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• W2010181423 abstract "The hippocampus remains uniquely popular as a prototypical cortical area for elucidating fundamental principles of synaptic transmission and the essentials of neuronal architecture and interconnectivity. “The Spring Hippocampal Research Conference,” traditionally held on Grand Cayman (B. W. I) and organized by Robert S. Sloviter (University of Arizona), Dan H. Lowenstein (University of California, San Francisco), and Robert K. S. Wong (State University of New York), brings together hippocampal aficionados interested in these complex issues. We have organized this report around some of the major themes that emerged from this year’s presentations and ensuing discussions, incorporating only the most salient and recent citations. Dendrites have long ceased to be regarded as passive cables. Although the usual site of action potential initiation is near the soma, new data indicate that in the CA1 area (Figure 1) sodium spikes can be generated in pyramidal cell dendrites under conditions of increased synaptic excitation. This may occur readily, owing to frequency facilitation during repetitive synaptic stimulation of the Schaffer collateral pathway (N. Spruston; Northwestern University). During tetanic synaptic activation, the first action potential is usually initiated in the axon, whereas the second and third spikes are generated in the dendrites. However, prolonged synaptic stimulation shifts the site of spike initiation back to the axon, as the availability of dendritic sodium channels is decreased due to inactivation (Spruston). What is the relevance of these data for the integration of dendritic signals in the intact animal? This issue was recently addressed with in vivo recordings from the apical dendrites of CA1 pyramidal neurons, showing the dendritic attenuation of backpropagating action potentials (12Kamondi A Acsady L Buzsaki G Dendritic spikes are enhanced by cooperative network activity in the intact hippocampus.J. Neurosci. 1998; 18: 3919-3928PubMed Google Scholar). Moreover, putative Ca2+ spikes as well as large amplitude fast spikes can be monitored in dendrites of CA1 pyramidal cells concurrent with extracellularly recorded sharp waves (Figure 2; G. Buzsáki, Rutgers University). Interestingly, during sharp waves a greater number of spikes can be observed in the dendrites than in the soma, suggesting both their local generation and their unreliable propagation to the soma (Buzsáki). Likewise, isolated dendritic spikes in CA1 pyramidal neurons have also been noted in vitro (Spruston), suggesting a functional role that is fundamentally different from that of action potentials propagating down the axon (Figure 2). Ionotropic and metabotropic receptors on dendrites can influence the spatial extent of action potential backpropagation as well as action potential–induced transient increases in dendritic [Ca2+]i. Dendritic inhibitory postsynaptic potentials (IPSPs) can decrease the amplitude of single spikes in pyramidal cell distal dendrites (22Tsubokawa H Ross W.N IPSPs modulate spike backpropagation and associated [Ca2+]i changes in the dendrites of hippocampal CA1 pyramidal neurons.J. Neurophysiol. 1996; 76: 2896-2906PubMed Google Scholar, 3Buzsáki G Penttonen M Nadasdy Z Bragin A Pattern and inhibition-dependent invasion of pyramidal cell dendrites by fast spikes in the hippocampus in vivo.Proc. Natl. Acad. Sci. USA. 1996; 93: 9921-9925Crossref PubMed Scopus (197) Google Scholar). Furthermore, muscarinic receptor activation antagonizes the activity-dependent decrease of action potential amplitudes and thereby enhances dendritic [Ca2+]i levels (23Tsubokawa H Ross W.N Muscarinic modulation of spike backpropagation in the apical dendrites of hippocampal CA1 pyramidal neurons.J. Neurosci. 1997; 17: 5782-5791PubMed Google Scholar). Phorbol ester application is effective in reversing the tetanically induced reduction of spike amplitudes, suggesting the involvement of protein kinase C (PKC) (W. Ross, New York Medical College; 4Colbert C.M Johnston D Protein kinase C activation decreases activity-dependent attenuation of dendritic Na+ current in hippocampal CA1 pyramidal neurons.J. Neurophysiol. 