von Cornelia Larissa Granz
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| [1.] Clg/Fragment 025 12 - Diskussion Zuletzt bearbeitet: 2014-05-11 19:54:57 Schumann | Baratta et al 2002, BauernOpfer, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop |
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| Untersuchte Arbeit: Seite: 25, Zeilen: 12-30 |
Quelle: Baratta et al 2002 Seite(n): 3078, 3082, 3084, Zeilen: 3078:right col. 20-28; 3082:right col. 31-36; 3084:right col. 13-23.25-29.42-46 |
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| In hippocampal CA1 area,
somatostatin activates postsynaptic K+ currents in pyramidal neurons (Moore et al., 1988; Schweitzer et al., 1998) to hyperpolarize neurons away from their threshold for firing. Somatostatin inhibits glutamatergic excitatory postsynaptic currents at CA1 Schaeffer collateral synapses, while not affecting GABAergic inhibitory postsynaptic currents (Boehm and Betz 1997; Tallent and Siggins 1997). In CA3, somatostatin inhibits excitatory postsynaptic currents generated at associational/commissural synapses (Tallent and Siggins 1999). In line with our results, it has been reported that is released during high-frequency activation of somatostatin containing interneurons and acts to prevent LTP in lateral perforant pathway (Baratta et al., 2002). However some other studies have suggested that somatostatin facilitates LTP at some synapses in the hippocampus. An in vitro study in guinea pig demonstrated that SST augmented mossy fiber LTP in CA3 neurons (Matsuoka et al. 1991). In dentate, a previous in vivo study in rat suggested facilitation by SST of medial perforant path LTP (Nakata et al. 1996). Several inhibitory neuropeptides depress LTP in different brain structures. In vitro studies have shown nociceptin (Yu and Xie 1998), dynorphin (Terman et al. 1994) to depress LTP at lateral perforant pathway synapses. These peptides likely have a presynaptic site of action in inhibiting glutamate releases, although they could also act postsynaptically (Yu and Xie 1998). Neuropeptide Y inhibits N-type Ca2+ currents and Ca2+ transients in dentate granule cells (McQuiston et al. 1996); thus, like somatostatin, this is a possible mechanism through which this peptide could attenuate LTP. |
[page 3078]
In CA1, SST activates postsynaptic K+ currents in pyramidal neurons (Moore et al. 1988; Schweitzer et al. 1998) to hyperpolarize neurons away from their threshold for firing. SST inhibits glutamatergic excitatory postsynaptic currents (EPSCs) at CA1 Schaeffer collateral synapses, while not affecting GABAergic inhibitory postsynaptic currents (Boehm and Betz 1997; Tallent and Siggins 1997). In CA3, SST inhibits EPSCs generated at associational/commissural synapses while not affecting mossy fiber EPSCs (Tallent and Siggins 1999). [page 3082] Previous studies have suggested that SST facilitates LTP at some synapses in the hippocampus. An in vitro study in guinea pig demonstrated that SST augmented mossy fiber LTP in CA3 neurons (Matsuoka et al. 1991). In dentate, a previous in vivo study in rat suggested facilitation by SST of medial perforant path LTP (Nakata et al. 1996).
Multiple inhibitory neuropeptides depress dentate gyrus LTP. An in vivo study showed neuropeptide Y (NPY)-mediated inhibition of dentate LTP (Whittaker et al. 1999), whereas in vitro studies have shown nociceptin (Yu and Xie 1998), dynorphin (Terman et al. 1994), galanin, and cortistatin (unpublished observations) to depress LTP at LPP synapses. Some of these peptides robustly depress baseline perforant-path fEPSPs (i.e., dynorphin, nociceptin); these peptides likely have a presynaptic site of action in inhibiting glutamate releases, although they could also act postsynaptically (Yu and Xie 1998). [...] NPY inhibits N-type Ca2+ currents and Ca2+ transients in dentate granule cells (McQuiston et al. 1996); thus, like SST, this is a possible mechanism through which this peptide could attenuate LTP. [...] Our results suggest SST is released during high-frequency activation of SST containing interneurons and acts to prevent LTP of LPP synapses. Seizure events have been shown to cause intense activation of SST/GABAergic hilar interneurons (Vezzani et al. 1996). |
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