The role of Ca2+ entry via synaptically activated NMDA receptors in the induction of long-term potentiation

Perkel, David J.; Petrozzino, Jeffrey J.; Nicoll, Roger A.; Connor, John A.

doi:10.1016/0896-6273(93)90111-4

Cited by 126 publications

(78 citation statements)

References 28 publications

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“…Consistent with this interpretation, synaptically initiated NMDA-dependent Ca 2+ signals within spiny dendrites of CA1 pyramidal neurons are larger in hippocampal slice cultures exposed to estradiol, an observation that again correlates with the higher spine density of estradiol-treated neurons (Pozzo-Miller et al, 1999). It is worth noting that those larger Ca 2+ signals in dendritic shafts in estrogen-treated neurons were evoked by afferent stimulation under voltage-clamp at depolarized potentials to evoke pharmacologically isolated NMDAR-mediated synaptic currents (Perkel et al, 1993;Malinow et al, 1994;Pozzo Miller et al, 1996), in contrast to the present observations that represent both voltage-and ligand-gated Ca 2+ influx during bAPs alone, EPSPs alone, or coincident bAPs and subthreshold EPSPs. It is currently unknown whether estradiol promotes the formation of a morphologically specific spine type, as BDNF does (Tyler and Pozzo-Miller, 2003).…”

Section: Discussionsupporting

confidence: 52%

BDNF enhances dendritic Ca2+ signals evoked by coincident EPSPs and back-propagating action potentials in CA1 pyramidal neurons

Pozzo-Miller

2006

Brain Research

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BDNF, a member of the neurotrophin family, is emerging as a key modulator of synaptic structure and function in the CNS. Due to the critical role of postsynaptic Ca 2+ signals in dendritic development and synaptic plasticity, we tested whether long-term exposure to BDNF affects Ca 2+ elevations evoked by coincident excitatory postsynaptic potentials (EPSPs) and back-propagating action potentials (bAPs) in spiny dendrites of CA1 pyramidal neurons within hippocampal slice cultures. In control neurons, a train of 5 coincident EPSPs and bAPs evoked Ca 2+ elevations in oblique radial branches of the main apical dendrite that were of similar amplitude than those evoked by a train of 5 bAPs alone. On the other hand, dendritic Ca 2+ signals evoked by coincident EPSPs and bAPs were always larger than those triggered by bAPs in CA1 neurons exposed to BDNF for 48 h. This difference was not observed after blockade of NMDA receptors (NMDARs) with D,L-APV, but only in BDNFtreated neurons, suggesting that Ca 2+ signals in oblique radial dendrites include a synaptic NMDARdependent component. Co-treatment with the receptor tyrosine kinase inhibitor k-252a prevented the effect of BDNF on coincident dendritic Ca 2+ signals, suggesting the involvement of neurotrophin Trk receptors. These results indicate that long-term exposure to BDNF enhances Ca 2+ signaling during coincident pre-and postsynaptic activity in small spiny dendrites of CA1 pyramidal neurons, representing a potential functional consequence of neurotrophin-mediated dendritic remodeling in developing neurons.

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Section: Discussionsupporting

confidence: 52%

BDNF enhances dendritic Ca2+ signals evoked by coincident EPSPs and back-propagating action potentials in CA1 pyramidal neurons

Pozzo-Miller

2006

Brain Research

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“…Activity-dependent accumulation of calcium in dendritic spines has been observed in rapidly-frozen tissue by electron probe x-ray microanalysis (Andrews et al, 1988) and in living brain slice using fluorescent calcium indicators (Mtiller and Connor, 1991;Regehr and Tank, 1992). These intradendritic elevations in Ca2+ reflect calcium entry via synaptically activated NMDAtype glutamate receptors (Alford et al, 1993;Perkel et al, 1993), possibly amplified by influx through voltage-gated calcium channels and/or calcium-induced release of calcium from internal stores (Alford et al, 1993;Jaffe et al, 1994) such as the spine apparatus (Wilson et al, 1983). Siman et al (1984) observed that brain spectrin (fodrin), a major component of the submembrane cytoskeleton and an actin-and calmodulin-binding protein, is degraded by the synaptosomal calcium-activated protease calpain I, and proposed that postsynaptic activity-induced calcium accumulation could, through this mechanism, alter the cytoskeleton leading to long-lasting changes in the shape of dendritic spines.…”

Section: Discussionmentioning

confidence: 99%

Repeated confocal imaging of individual dendritic spines in the living hippocampal slice: evidence for changes in length and orientation associated with chemically induced LTP

et al. 1995

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Using confocal microscopy in conjunction with microdrop application of Dil, we have imaged and measured individual dendritic spines of living hippocampal CA1 pyramidal neurons in acute brain slices, before and approximately 3 hr after induction of long-term potentiation by chemical means. Statistical analysis of changes in the length of individual spines, and comparison with results of Monte Carlo simulations, suggests that two forms of structural change occur in chemically induced long-term potentiation: growth of a subpopulation of small spines, and angular displacement of spines. These changes could provide a structural basis for the expression of long-term potentiation.

