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Enduring medial perforant path short-term synaptic depression at high pressure.

Talpalar AE, Giugliano M, Grossman Y - Front Cell Neurosci (2010)

Bottom Line: We used rat cortico-hippocampal slices and computer simulations for studying the effects of pressure and its interaction with extracellular Ca(2+) ([Ca(2+)](o)) on FDD at the MPP synapses.Mathematical model analysis of the fractions of synaptic resources used by each fEPSP during trains (normalized to their maximum) and the total fraction utilized within a train indicate that HP depresses synaptic activity also by reducing synaptic resources.This data suggest that MPP synapses may be modulated, in addition to depression of single events, by reduction of synaptic resources and then may have the ability to conserve their dynamic properties under different conditions.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Neurobiology, Faculty of Health Sciences, and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev Beer-Sheva, Israel.

ABSTRACT
The high pressure neurological syndrome develops during deep-diving (>1.1 MPa) involving impairment of cognitive functions, alteration of synaptic transmission and increased excitability in cortico-hippocampal areas. The medial perforant path (MPP), connecting entorhinal cortex with the hippocampal formation, displays synaptic frequency-dependent-depression (FDD) under normal conditions. Synaptic FDD is essential for specific functions of various neuronal networks. We used rat cortico-hippocampal slices and computer simulations for studying the effects of pressure and its interaction with extracellular Ca(2+) ([Ca(2+)](o)) on FDD at the MPP synapses. At atmospheric pressure, high [Ca(2+)](o) (4-6 mM) saturated single MPP field EPSP (fEPSP) and increased FDD in response to short trains at 50 Hz. High pressure (HP; 10.1 MPa) depressed single fEPSPs by 50%. Increasing [Ca(2+)](o) to 4 mM at HP saturated synaptic response at a subnormal level (only 20% recovery of single fEPSPs), but generated a FDD similar to atmospheric pressure. Mathematical model analysis of the fractions of synaptic resources used by each fEPSP during trains (normalized to their maximum) and the total fraction utilized within a train indicate that HP depresses synaptic activity also by reducing synaptic resources. This data suggest that MPP synapses may be modulated, in addition to depression of single events, by reduction of synaptic resources and then may have the ability to conserve their dynamic properties under different conditions.

No MeSH data available.


Related in: MedlinePlus

High [Ca2+]o promotes paired-pulse-depression of MPP fEPSPs under HP. (A) Single experiment shows the antagonistic effect of high (4 mM) [Ca2+]o on HP (10.1 MPa) paired-pulse modulation. At 10.1 MPa the initial phase of paired-pulse-depression (PPD) was attenuated, while the later paired-pulse-facilitation (PPF) was increased. Increased [Ca2+]o at HP partially restored the slope of E1, but increased PPD for short ISI and abolished the later phase of PPF for ISI 35–120 ms. (B) Comparison between PPM at 5.1 MPa (2 mM [Ca2+]o) and 10.1 MPa (4 mM [Ca2+]o). Note that E1 under these two conditions is almost equal; however PPD is much greater under the latter condition.
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Figure 3: High [Ca2+]o promotes paired-pulse-depression of MPP fEPSPs under HP. (A) Single experiment shows the antagonistic effect of high (4 mM) [Ca2+]o on HP (10.1 MPa) paired-pulse modulation. At 10.1 MPa the initial phase of paired-pulse-depression (PPD) was attenuated, while the later paired-pulse-facilitation (PPF) was increased. Increased [Ca2+]o at HP partially restored the slope of E1, but increased PPD for short ISI and abolished the later phase of PPF for ISI 35–120 ms. (B) Comparison between PPM at 5.1 MPa (2 mM [Ca2+]o) and 10.1 MPa (4 mM [Ca2+]o). Note that E1 under these two conditions is almost equal; however PPD is much greater under the latter condition.

Mentions: The above assessment of SR status showed reduction of the estimated SR at HP whereas change in [Ca2+]o was not effective. Paired-pulse protocols normally allow the study of short-term synaptic plasticity, namely paired-pulse-facilitation (PPF) or paired-pulse-depression (PPD). By comparing the strength (slope) of the second fEPSP (E2) with respect to E1 we can also estimate the proportion of ET used by subsequent Ei for the two responses. In a previous study (Talpalar and Grossman, 2003) we showed that under control conditions of [Ca2+]o and pressure, the MPP input displayed variable plasticity depending on the duration of the inter-stimulus interval (ISI): ISIs of <30 ms produced pure PPD (E2/E1 < 1) while ISIs of 35–80 ms produced a small∼5% PPF (E2/E1 > 1). HP reduced PPD at short ISIs, and increased PPF of longer ISIs (Talpalar and Grossman, 2003), suggesting that synaptic release of E1 was reduced shifting away from saturation. These observations were reproduced in the present set of experiments, in which 10.1 MPa pressure reduced PPD at the 10–20 ms ISIs and increased PPF at the 40–120 ms ISIs (Figure 3A). In addition, we compared the effect of raising [Ca2+]o on similar paired-pulse modulation at control and HP.