1998; 79: 491-495PubMed Google Scholar). Apart from the modulation of action potential backpropagation due to ionotropic and metabotropic receptor types, there is also evidence to suggest a major involvement of voltage-gated IA-type potassium channels (10Hoffman D.A Magee J.C Colbert C.M Johnston D K+ channel regulation of signal propagation in dendrites of hippocampal pyramidal neurons.Nature. 1997; 387: 869-875Crossref PubMed Scopus (30) Google Scholar). With the somato-dendritic gradient of channel density showing a steep increase toward distal dendrites, at any given membrane potential disproportionally more IA will be activated in the dendrites when compared to the soma (D. Johnston, Baylor College of Medicine). It also appears that the activity of IA channels can be modulated, since their phosphorylation via protein kinases A and C (PKA and PKC) causes a shift in the voltage activation of the channels, resulting in a reduction of IA activation and, accordingly, an increased amplitude of backpropagating action potentials (Figure 2; 9Hoffman D.A Johnston D Downregulation of transient K+ channels in dendrites of hippocampal CA1 pyramidal neurons by activation of PKA and PKC.J. Neurosci. 1998; 18: 3521-3528Crossref PubMed Google Scholar). Just as with dendritic information processing, the conventional picture of the inhibitory role of the amino acid transmitter GABA is currently under profound revision. During the early development of CNS neurons, GABAA receptor–mediated responses are often strongly depolarizing. The ontogenetic change in GABAergic transmission from excitatory to inhibitory is set by the developmental regulation of the expression of the recently cloned neuronal K+/Cl− cotransporter, KCC2 (K. Kaila, University of Helsinki). Therefore, this transporter appears to be mainly responsible for the extrusion of chloride that is needed for the switch to hyperpolarizing GABAA responses in mature neurons. Already during early development, the release of GABA appears to be under presynaptic control, as it is inhibited by the activation of neuropeptide Y (NPY) and GABAB receptors (A. van den Pol, Yale University). In the adult hippocampus, GABAA receptor–mediated excitation also takes place under conditions that involve intense activation of the network of interneurons. Whether dendritic concentration changes of the two major anions that penetrate the GABAA receptor channel, chloride and bicarbonate, can account for those changes has been addressed using computational modeling, incorporating a K+/Cl− cotransporter with an experimentally determined affinity and maximum transport rate (K. Staley, University of Colorado Health Science Center). The model shows that GABA-gated chloride flux is theoretically sufficient to overwhelm the transporter’s capacity, resulting in a prominent shift of dendritic chloride and hence in a large positive shift in the GABAA reversal potential. Similar shifts in the concentration gradient of anions may also occur in adult hippocampal neurons following exposure to the potassium channel blocker 4-AP. Using this paradigm, the experimental manipulation of chloride and bicarbonate ions suggests that the depolarizing component of GABA responses may be carried by bicarbonate ions (R. Wong). Apart from the redistribution of anions, an additional mechanism—probably a direct depolarizing action of activity-dependent increases in the extracellular potassium concentration—plays a role in the long-lasting depolarizations seen in pyramidal neurons both during tetanic stimulation and in the presence of 4-AP (Kaila). Although the functional role of many synaptically released neuropeptides remains enigmatic, insights are gradually emerging owing to the availability of specific pharmacological modulators and/or transgenic mice. The peptide NPY can presynaptically inhibit the release of glutamate, and the ensuing excitability change in the network can be imaged by dyes sensitive to mitochondrial depolarizations and calcium level changes (V. Bindokas, University of Chicago). While NPY-deficient mice exhibit no changes in normal synaptic hippocampal function, these animals are less able to terminate limbic seizures (S. Baraban, Case Western Reserve University). Furthermore, in transgenic mice the excitotoxic action of kainic acid evokes prolonged periods of status epilepticus and death; the