The field EPSP recorded in the CA1 region of rat hippocampal slices is potentiated by bath application of the direct adenylate cyclase activator forskolin (Chavez-Noriega and Stevens, 1992a). We have now used the whole-cell patch-clamp technique to analyze the effect of forskolin on evoked synaptic currents and on spontaneous and miniature excitatory postsynaptic currents (sEPSCs and mEPSCs) recorded in rat hippocampal slices in order to determine the relative contributions of pre- and postsynaptic mechanisms to this increased synaptic strength. Application of 50 microM forskolin in the presence of 3-isobutyl-1-methylxanthine (IBMX; a phosphodiesterase inhibitor) enhanced the evoked EPSC (eEPSC) peak amplitude to 230 +/- 43% of control (n = 13). No significant change in sEPSC or in mEPSC amplitude was detected after forskolin addition (106 +/- 7%, n = 9), indicating that postsynaptic receptor sensitivity at synaptic junctions is not greatly affected. In contrast, a large increase in sEPSC and mEPSC frequency was noted in all cells (299 +/- 81%). Following forskolin application, the amplitude distribution of evoked synaptic currents shifted to larger values, but more significantly, a sharp decrease in failure rate was produced in all cells tested. Also, a significant correlation was found between the potentiation produced by forskolin in IBMX on the eEPSC and the ratio of the squared coefficient of variation (CV = SD/mean). Finally, a quantal analysis of four cells was consistent with the hypothesis that transmitter release was increased by forskolin/IBMX with, if anything, a concomitant decrease in quantal size. Together, these observations indicate that presynaptic mechanisms significantly contribute to the enhancement produced by this diterpene.(ABSTRACT TRUNCATED AT 250 WORDS)

Ca 2 ÷/phospholipid-dependent protein kinase has long been thought to play an important role in modulating synaptic efficacy. It has been shown previously that mice lacking the brain-specific ~/subtype of PKC display abnormal long-term potentiation (LTP), whereas ordinary synaptic transmission is unaffected by the mutation. We now examine the effects of phorbol esters, which are nonselective activators of PKC, on synaptic modulation in these mutant mice. In wild-type mice, phorbol esters produce marked enhancement of synaptic transmission that is largely presynaptic in origin, an effect that has been thought to share mechanisms with LTP. In mutant mice, phorbol ester-mediated potentiation is normal despite the absence of the major PKC isoform. As in wild-type mice, this synaptic enhancement is at least partly attributable to presynaptic changes. Our results demonstrate that the ~, isotype of PKC is not essential for phorbol ester-mediated synaptic facilitation, and place limitations on the possible roles of PKC in LTP.

In this report, we provide a quantitative description for 2 aspects of the mouse piriform cortex. First, we give volumetric estimates of regions within the anterior and posterior piriform cortex. Second, we estimate the neuronal densities in each of these regions. From these two estimates, we calculate that the mouse piriform contains around half a million neurons equally distributed over the anterior and posterior piriform cortex. Quantitative descriptions such as these are important because they make it possible to construct realistic models and provide a constraint that theories of the olfactory circuit must fulfil. We show how quantitative descriptions can be useful for modelling by using our data to refine and improve earlier models of piriform cortex activity. BackgroundIn this report, we provide a quantitative description of the mouse piriform cortex (Neville & Haberly 2004;Bekkers & Suzuki 2013). The piriform cortex, also called the pyriform or pre-piriform cortex, is the largest olfactory region in the cortex, and is responsible for encoding experience and learning dependent odors. It forms the third stage of the olfactory circuit that begins with the olfactory epithelium in the nose followed by the olfactory bulb. A quantitative description of the piriform cortex is needed for 2 reasons.