Ultrastructural features of hippocampal CA1 synapses with respect to synaptic enhancement following repeated PKA activation

Urakubo, Tomoyoshi; Ogura, Akihiko; Tominaga-Yoshino, Keiko

doi:10.1016/j.neulet.2006.07.057

Cited by 10 publications

(11 citation statements)

References 20 publications

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“…More recently it has been demonstrated that repeated activation of PKA induces a long‐lasting (> 2 weeks) increase in the number of synaptic sites in primary hippocampal neuron cultures (Yamamoto et al. , 2005) and in hippocampal slices (Urakubo et al. , 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Both PKA activity and protein synthesis are involved in synaptogenesis occurring during the late phase of long-term potentiation in the hippocampus in vitro (Pita-Almenar et al, 2006). More recently it has been demonstrated that repeated activation of PKA induces a long-lasting (> 2 weeks) increase in the number of synaptic sites in primary hippocampal neuron cultures (Yamamoto et al, 2005) and in hippocampal slices (Urakubo et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

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Chronic activation of the D2 dopamine autoreceptor inhibits synaptogenesis in mesencephalic dopaminergic neurons in vitro

Fasano

Poirier

DesGroseillers

et al. 2008

Eur J of Neuroscience

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Chronic blockade or activation of dopamine receptors is critical for the pharmacological treatment of diseases like schizophrenia, Parkinson's or attention deficit and hyperactivity disorder. However, the long-term impact of such treatments on dopamine neurons is unclear. Chronic blockade of the dopamine D2 receptor in vivo triggers an increase in the axonal arborization of dopamine neurons [European Journal of Neuroscience, 2002, 16, 787-794]. However, the specific involvement of presynaptic (autoreceptors) vs. postsynaptic D2 receptors as well as the molecular mechanisms involved have not been determined. Here, we examined the role of D2 autoreceptors in regulating the ability of mouse dopamine neurons to establish axon terminals. Chronic activation of this receptor with quinpirole, a specific agonist, decreased the number of axon terminals established by isolated dopamine neurons. This effect was accompanied by a decrease in dopamine release and was mediated through inhibition of protein kinase A. The decrease in axon terminal number induced by D2 receptor activation was also occluded when the mammalian Target of Rapamycin pathway of mRNA translation was blocked. Our results suggest that chronic activation of the D2 autoreceptor inhibits synaptogenesis by mesencephalic dopamine neurons through translational regulation of the synthesis of proteins required for synapse formation. This study provides a better understanding of the impact of long-term pharmacological interventions acting through the D2 receptor.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chronic activation of the D2 dopamine autoreceptor inhibits synaptogenesis in mesencephalic dopaminergic neurons in vitro

Fasano

Poirier

DesGroseillers

et al. 2008

Eur J of Neuroscience

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“…Neuronal injury induced by transient global ischemia was previously considered a necrotic form of cell death, 2,25–28 based on electron microscope observations such as early cell swelling, mitochondrial shrinkage, dilation of the ER, polyribosome dispersion, and eventual rupture of nuclear, organelle, and plasma membranes 26,27,29,30 . Li et al.…”

Section: Discussionmentioning

confidence: 99%

Glucose/oxygen deprivation and reperfusion upregulate SNAREs and complexin in organotypic hippocampal slice cultures

Park¹,

Jung

Kim³

et al. 2008

Neuropathology

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Brain ischemia activates Ca(2+)-dependent synaptic vesicle exocytosis. The synaptosomal-associated protein 25 (SNAP-25) and syntaxin proteins, located on presynaptic terminals, are components of the SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complex and play a key role in regulating exocytosis. Changes in the expression of SNAREs could affect SNARE complex formation, fusion of vesicles with the presynaptic membrane, and release of neurotransmitters through exocytosis. To investigate the relationship of glucose/oxygen deprivation (GOD)/reperfusion-induced neuronal damage and alteration of presynaptic function, we examined the expression of SNAREs and complexin during GOD and reperfusion using organotypic hippocampal slice cultures. Microtubule-associated protein 2 (MAP-2) staining and transmission electron microscopy showed that neuronal damage increased in a time-dependent manner and both types of neuronal death can occur at different times during GOD and reperfusion. The immunoreactivity of SNAREs such as SNAP-25, vesicle-associated membrane protein and syntaxin and complexin increased in pyramidal cell bodies in the CA1 and CA3 areas in a time-dependent manner following reperfusion. Our data suggest that alteration of presynaptic function may play a partial role in delayed neuronal death during GOD and reperfusion in organotypic hippocampal slice cultures.

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“…This synaptic enhancement is independent of cell survival but is accompanied by the formation of new synapses101112 requires protein synthesis13, and is specific to the stimulated input pathway14. Electrical tetanization can replace chemical induction of LTP14.…”

mentioning

confidence: 99%

“…The first question is related to the fact that the spines are perpetually fluctuating15. The second question is related to the fact that there is a considerably long delay before the spine number increase becomes apparent101112. The third question is related to a recently emerging theory of “clustered synaptogenesis” in which synapse formation is regulated not on a basis of individual synapse but on a basis of population of synapses161718.…”

mentioning

confidence: 99%

Dendritic spine dynamics in synaptogenesis after repeated LTP inductions: Dependence on pre-existing spine density

Tominaga-Yoshino

Hasegawa

et al. 2013

Sci Rep

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Not only from our daily experience but from learning experiments in animals, we know that the establishment of long-lasting memory requires repeated practice. However, cellular backgrounds underlying this repetition-dependent consolidation of memory remain largely unclear. We reported previously using organotypic slice cultures of rodent hippocampus that the repeated inductions of LTP (long-term potentiation) lead to a slowly developing long-lasting synaptic enhancement accompanied by synaptogenesis distinct from LTP itself, and proposed this phenomenon as a model system suitable for the analysis of the repetition-dependent consolidation of memory. Here we examined the dynamics of individual dendritic spines after repeated LTP-inductions and found the existence of two phases in the spines' stochastic behavior that eventually lead to the increase in spine density. This spine dynamics occurred preferentially in the dendritic segments having low pre-existing spine density. Our results may provide clues for understanding the cellular bases underlying the repetition-dependent consolidation of memory.

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Ultrastructural features of hippocampal CA1 synapses with respect to synaptic enhancement following repeated PKA activation

Cited by 10 publications

References 20 publications

Chronic activation of the D2 dopamine autoreceptor inhibits synaptogenesis in mesencephalic dopaminergic neurons in vitro

Chronic activation of the D2 dopamine autoreceptor inhibits synaptogenesis in mesencephalic dopaminergic neurons in vitro

Glucose/oxygen deprivation and reperfusion upregulate SNAREs and complexin in organotypic hippocampal slice cultures

Dendritic spine dynamics in synaptogenesis after repeated LTP inductions: Dependence on pre-existing spine density

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