seizure-induced fatality can be prevented by ventricular infusion of NPY. The involvement of NPY in the control of hippocampal excitability is also apparent in an experimental model of epilepsy, the stimulus train–induced bursting (STIB) model of epilepsy (G. Klapstein, University of California, Los Angeles). In this experimental in vitro paradigm, NPY and Y2 receptor agonists potently inhibit excitatory ictal and interictal events, while the rhythmic AMPA receptor–mediated glutamatergic drive to interneurons is insensitive to inhibition by NPY. Recent findings suggested that NPY Y5 receptors suppress seizure activity in kainate-treated rats in vivo. However, in the STIB paradigm, NPY Y5 receptor agonists are ineffective, while NPY itself and NPY Y2 receptor agonists inhibit the evoked afterdischarges, suggesting that NPY Y2 receptors predominate in regulating excitability in the normal hippocampus (W. Colmers, University of Alberta). Metabotropic glutamate receptors (mGluRs) are rapidly moving center stage owing to their importance in regulating the function of several major ionotropic and metabotropic amino acid receptors. Low nanomolar concentrations of group II mGluR agonists act differentially and selectively to potentiate NMDA and GABAA while depressing GABAB receptor–mediated synaptic potentials recorded in vitro from the rat dorsolateral septal nucleus (J. Gallagher, University of Texas, Galveston). In addition to presynaptic inhibitory effects, group I mGluRs can directly excite neocortical interneurons, resulting in a facilitation of inhibitory neurotransmission (J. Hablitz, University of Alabama). In hippocampal slices, the activation of group I mGluRs produces synchronized discharges that resemble ictal events in epilepsy and remain in the absence of agonist. Moreover, the induction of these discharges by mGluR I agonists may require new protein synthesis (Wong). In kindled amygdala neurons, a nonselective mGluR antagonist is effective in blocking group I mGluR agonist–induced bursting but had no effect on synaptically induced kindled bursting (P. Shinnick-Gallagher, University of Texas, Galveston). Thus, these data support the emerging view that mGluR effects are synapse specific. Protein kinases and phosphatases not only regulate the function of many ionotropic channels, they also modulate signaling by mGluRs (J. Conn, Emory University). One mGluR subtype, mGluR5, plays an important role in potentiating NMDA receptor currents in hippocampal pyramidal cells. In turn, NMDA receptor activation can potentiate mGluR5-mediated responses by reversing PKC-mediated desensitization of mGluR5. Apart from mGluR5, NMDA receptor function may also be modulated by thrombin receptors, which can potentiate NMDA receptor function, presumably by relieving the channel’s magnesium block (S. Traynelis, Emory University). Thus, thrombin extravasation could promote NMDA-mediated excitotoxicity after stroke or traumatic brain injury. As outlined above, kinases affect the function of hippocampal G protein–coupled receptors, and, conversely, the latter are also known to regulate the function of protein kinases, such as the mitogen-activated protein kinase (MAPK). A wide variety of neuromodulatory neurotransmitter receptors couple to MAPK activation in the hippocampus (D. Sweatt, Baylor College of Medicine). In turn, MAPK plays a critical role in transcriptional regulation by PKA and PKC. This unexpected diversity in the regulation of MAPK suggests a broad role for the MAPK cascade in the modulation of hippocampal synaptic plasticity. The role of G protein–coupled receptors also extends to the modulation of voltage-gated ion channels, exemplified by the recently discovered cannabinoid receptors. Curiously, the cannabinoid receptor–mediated action through negative (Gi/Go protein) coupling to adenylyl cyclase leads to simultaneous and reciprocal changes in two major potassium channel currents, IA and ID (S. Deadwyler, Wake Forest University). Since neither current can be altered individually via changes in cannabinoid receptor occupancy, action potential parameters in hippocampal neurons will be altered by a composite potassium current that either minimizes spike duration and maximizes frequency or extends spike duration but reduces spike frequency. The theta rhythm (∼3–10 Hz) remains a major focus of hippocampal research. Theta-modulated hippocampal network activity is likely to contribute to the neural coding of spatial information (W. Skaggs, University of Pittsburgh). Remarkably, the firing time of a hippocampal neuron systematically advances in phase with respect to the theta cycle, when the animal moves across the place field of the recorded cell (16O’Keefe J Recce M.L Phase relationship between hippocampal place units and the EEG theta-rhythm.Hippocampus. 