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How voltage-gated calcium channels gate forms of homeostatic synaptic plasticity.

Frank CA - Front Cell Neurosci (2014)

Bottom Line: Postsynaptically, there is a great deal of evidence that reduced network activity and loss of calcium influx through CaV1-type calcium channels also results in adaptive homeostatic signaling.The episodic nature of some of these disorders suggests alternating periods of stable and unstable function.Uncovering information about how calcium channels are regulated in the context of HSP could be relevant toward understanding these and other disorders.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Cell Biology, University of Iowa Carver College of Medicine Iowa City, IA, USA.

ABSTRACT
Throughout life, animals face a variety of challenges such as developmental growth, the presence of toxins, or changes in temperature. Neuronal circuits and synapses respond to challenges by executing an array of neuroplasticity paradigms. Some paradigms allow neurons to up- or downregulate activity outputs, while countervailing ones ensure that outputs remain within appropriate physiological ranges. A growing body of evidence suggests that homeostatic synaptic plasticity (HSP) is critical in the latter case. Voltage-gated calcium channels gate forms of HSP. Presynaptically, the aggregate data show that when synapse activity is weakened, homeostatic signaling systems can act to correct impairments, in part by increasing calcium influx through presynaptic CaV2-type channels. Increased calcium influx is often accompanied by parallel increases in the size of active zones and the size of the readily releasable pool of presynaptic vesicles. These changes coincide with homeostatic enhancements of neurotransmitter release. Postsynaptically, there is a great deal of evidence that reduced network activity and loss of calcium influx through CaV1-type calcium channels also results in adaptive homeostatic signaling. Some adaptations drive presynaptic enhancements of vesicle pool size and turnover rate via retrograde signaling, as well as de novo insertion of postsynaptic neurotransmitter receptors. Enhanced calcium influx through CaV1 after network activation or single cell stimulation can elicit the opposite response-homeostatic depression via removal of excitatory receptors. There exist intriguing links between HSP and calcium channelopathies-such as forms of epilepsy, migraine, ataxia, and myasthenia. The episodic nature of some of these disorders suggests alternating periods of stable and unstable function. Uncovering information about how calcium channels are regulated in the context of HSP could be relevant toward understanding these and other disorders.

No MeSH data available.


Related in: MedlinePlus

Invertebrate models of CaV-directed homeostatic plasticity. Inspection of the Drosophila melanogaster NMJ has provided a wealth of information regarding the roles VGCCs and associated molecules play in homeostatic plasticity, as has examination of C. elegans preparations, such as the ventral nerve cord (VNC) or the NMJ. (A) Drosophila NMJ. Pharmacological or genetic impairment of postsynaptic glutamate receptors triggers a retrograde signaling process that results in enhanced presynaptic Cac/CaV2 function and increased neurotransmitter release. Additionally, Cac/CaV2, α2δ, and Dmca1D/CaV1 all affect synaptic bouton development or maturation at the NMJ. (B)C. elegans synapses. At the C. elegans VNC, the coordinated functions of UNC-2/CaV2, EGL-19/CaV1, UNC-36/α2δ and UNC-43/CaMKII ensure proper coupling of GLR-1 glutamate receptor density to developmental growth.
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Figure 2: Invertebrate models of CaV-directed homeostatic plasticity. Inspection of the Drosophila melanogaster NMJ has provided a wealth of information regarding the roles VGCCs and associated molecules play in homeostatic plasticity, as has examination of C. elegans preparations, such as the ventral nerve cord (VNC) or the NMJ. (A) Drosophila NMJ. Pharmacological or genetic impairment of postsynaptic glutamate receptors triggers a retrograde signaling process that results in enhanced presynaptic Cac/CaV2 function and increased neurotransmitter release. Additionally, Cac/CaV2, α2δ, and Dmca1D/CaV1 all affect synaptic bouton development or maturation at the NMJ. (B)C. elegans synapses. At the C. elegans VNC, the coordinated functions of UNC-2/CaV2, EGL-19/CaV1, UNC-36/α2δ and UNC-43/CaMKII ensure proper coupling of GLR-1 glutamate receptor density to developmental growth.

Mentions: With the backdrop of this considerable knowledge, we consider the emerging roles that VGCCs play in HSP. We review electrophysiological, biochemical, and imaging data that have established the important roles CaV channels play in multiple forms of HSP across diverse experimental systems (Figures 1, 2). We also briefly consider the idea that CaV channels might link HSP to disorders in which underlying neuronal stability is lost.


