Multifunctional Role of Protein Kinase C in Regulating the Formation and Maturation of Specific Synapses

Hu, Jiang-Yuan; Chen, Yang; Schacher, Samuel

doi:10.1523/jneurosci.3305-07.2007

Cited by 11 publications

(20 citation statements)

References 86 publications

(134 reference statements)

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“…Sensorin translation is required for synapse stabilization between SNs and MNs (27, 30) and both sensorin translation and secretion are required for 5HT-induced LTF of Aplysia SN-MN synapses (31). To generate sensorin translational reporters, we fused the 5’ and 3’ UTRs of sensorin to the coding region of the photoconvertible fluorescent protein dendra2 (32).…”

Section: Sensorin Translational Reportermentioning

confidence: 99%

Synapse- and Stimulus-Specific Local Translation During Long-Term Neuronal Plasticity

Wang

Kim²,

Zhao

et al. 2009

Science

203

199

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Long-term memory and synaptic plasticity require changes in gene expression and yet can occur in a synapse-specific manner. mRNA localization and regulated translation at synapses are thus critical for establishing synapse specificity. Using live cell microscopy of photoconvertible fluorescent protein translational reporters, we directly visualized local translation at synapses during long-term facilitation of Aplysia sensory-motor synapses. Translation of the reporter required multiple applications of serotonin, was spatially restricted to stimulated synapses, was transcript-and stimulus-specific, and occurred during long-term facilitation but not during longterm depression of sensory-motor synapses. Translational regulation only occurred in the presence of a chemical synapse and required calcium signaling in the postsynaptic motor neuron. Thus highly regulated local translation occurs at synapses during long-term plasticity and requires transsynaptic signals.Long-lasting learning-related synaptic plasticity requires transcription for its persistence (1-3) and yet can occur in a synapse-specific manner (4-7). One mechanism that has been proposed to mediate this spatial restriction of gene expression during neuronal plasticity involves regulated translation of localized mRNAs at stimulated synapses (8-10). Many findings support the existence of local translation at synapses. First, all of the machinery required for translation is present in neuronal processes, including polyribosomes (11,12), translation factors (13), and a select population of mRNAs (14-18). Second, studies using

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Section: Sensorin Translational Reportermentioning

confidence: 99%

Synapse- and Stimulus-Specific Local Translation During Long-Term Neuronal Plasticity

Wang

Kim²,

Zhao

et al. 2009

Science

203

199

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“…Sensory neurons were isolated from pleural ganglia dissected from adult animals (80 g) and motor neurons L7 and L11 were isolated from abdominal ganglia dissected from juvenile animals (2 g) and maintained in culture for varying times (see below) under conditions previously described (Rayport and Schacher, 1986; Hu et al, 2007b). Each cell body was isolated with a segment (300-600 μm) of its original axon as well as some fine dendritic-like branches extending from the axons of the motor neurons.…”

Section: Methodsmentioning

confidence: 99%

“…Assays for synaptic connections were monitored with standard electrophysiological recordings (Hu et al, 2007b). Starting 2 h after onset of interaction between sensory neuron and L7 (or L11), an intracellular electrode was used to monitor excitatory postsynaptic potentials (EPSPs) following action potentials evoked with an extracellular electrode placed near the cell body of the sensory neurons (Schacher and Montarolo, 1991; Hu et al, 2007b).…”

Section: Methodsmentioning

confidence: 99%

“…Starting 2 h after onset of interaction between sensory neuron and L7 (or L11), an intracellular electrode was used to monitor excitatory postsynaptic potentials (EPSPs) following action potentials evoked with an extracellular electrode placed near the cell body of the sensory neurons (Schacher and Montarolo, 1991; Hu et al, 2007b). The membrane potential of the motor neuron was held at −80 mV.…”

Section: Methodsmentioning

confidence: 99%

“…PKC activity is critical for initiating synapse formation and growth by sensory neurons contacting L7 (Hu et al, 2007b). Pharmacological inhibition of all PKC isoforms blocked growth and initial synapse formation by sensory neurons but did not interfere with sensory neuron growth contacting the non-target L11.…”