1993; 3: 317-330Crossref PubMed Scopus (1780) Google Scholar). Therefore, at the beginning of the theta cycle the hippocampal population activity encodes a rat’s current location, and as the cycle progresses it shifts forward to represent locations ahead of the rat along its trajectory (21Skaggs W.E McNaughton B.L Wilson M.A Barnes C.A Theta phase precession in hippocampal neuronal populations and the compression of temporal sequences.Hippocampus. 1996; 6: 149-172Crossref PubMed Scopus (1141) Google Scholar). In terms of intrinsic rhythmogenesis, layer II stellate cells in the entorhinal cortex (EC) display robust membrane potential oscillations in the theta frequency range. The oscillatory activity may arise owing to the ongoing interplay between the activation of a low threshold, persistent sodium current and the deactivation of a nonspecific cation current (IH; A. Alonso, McGill University). Apart from principal neurons, particular classes of hippocampal interneurons may also exhibit low threshold membrane oscillations (J.-C. Lacaille, University of Montreal). They occur in a class of hippocampal interneurons within the stratum lacunosum-moleculare, whereas other interneurons in the stratum oriens are less prone to oscillate. Somatostatin-containing interneurons are also likely to partake in the downstream processing of theta activity (T. Freund, Institute of Experimental Medicine, Budapest). Somatostatin cells receive their main excitatory inputs from the local collaterals of pyramidal neurons and, in turn, preferentially innervate the distal dendrites of pyramidal cells. Published data suggest that disynaptic inhibition arising in this circuit is appropriately timed to affect the dendritic invasion and backpropagation of action potentials. However, this may only occur during the peak population activity of the theta cycle, when the concerted activity of pyramidal cells will provide enough convergent excitation for somatostatin cells to fire an action potential. Apart from hippocampal interneurons, the GABAergic septo-hippocampal input may also have a major role in generating hippocampal theta. Interestingly, computational modeling predicts that GABAA receptor–mediated interactions are unlikely to be sufficient for synchronizing theta frequency oscillations of GABAergic medial septal neurons (Figure 3; X.-J. Wang, Brandeis University), since the ionic model of membrane oscillations in these cells depends critically on a low threshold, slowly inactivating potassium current. When extending the model to incorporate the entire reciprocal septo-hippocampal circuit, network simulations indicate that the medial septum may be a prerequisite for theta rhythm generation. However, the emergence of synchrony across the entire network may crucially depend on the presence of the hippocampo-septal inhibitory feedback loop. Rhythmic hippocampal network activities within different frequency bands are not necessarily mutually exclusive. On the contrary, in the hippocampus of intact animals, gamma frequency (20–70 Hz) oscillations are frequently nested in concurrently occurring theta (19Penttonen M Kamondi A Acsady L Buzsaki G Gamma frequency oscillation in the hippocampus of the rat intracellular analysis in vivo.Eur. J. Neurosci. 1998; 10: 718-728Crossref PubMed Scopus (241) Google Scholar). Intracellular in vivo recordings demonstrate the interdependence of concurrently recorded extra- and intracellular gamma frequency. The voltage dependence of intracellularly recorded activity is suggestive of chloride-mediated IPSPs contributing to gamma oscillations. What are the presynaptic sources for these events? Recordings from anatomically verified basket cells, which innervate the perisomatic region of pyramidal cells, demonstrate that they not only discharge at gamma frequencies but are also phase locked to field recordings (Buzsáki). Conceivably, they will therefore impose their rhythmic output onto postsynaptic pyramidal neurons (1Buhl E.H Halasy K Somogyi P Diverse sources of hippocampal unitary inhibitory postsynaptic potentials and the number of synaptic release sites.Nature. 