scholarly journals Serotonin produces long-term changes in the excitability of Aplysia sensory neurons in culture that depend on new protein synthesis

1987 ◽  
Vol 7 (7) ◽  
pp. 2232-2238 ◽  
Author(s):  
N Dale ◽  
ER Kandel ◽  
S Schacher
Keyword(s):  
Protein Synthesis ◽  
Sensory Neurons ◽  
Long Term Changes ◽  
New Protein

cAMP evokes long-term facilitation in Aplysia sensory neurons that requires new protein synthesis

Science ◽  
1988 ◽  
Vol 240 (4859) ◽  
pp. 1667-1669 ◽  
Author(s):  
S Schacher ◽  
V. Castellucci ◽  
E. Kandel
Keyword(s):  
Protein Synthesis ◽  
Sensory Neurons ◽  
Long Term Facilitation ◽  
New Protein

Long-Term Changes in Excitability Induced by Protein Kinase C Activation in Aplysia Sensory Neurons

1998 ◽  
Vol 79 (3) ◽  
pp. 1210-1218 ◽  
Author(s):  
Frédéric Manseau ◽  
Wayne S. Sossin ◽  
Vincent F. Castellucci
Keyword(s):  
Protein Synthesis ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Sensory Neurons ◽  
Dependent Manner ◽  
Kinase C ◽  
Long Term Changes ◽  
Protein Kinase C Activation ◽  
Time Point

Manseau, Frédéric, Wayne S. Sossin, and Vincent F. Castellucci. Long-term changes in excitability induced by protein kinase C activation in Aplysia sensory neurons. J. Neurophysiol. 79: 1210–1218, 1998. Protein kinases A (PKA) and C (PKC) play a central role as intracellular transducers during simple forms of learning in Aplysia. These two proteins seem to cooperate in mediating the different forms of plasticity underlying behavioral modifications of defensive reflexes in a state- and time-dependent manner. Although short- and long-term changes in the synaptic efficacy of the connections between mechanosensory neurons and motoneurons of the reflex have been well characterized, there is also a distinct intermediate phase of plasticity that is not as well understood. Biochemical and physiological experiments have suggested a role for PKC in the induction and expression of this form of facilitation. In this report, we demonstrate that PKC activation can induce both intermediate- and long-term changes in the excitability of sensory neurons (SNs). Short application of 4β-phorbol ester 12,13-dibutyrate (PDBU), a potent activator of PKC, produced a long-lasting increase in the number of spikes fired by SNs in response to depolarizing current pulses. This effect was observed in isolated cell culture and in the intact ganglion; it was blocked by a selective PKC inhibitor (chelerythrine). Interestingly, the increase in excitability measured at an intermediate-term time point (3 h) after treatment was independent of protein synthesis, while it was disrupted at the long-term (24 h) time point by the general protein synthesis inhibitor, anisomycin. In addition to suggesting that PKC as well as PKA are involved in long-lasting excitability changes, these findings support the idea that memory formation involves multiple stages that are mechanistically distinct at the biochemical level.

scholarly journals The long-term stability of new hippocampal place fields requires new protein synthesis

2004 ◽  
Vol 101 (10) ◽  
pp. 3656-3661 ◽  
Author(s):  
N. T. Agnihotri ◽  
R. D. Hawkins ◽  
E. R. Kandel ◽  
C. Kentros
Keyword(s):  
Protein Synthesis ◽  
Term Stability ◽  
Long Term Stability ◽  
Place Fields ◽  
New Protein

5-HT modulates protein synthesis and the expression of specific proteins during long-term facilitation in aplysia sensory neurons

Neuron ◽  
1989 ◽  
Vol 2 (6) ◽  
pp. 1577-1586 ◽  
Author(s):  
A. Barzilai ◽  
T.E. Kennedy ◽  
J.D. Sweatt ◽  
E.R. Kandel
Keyword(s):  
Protein Synthesis ◽  
Sensory Neurons ◽  
Specific Proteins ◽  
Long Term Facilitation

scholarly journals Mammalian target of rapamycin is required for phrenic long-term facilitation following severe but not moderate acute intermittent hypoxia

2015 ◽  
Vol 114 (3) ◽  
pp. 1784-1791 ◽  
Author(s):  
Brendan J. Dougherty ◽  
Daryl P. Fields ◽  
Gordon S. Mitchell
Keyword(s):  
Protein Synthesis ◽  
Phrenic Nerve ◽  
Intermittent Hypoxia ◽  
Mammalian Target Of Rapamycin ◽  
Nerve Activity ◽  
Long Term Facilitation ◽  
New Protein ◽  
Mtor Activity ◽  
Dependent Mechanism

Phrenic long-term facilitation (pLTF) is a persistent increase in phrenic nerve activity after acute intermittent hypoxia (AIH). Distinct cell-signaling cascades give rise to pLTF depending on the severity of hypoxemia within hypoxic episodes. Moderate AIH (mAIH; three 5-min episodes, PaO2 ∼35–55 mmHG) elicits pLTF by a serotonin (5-HT)-dependent mechanism that requires new synthesis of brain-derived neurotrophic factor (BDNF), activation of its high-affinity receptor (TrkB), and ERK MAPK signaling. In contrast, severe AIH (sAIH; three 5-min episodes, PaO2 ∼25–30 mmHG) elicits pLTF by an adenosine-dependent mechanism that requires new TrkB synthesis and Akt signaling. Although both mechanisms require spinal protein synthesis, the newly synthesized proteins are distinct, as are the neurochemicals inducing plasticity (serotonin vs. adenosine). In many forms of neuroplasticity, new protein synthesis requires translational regulation via mammalian target of rapamycin (mTOR) signaling. Since Akt regulates mTOR activity, we hypothesized that mTOR activity is necessary for sAIH- but not mAIH-induced pLTF. Phrenic nerve activity in anesthetized, paralyzed, and ventilated rats was recorded before, during, and 60 min after mAIH or sAIH. Rats were pretreated with intrathecal injections of 20% DMSO (vehicle controls) or rapamycin (0.1 mM, 12 μl), a selective mTOR complex 1 inhibitor. Consistent with our hypothesis, rapamycin blocked sAIH- but not mAIH-induced pLTF. Thus spinal mTOR activity is required for adenosine-dependent (sAIH) but not serotonin-dependent (mAIH) pLTF, suggesting that distinct mechanisms regulate new protein synthesis in these forms of spinal neuroplasticity.

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