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confidence: 99%

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Aplysia Cell Adhesion Molecule and a Novel Protein Kinase C Activity in the Postsynaptic Neuron Are Required for Presynaptic Growth and Initial Formation of Specific Synapses

Chen²,

Bougie³

et al. 2010

Journal of Neuroscience

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To explore the role of both Aplysia cell adhesion molecule (ApCAM) and activity of specific protein kinase C (PKC) isoforms in the initial formation of sensory neuron synapses with specific postsynaptic targets (L7 but not L11), we examined presynaptic growth, initial synapse formation, and the expression of the presynaptic neuropeptide sensorin following cell-specific reduction of ApCAM or of a novel PKC activity. Synapse formation between sensory neurons and L7 begins by 3 h after plating and is accompanied by a rapid accumulation of a novel PKC to sites of synaptic interaction. Reducing ApCAM expression specifically from the surface of L7 blocks presynaptic growth and initial synapse formation, target-induced increase of sensorin in sensory neuron cell bodies and the rapid accumulation of the novel PKC to sites of interaction. Selective blockade of the novel PKC activity in L7, but not in sensory neurons, with injection of a dominant negative construct that interferes with the novel PKC activity, produces the same actions as downregulating ApCAM; blockade of presynaptic growth and initial synapse formation, and the target-induced increase of sensorin in sensory neuron cell bodies. The results indicate that signals initiated by postsynaptic cell adhesion molecule ApCAM coupled with the activation of a novel PKC in the appropriate postsynaptic neuron produce the retrograde signals required for presynaptic growth associated with initial synapse formation, and the target-induced expression of a presynaptic neuropeptide critical for synapse maturation.

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Altered expression and alpha‐1 adrenergic receptor mediated activity of protein kinase C in the prefrontal cortex of rats with neonatal ventral hippocampus lesions

Al-Khairi

Baharnoori

Kamath

et al. 2009

Synapse

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The neonatal ventral hippocampus (nVH) lesion in rats captures many features of schizophrenia at the levels of behavior and neurobiological markers. We have previously reported enhanced expression of alpha-1 adrenergic receptors (AR) in the prefrontal cortex (PFC) of postpubertal nVH-lesioned rats and proposed that enhanced alpha-1 AR signaling might participate in some of the behavioral abnormalities observed in the nVH-lesioned rats. To assess the components of alpha-1 adrenergic signaling in nVH-lesion rats, we examined prefrontal cortical expression of protein kinase C (PKC) subtypes by Western blotting and alpha-1 AR-stimulated PKC activity by in vitro enzyme assay in postpubertal animals. Neonatal VH-lesioned animals showed significantly increased expression of membrane-bound PKC-alpha and the phosphorylated form of PKC. Cytosolic PKC-beta II and PKC-gamma expression were found to be decreased in the PFC of lesioned animals with no change in the expression of PKC-beta I either in the cytosol or membrane. PKC activity assays showed an increase in basal PKC activity in the PFC slices of nVH-lesioned animals. Stimulation of alpha-1 adrenergic receptor with different concentrations of the agonist phenylephrine (PE), while increasing PKC activity in the sham-lesioned animals surprisingly decreased the activity in nVH-lesioned animals. Increased basal levels as well as activity of prefrontal PKC and its anomalous regulation by alpha-1 adrenergic receptors may participate in the cognitive and stress-induced behavioral alterations in nVH-lesioned animals.

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Multifunctional Role of Protein Kinase C in Regulating the Formation and Maturation of Specific Synapses

Cited by 11 publications

References 86 publications

Synapse- and Stimulus-Specific Local Translation During Long-Term Neuronal Plasticity

Synapse- and Stimulus-Specific Local Translation During Long-Term Neuronal Plasticity

Aplysia Cell Adhesion Molecule and a Novel Protein Kinase C Activity in the Postsynaptic Neuron Are Required for Presynaptic Growth and Initial Formation of Specific Synapses

Altered expression and alpha‐1 adrenergic receptor mediated activity of protein kinase C in the prefrontal cortex of rats with neonatal ventral hippocampus lesions

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