1994; 368: 823-828Crossref PubMed Scopus (590) Google Scholar) and will thus, fostered by the resonant properties of principal cells, pace their activity in the gamma frequency range (Buzsáki). Recent findings reveal that cholinergic-muscarinic activation of the hippocampal CA3 region in vitro can induce persistent gamma frequency network oscillations (Figure 4; 7Fisahn A.F Pike F.G Buhl E.H Paulsen O Cholinergic induction of network oscillations at 40 Hz in the hippocampus in vitro.Nature. 1998; 394: 186-189Crossref PubMed Scopus (678) Google Scholar). Simultaneous whole-cell patch and extracellular field recordings demonstrate that within an oscillatory cycle action potentials, excitatory postsynaptic currents (EPSCs), and inhibitory postsynaptic currents (IPSCs) occur in a well-defined temporal sequence, with the relative timing of events strongly suggesting that inhibitory events have a crucial role in phasing population activity (E. Buhl, MRC Anatomical Neuropharmacology Unit, Oxford). Within the hippocampal CA1 area, gamma oscillations may also act as a powerful filter for afferent inputs (24Whittington M.A Traub R.D Jefferys J.G.R Synchronized oscillations in interneuron networks driven by metabotropic glutamate receptor activation.Nature. 1995; 373: 612-615Crossref PubMed Scopus (1254) Google Scholar). Volleys arriving in phase with the local gamma oscillations will generate additional action potentials, whereas inappropriately timed inputs disrupt the background pyramidal cell involvement to such an extent that only a subthreshold gamma oscillation remains, thus effectively abolishing output from the oscillating area. Such tetanically induced gamma oscillations may transform rather abruptly to beta frequencies (R. Traub, University of Birmingham). Experiments and network simulations suggest that the temporal evolution of two parameters can account for the frequency switch: the gradual recovery of a slow Ca2+-activated potassium conductance and the concomitant increase of recurrent excitatory feedback between pyramidal neurons. Although chemical synaptic neurotransmission is of unequivocal importance for the generation of network activity, it has been recently shown that spontaneous high frequency oscillations (150–200 Hz) can emerge in electrotonically coupled networks of hippocampal neurons (6Draguhn A Traub R.D Schmitz D Jefferys J.G.R Electrical coupling underlies high frequency oscillations in the hippocampus in vitro.Nature. 1998; 394: 189-192Crossref PubMed Scopus (539) Google Scholar). This phenomenon was linked to the firing of small sets of pyramidal cells, with the pharmacological block of gap junctions showing that synchronization was not synaptic but rather occurred through gap junctional–mediated electrical coupling (J. Jefferys, University of Birmingham). Considerable interest has focused on the synaptic reorganization of dentate granule cells in the adult hippocampus and their possible role in epileptogenesis. It has remained controversial whether sprouting axon collaterals form recurrent excitatory and/or inhibitory circuits, and whether they are epileptogenic or rather restorative (E. Dudek, Colorado State University). Recent data suggests that mossy fiber “sprouting” leads to new recurrent excitatory circuits in the dentate gyrus, which are masked by local inhibitory circuits. Moreover, mossy fiber sprouting may also lead to new excitatory synapses onto inhibitory interneurons. Likewise, in the CA1 area an increase of principal cell axon collaterals in hippocampal slices of kainate-treated epileptic rats may provide the anatomical substrate for the ensuing synaptic reorganization (Lacaille; 20Perez Y Morin F Beaulieu C Lacaille J.-C Axonal sprouting of CA1 pyramidal cells in hyperexcitable hippocampal slices of kainate-treated rats.Eur. J. Neurosci. 