon L. Voronin, and Enrico Cherubini. "Frequency‐dependent shift from paired‐pulse facilitation to paired‐pulse depression at unitary CA3‐CA3 synapses in the rat hippocampus." Journal of Physiology 544, no. 2 (2002): 469–76. http://dx.doi.org/10.1113/jphysiol.2002.026609.

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5

Sui, Li, and M. E. Gilbert. "Pre- and Postnatal Propylthiouracil-Induced Hypothyroidism Impairs Synaptic Transmission and Plasticity in Area CA1 of the Neonatal Rat Hippocampus." Endocrinology 144, no. 9 (2003): 4195–203. http://dx.doi.org/10.1210/en.2003-0395.

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Abstract Thyroid hormones are essential for neonatal brain development. It is well established that insufficiency of thyroid hormone during critical periods of development can impair cognitive functions. The mechanisms that underlie learning deficits in hypothyroid animals, however, are not well understood. As impairments in synaptic function are likely to contribute to cognitive deficits, the current study tested whether thyroid hormone insufficiency during development would alter quantitative characteristics of synaptic function in the hippocampus. Developing rats were exposed in utero and p

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Tanner, Kylie M., Chinyere Obasi, Ian A. Herrick, and L. Stan Leung. "Effects of Propofol on Hippocampal Synaptic Transmission in Behaving Rats." Anesthesiology 93, no. 2 (2000): 463–72. http://dx.doi.org/10.1097/00000542-200008000-00026.

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Background The action of propofol has been studied in vitro and in vivo, but the effects of intravenously administered propofol on synaptic transmission in freely behaving rats have not been studied before. Methods Rats were implanted with recording electrodes in the dentate gyrus and with stimulation electrodes in the medial perforant path (MPP). Paired pulses at different interpulse intervals (IPIs) were delivered to the MPP, and average evoked potentials were recorded in the dentate gyrus before and after a bolus of propofol (10 or 20 mg/kg administered intravenously) or control vehicle was

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7

Ferchmin, P. A., P. G. DiScenna, E. M. Rivera, V. A. Eterović, and T. J. Teyler. "26. Spermine increases paired-pulse facilitation in area CA1 of hippocampus: Effect of calcium." Journal of Neuroscience Methods 52, no. 1 (1994): A12. http://dx.doi.org/10.1016/0165-0270(94)90086-8.

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8

Andreasen, M., and J. J. Hablitz. "Paired-pulse facilitation in the dentate gyrus: a patch-clamp study in rat hippocampus in vitro." Journal of Neurophysiology 72, no. 1 (1994): 326–36. http://dx.doi.org/10.1152/jn.1994.72.1.326.

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1. Whole-cell patch-clamp recordings were used to study paired-pulse facilitation (PPF) of the lateral perforant path input to the dentate gyrus in thin hippocampal slices. 2. Orthodromic stimulation of the lateral perforant pathway evoked a excitatory postsynaptic current (EPSC) with a latency of 3.3 +/- 0.1 ms (mean +/- SE) that fluctuated in amplitude. The EPSC had a rise time (10-90%) of 2.79 +/- 0.06 ms (n = 35) and decayed with a single exponential time course with a time-constant of 9.14 +/- 0.24 ms (n = 35). No correlation was found between the amplitude of the EPSC and the rise time o

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Takamatsu, Isao, Ayano Iwase, Makoto Ozaki, Tomiei Kazama, Keiji Wada, and Masayuki Sekiguchi. "Dexmedetomidine Reduces Long-term Potentiation in Mouse Hippocampus." Anesthesiology 108, no. 1 (2008): 94–102. http://dx.doi.org/10.1097/01.anes.0000296076.04510.e1.

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Background Dexmedetomidine (Precedex; Abbott Laboratories, Abbott Park, IL) is a selective alpha2-adrenergic agonist that also has affinity for imidazoline receptors. In clinical studies, dexmedetomidine has sedative effects and impairs memory, but the action of dexmedetomidine on synaptic plasticity in the brain has yet to be established. In the present study, the authors investigated the effects of dexmedetomidine on two forms of synaptic plasticity-long-term potentiation (LTP) and paired-pulse facilitation-in the CA1 region of mouse hippocampal slices. Methods The authors recorded Schaffer

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10

Ferchmin, P. A., Vesna A. Eterović, Edna M. Rivera, and Timothy J. Teyler. "Spermine increases paired-pulse facilitation in area CA1 of hippocampus in a calcium-dependent manner." Brain Research 689, no. 2 (1995): 189–96. http://dx.doi.org/10.1016/0006-8993(95)00568-b.

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