Enduring medial perforant path short-term synaptic depression at high pressure.

Talpalar AE, Giugliano M, Grossman Y - Front Cell Neurosci (2010)

High [Ca2+]o promotes paired-pulse-depression of MPP fEPSPs under HP. (A) Single experiment shows the antagonistic effect of high (4 mM) [Ca2+]o on HP (10.1 MPa) paired-pulse modulation. At 10.1 MPa the initial phase of paired-pulse-depression (PPD) was attenuated, while the later paired-pulse-facilitation (PPF) was increased. Increased [Ca2+]o at HP partially restored the slope of E1, but increased PPD for short ISI and abolished the later phase of PPF for ISI 35–120 ms. (B) Comparison between PPM at 5.1 MPa (2 mM [Ca2+]o) and 10.1 MPa (4 mM [Ca2+]o). Note that E1 under these two conditions is almost equal; however PPD is much greater under the latter condition.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2967425&req=5

Figure 3: High [Ca2+]o promotes paired-pulse-depression of MPP fEPSPs under HP. (A) Single experiment shows the antagonistic effect of high (4 mM) [Ca2+]o on HP (10.1 MPa) paired-pulse modulation. At 10.1 MPa the initial phase of paired-pulse-depression (PPD) was attenuated, while the later paired-pulse-facilitation (PPF) was increased. Increased [Ca2+]o at HP partially restored the slope of E1, but increased PPD for short ISI and abolished the later phase of PPF for ISI 35–120 ms. (B) Comparison between PPM at 5.1 MPa (2 mM [Ca2+]o) and 10.1 MPa (4 mM [Ca2+]o). Note that E1 under these two conditions is almost equal; however PPD is much greater under the latter condition.
Mentions: The above assessment of SR status showed reduction of the estimated SR at HP whereas change in [Ca2+]o was not effective. Paired-pulse protocols normally allow the study of short-term synaptic plasticity, namely paired-pulse-facilitation (PPF) or paired-pulse-depression (PPD). By comparing the strength (slope) of the second fEPSP (E2) with respect to E1 we can also estimate the proportion of ET used by subsequent Ei for the two responses. In a previous study (Talpalar and Grossman, 2003) we showed that under control conditions of [Ca2+]o and pressure, the MPP input displayed variable plasticity depending on the duration of the inter-stimulus interval (ISI): ISIs of <30 ms produced pure PPD (E2/E1 < 1) while ISIs of 35–80 ms produced a small∼5% PPF (E2/E1 > 1). HP reduced PPD at short ISIs, and increased PPF of longer ISIs (Talpalar and Grossman, 2003), suggesting that synaptic release of E1 was reduced shifting away from saturation. These observations were reproduced in the present set of experiments, in which 10.1 MPa pressure reduced PPD at the 10–20 ms ISIs and increased PPF at the 40–120 ms ISIs (Figure 3A). In addition, we compared the effect of raising [Ca2+]o on similar paired-pulse modulation at control and HP.

Bottom Line: We used rat cortico-hippocampal slices and computer simulations for studying the effects of pressure and its interaction with extracellular Ca(2+) ([Ca(2+)](o)) on FDD at the MPP synapses.Mathematical model analysis of the fractions of synaptic resources used by each fEPSP during trains (normalized to their maximum) and the total fraction utilized within a train indicate that HP depresses synaptic activity also by reducing synaptic resources.This data suggest that MPP synapses may be modulated, in addition to depression of single events, by reduction of synaptic resources and then may have the ability to conserve their dynamic properties under different conditions.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Neurobiology, Faculty of Health Sciences, and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev Beer-Sheva, Israel.

ABSTRACT
The high pressure neurological syndrome develops during deep-diving (>1.1 MPa) involving impairment of cognitive functions, alteration of synaptic transmission and increased excitability in cortico-hippocampal areas. The medial perforant path (MPP), connecting entorhinal cortex with the hippocampal formation, displays synaptic frequency-dependent-depression (FDD) under normal conditions. Synaptic FDD is essential for specific functions of various neuronal networks. We used rat cortico-hippocampal slices and computer simulations for studying the effects of pressure and its interaction with extracellular Ca(2+) ([Ca(2+)](o)) on FDD at the MPP synapses. At atmospheric pressure, high [Ca(2+)](o) (4-6 mM) saturated single MPP field EPSP (fEPSP) and increased FDD in response to short trains at 50 Hz. High pressure (HP; 10.1 MPa) depressed single fEPSPs by 50%. Increasing [Ca(2+)](o) to 4 mM at HP saturated synaptic response at a subnormal level (only 20% recovery of single fEPSPs), but generated a FDD similar to atmospheric pressure. Mathematical model analysis of the fractions of synaptic resources used by each fEPSP during trains (normalized to their maximum) and the total fraction utilized within a train indicate that HP depresses synaptic activity also by reducing synaptic resources. This data suggest that MPP synapses may be modulated, in addition to depression of single events, by reduction of synaptic resources and then may have the ability to conserve their dynamic properties under different conditions.

No MeSH data available.


Related in: MedlinePlus