1996; 8: 736-748Crossref PubMed Scopus (149) Google Scholar). New evidence suggests that the initial effect of kainate treatment is a reduction in inhibition, whereas several months later additional alterations occur, which lead to repetitive bursts of population activity that appear to be mediated by new recurrent excitatory circuits (B. Smith, Colorado State University). Hippocampal neurons also show an increase of excitability following a prenatal irradiation paradigm (S. Roper, University of Florida). It appears that irradiation induces heterotopic clusters of neurons and the dispersion of hippocampal pyramidal neurons, with the conjoint formation of new recurrent circuits resulting in an overall increase of excitability within these heterotopic islands. Neurogenesis in the granule cell layer of the rodent dentate gyrus continues throughout adult life. A number of pathogenic stimuli, such as fluid-percussion trauma or prolonged epileptic seizures, may further kindle dentate granule cell neurogenesis, presumably resulting in the formation of aberrant connections by newly born granule cells (18Parent J.M Yu T.W Leibowitz R.T Geschwind D.H Sloviter R.S Lowenstein D.H Dentate granule cell neurogenesis is increased by seizures and contributes to aberrant network reorganization in the adult rat hippocampus.J. Neurosci. 1997; 17: 3727-3738Crossref PubMed Google Scholar; D. Lowenstein). The increased mitotic rate after status epilepticus leads to an increase in the total number of dentate granule cells (L. Mello, Federal University of Sao Paulo). Interestingly, the experimental reduction of mossy fiber outgrowth is ineffective in reducing kainate-induced epileptogenesis; hence, it is conceivable that mossy fiber sprouting and dentate granule cell neurogenesis in epilepsy are adaptive phenomena. Indeed, granule cell neurogenesis/synaptogenesis can be also induced by long-term potentiation–inducing (LTP-inducing) paradigms, although they are not necessarily correlated with LTP induction (B. Derrick, University of Texas, San Antonio). What are the underlying molecular mechanisms that may orchestrate plastic changes in synaptic organization and function? Neurotrophins seem suitable candidate molecules, with brain-derived neurotrophic factor (BDNF) modulating synaptic function in the hippocampus and acting presynaptically to facilitate high frequency synaptic transmission at CA1 synapses in the developing hippocampus (W. Gottschalk, USDP, NICHD, and NIH). The BDNF-mediated effects are regulated by the expression and/or distribution of specific synaptic proteins involved in vesicle mobilization and/or docking at presynaptic active zones (L. Pozzo-Miller, NINDS and NIH). Synapses in the CA1 area of BDNF knockout mice are less likely to express LTP, and when they do, its magnitude is reduced compared to wild-type littermates. The transgenic mice also reveal a reduction in the number of vesicles docked at presynaptic active zones and a marked decrease in the levels of synaptobrevin (VAMP-2) as well as synaptophysin. These observations are consistent with the hypothesis that BDNF modulates high frequency synaptic transmission through a presynaptic mechanism (Pozzo-Miller). However, BDNF can also modulate synaptic inhibition via postsynaptic mechanisms, inducing a rapid downregulation of various GABAA receptor subunits from the cell surface of hippocampal neurons in culture (B. Berninger, University of California, San Diego), which may account for the previously observed decrease in synaptic inhibition. Synaptic modulation of GABAergic interneurons may genuinely differ from what has been observed in principal cells. Indeed, mossy fiber synaptic transmission onto pyramidal cells and interneurons of the CA3 area is strikingly different (14Maccaferri G Toth K McBain C.J Target-specific expression of presynaptic mossy fiber plasticity.Science. 