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Section: Functional Roles Of Dopamine Modulation Of Dendritic Ca 2ϩ Pmentioning

confidence: 99%

“…The depolarizing Ca 2ϩ "hump" potential (together with the I NaP activated at the subthreshold voltage range) can also serve to relieve the voltage-dependent Mg 2ϩ block of the dendritic NMDA receptor channel complex, thus allowing additional Ca 2ϩ entry. Elevation of [Ca 2ϩ ] i has been shown to activate diverse intracellular biochemical processes responsible for altering synaptic efficacy (Hirsch and Crépel 1990, 1992a, 1992bRegehr and Tank 1990;Sah and Nicoll 1991; Alford et al 1993;Perkel et al 1993;Ghosh and Greenberg 1995).Dendritic high-voltage-activated Ca 2ϩ spikes and plateau potentials are likely to participate in multiple functions that are important for burst firing mechanisms, sustaining repetitive firing, and enduring forms of changes in synaptic plasticity ( Figure 5). Moderate attenuating effects on the amplitude of the dendritic Ca 2ϩ spikes following D1/5 receptor activation may "focus" or "sharpen" the effects of suprathreshold inputs arising primarily from different cortical association areas.…”

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confidence: 99%

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Yang

Seamans

Gorelova

1999

Neuropsychopharmacology

164

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This review covers some recent findings of the electrophysiological mechanisms through which mesocortical dopamine modulates prefrontal cortical neurons. Dopamine has been shown to modulate several ionic conductances located along the soma-dendritic axis of prefrontal cortical pyramidal neurons. These ionic currents include high-voltage-activated calcium currents and slowly inactivating NaReceived May 12, 1998; revised May 27, 1998; accepted May 29, 1998. 162 C.R. Yang et al. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO Schizophrenia strikes one in one hundred people worldwide, regardless of cultural or racial origins. As the illness progresses and if it remains unattended, patients are frequently trapped in psychological, social, and economic devastation (Gottesman 1991;Jablensky 1995). Currently, our incomplete understanding of the neurobiological bases of schizophrenia suggests that defects in the genetic controls of brain development in such limbic regions (including temporal lobe structures such as hippocampus and the amygdala) as well as the prefrontal cortex (PFC) lead to cell loss or deformation, cytoarchitectural disorganization, and abnormal innervation in these brain regions (Roberts and Bruton 1990;Stevens 1992; Bogerts 1993;Shapiro 1993; Akbarian et al. 1993 Akbarian et al. , 1996Ross and Pearlson 1996;Weinberger 1996; Karayiorgou and Gogos 1997; Lewis 1997;Selemon et al. 1995Selemon et al. , 1998.Some results from recent imaging studies of brains from living schizophrenics have suggested that there are defective functional communications between the interconnected cortical (PFC and cingulate cortex) and limbic subcortical structures (thalamus, striatum, and temporal lobe limbic structures)(see reviews of Liddle 1996; Pfefferbaum and Marsh 1995; Andreasen 1997; Heckers et al. 1998). Findings from these studies suggest that in schizophrenics, abnormal recruitment of several interconnected cortical and subcortical structures may underlie such symptom clusters as psychomotor poverty, thought disorganization, and reality distortion (Liddle et al. 1992; Liddle 1996; Fletcher 1998; Heckers et al. 1998).As noted in Figure 1, the PFC receives converging limbic, association cortical, and mesocortical dopamine inputs. These inputs interact in the PFC and are involved functionally in high-level cognitive processes (Fuster 1995). Among the many brain regions that PFC output innervates, two important subcortical regions are emphasized in this review. These are the nucleus accumbens (where mesoaccumbens dopamine neurons terminate) and the ventral tegmental area (VTA, where the midbrain dopamine neurons reside) Groenewegen et al. 1990; Berendse et al. 1992a Berendse et al. , 1992bSesack and Pickel 1992;Gorelova and Yang 1997b). Several of the interconnected limbic, cortical, and subcortical structures known to be affected in schizophrenia are targets of the ascending midbrain dopamine systems that normally provide functional modulation of neurotransmission (Björklund and Lindvall 1984;Mogenson et ...

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The role of Ca2+ entry via synaptically activated NMDA receptors in the induction of long-term potentiation

Cited by 126 publications

References 28 publications

BDNF enhances dendritic Ca2+ signals evoked by coincident EPSPs and back-propagating action potentials in CA1 pyramidal neurons

BDNF enhances dendritic Ca2+ signals evoked by coincident EPSPs and back-propagating action potentials in CA1 pyramidal neurons

Repeated confocal imaging of individual dendritic spines in the living hippocampal slice: evidence for changes in length and orientation associated with chemically induced LTP

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

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