How voltage-gated calcium channels gate forms of homeostatic synaptic plasticity.

Frank CA - Front Cell Neurosci (2014)

Invertebrate models of CaV-directed homeostatic plasticity. Inspection of the Drosophila melanogaster NMJ has provided a wealth of information regarding the roles VGCCs and associated molecules play in homeostatic plasticity, as has examination of C. elegans preparations, such as the ventral nerve cord (VNC) or the NMJ. (A) Drosophila NMJ. Pharmacological or genetic impairment of postsynaptic glutamate receptors triggers a retrograde signaling process that results in enhanced presynaptic Cac/CaV2 function and increased neurotransmitter release. Additionally, Cac/CaV2, α2δ, and Dmca1D/CaV1 all affect synaptic bouton development or maturation at the NMJ. (B)C. elegans synapses. At the C. elegans VNC, the coordinated functions of UNC-2/CaV2, EGL-19/CaV1, UNC-36/α2δ and UNC-43/CaMKII ensure proper coupling of GLR-1 glutamate receptor density to developmental growth.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3924756&req=5

Figure 2: Invertebrate models of CaV-directed homeostatic plasticity. Inspection of the Drosophila melanogaster NMJ has provided a wealth of information regarding the roles VGCCs and associated molecules play in homeostatic plasticity, as has examination of C. elegans preparations, such as the ventral nerve cord (VNC) or the NMJ. (A) Drosophila NMJ. Pharmacological or genetic impairment of postsynaptic glutamate receptors triggers a retrograde signaling process that results in enhanced presynaptic Cac/CaV2 function and increased neurotransmitter release. Additionally, Cac/CaV2, α2δ, and Dmca1D/CaV1 all affect synaptic bouton development or maturation at the NMJ. (B)C. elegans synapses. At the C. elegans VNC, the coordinated functions of UNC-2/CaV2, EGL-19/CaV1, UNC-36/α2δ and UNC-43/CaMKII ensure proper coupling of GLR-1 glutamate receptor density to developmental growth.
Mentions: With the backdrop of this considerable knowledge, we consider the emerging roles that VGCCs play in HSP. We review electrophysiological, biochemical, and imaging data that have established the important roles CaV channels play in multiple forms of HSP across diverse experimental systems (Figures 1, 2). We also briefly consider the idea that CaV channels might link HSP to disorders in which underlying neuronal stability is lost.

Bottom Line: Postsynaptically, there is a great deal of evidence that reduced network activity and loss of calcium influx through CaV1-type calcium channels also results in adaptive homeostatic signaling.The episodic nature of some of these disorders suggests alternating periods of stable and unstable function.Uncovering information about how calcium channels are regulated in the context of HSP could be relevant toward understanding these and other disorders.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Cell Biology, University of Iowa Carver College of Medicine Iowa City, IA, USA.

ABSTRACT
Throughout life, animals face a variety of challenges such as developmental growth, the presence of toxins, or changes in temperature. Neuronal circuits and synapses respond to challenges by executing an array of neuroplasticity paradigms. Some paradigms allow neurons to up- or downregulate activity outputs, while countervailing ones ensure that outputs remain within appropriate physiological ranges. A growing body of evidence suggests that homeostatic synaptic plasticity (HSP) is critical in the latter case. Voltage-gated calcium channels gate forms of HSP. Presynaptically, the aggregate data show that when synapse activity is weakened, homeostatic signaling systems can act to correct impairments, in part by increasing calcium influx through presynaptic CaV2-type channels. Increased calcium influx is often accompanied by parallel increases in the size of active zones and the size of the readily releasable pool of presynaptic vesicles. These changes coincide with homeostatic enhancements of neurotransmitter release. Postsynaptically, there is a great deal of evidence that reduced network activity and loss of calcium influx through CaV1-type calcium channels also results in adaptive homeostatic signaling. Some adaptations drive presynaptic enhancements of vesicle pool size and turnover rate via retrograde signaling, as well as de novo insertion of postsynaptic neurotransmitter receptors. Enhanced calcium influx through CaV1 after network activation or single cell stimulation can elicit the opposite response-homeostatic depression via removal of excitatory receptors. There exist intriguing links between HSP and calcium channelopathies-such as forms of epilepsy, migraine, ataxia, and myasthenia. The episodic nature of some of these disorders suggests alternating periods of stable and unstable function. Uncovering information about how calcium channels are regulated in the context of HSP could be relevant toward understanding these and other disorders.

No MeSH data available.


Related in: MedlinePlus