1998; 279: 1368-1370Crossref PubMed Scopus (184) Google Scholar; C. McBain, Laboratory for Cell and Molecular Neuroscience, NIH). LTP of mossy fiber inputs to CA3 pyramidal neurons is presynaptic and relies on the elevation of cAMP. In contrast, neither tetanic stimulation nor agents that elevate cAMP enhance mossy fiber transmission onto interneurons. These data demonstrate that synaptic terminals arising from a common afferent pathway do not function as a single computational unit but are specialized, depending on their postsynaptic target. This lack of plasticity may be explained by the conspicuous lack of calcineurin in inhibitory interneurons, the former being a key molecule in a major Ca2+-signaling pathway (I. Mody, University of California, Los Angeles). In support of this notion, calcineurin inhibitors fail to prolong NMDA single channel openings in interneurons, as readily observed in calcineurin-containing principal neurons. Although interneurons may lack conventional forms of synaptic plasticity, they can nevertheless express activity-dependent changes of their synaptic properties. Thus, an experimental paradigm that induced LTP in pyramidal neurons concomitantly elicited long-term depression (LTD) in interneurons. Interneuron LTD was shown to be synapse-nonspecific because depression was also observed at untetanized synapses (15McMahon L.L Kauer J.A Hippocampal interneurons express a novel form of synaptic plasticity.Neuron. 1997; 18: 295-305Abstract Full Text Full Text PDF PubMed Scopus (160) Google Scholar). In addition, interneuron LTD could not be induced by a pairing protocol and was not blocked by NMDA receptor antagonists, suggesting that the underlying mechanism is different from LTP that was simultaneously evoked in pyramidal neurons (J. Kauer, Duke University). Some interneurons in stratum oriens may also show unusual Ca2+ dynamics. Activation of MCPG-sensitive mGluRs induces voltage- and Ca2+-dependent oscillations in single interneurons, involving a functional coupling between voltage-dependent Ca2+ channels and the release of intracellular Ca2+ from ryanodine-sensitive stores (Lacaille). Thus, data are accumulating to suggest that different form(s) of activity-dependent phenomena are present in most inhibitory interneurons of the hippocampus. The association of pre- and/or postsynaptic activity may result in changes of synaptic efficacy. Either cooperative pre- and postsynaptic activity leads to synaptic strengthening or, alternatively, simultaneous activity in afferent pathways leads to the strong pathway associatively potentiating the weaker one. When using the granule cell mossy fiber output as the weak input and the commissural fibers as the strong input, associative LTP and LTD can be observed in the CA3 area in vivo (J. Martinez, University of Texas, San Antonio). Interestingly, associative LTP of the NMDA receptor–independent mossy fiber input is dependent on the NMDA receptor–dependent commissural input (5Derrick B.E Martinez Jr., J.L Associative, bidirectional modifications at the hippocampal mossy fibre–CA3 synapse.Nature. 1996; 381: 429-434Crossref PubMed Scopus (39) Google Scholar). The medial and lateral perforant path projections to the CA3 area also show associative LTP induction in vivo (Derrick). When the lateral perforant path was the strong input, associative LTP induction due to medial perforant path activation was blocked by the opioid receptor antagonist naloxone. However, when the lateral perforant pathway was the weak input, naloxone had no effect on the medial perforant path, suggesting that the former pathway exerts an obligatory role in information associatively transmitted to the hippocampus via the latter. Interactions between afferent pathways converging onto CA3 pyramidal neurons also become apparent during near-simultaneous activation of the mossy fiber input and the perforant path, resulting in the attenuation of the perforant path response (G. Barrionuevo, University of Pittsburgh). Thus, the mossy fiber input may regulate information flow into the CA3 area via the perforant path when both systems are simultaneously active. The complexity of pre- as well as postsynaptic factors contributing to the modulation of synaptic strength is particularly evident in plastic changes of the mossy fiber pathway. When using chelators (BAPTA) of postsynaptic Ca2+, it is apparent that mossy fiber LTP induction depends on postsynaptic Ca2+, and that differences in induction between both forms of mossy fiber LTP (pre- and postsynaptic) may be more quantitative than qualitative (Johnston; 13Kapur A Yeckel M.F Gray R Johnston D L-type calcium channels are required for one form of hippocampa" @default.
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• W2010181423 title "Remembering the Caribbean" @default.
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