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Titolo:
Modulation of excitability in Aplysia tail sensory neurons by tyrosine kinases
Autore:
Purcell, AL; Carew, TJ;
Indirizzi:
Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA Univ CalifIrvine Irvine CA USA 92697 obiol & Behav, Irvine, CA 92697 USA Yale Univ, Interdept Neurosci Program, New Haven, CT 06520 USA Yale Univ New Haven CT USA 06520 eurosci Program, New Haven, CT 06520 USA
Titolo Testata:
JOURNAL OF NEUROPHYSIOLOGY
fascicolo: 6, volume: 85, anno: 2001,
pagine: 2398 - 2411
SICI:
0022-3077(200106)85:6<2398:MOEIAT>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; DEPENDENT PROTEIN-KINASE; PRE-SYNAPTIC FACILITATION; KV1.3 POTASSIUM CHANNEL; MAP KINASE; SEROTONERGIC MODULATION; TRANSMITTER RELEASE; CATALYTIC SUBUNITS; CELLULAR MECHANISM; WITHDRAWAL REFLEX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
77
Recensione:
Indirizzi per estratti:
Indirizzo: Carew, TJ Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA Univ Calif Irvine Irvine CA USA 92697 hav, Irvine, CA 92697 USA
Citazione:
A.L. Purcell e T.J. Carew, "Modulation of excitability in Aplysia tail sensory neurons by tyrosine kinases", J NEUROPHYS, 85(6), 2001, pp. 2398-2411

Abstract

Tyrosine kinases have recently been shown to modulate synaptic plasticity and ion channel function. We show here that tyrosine kinases can also modulate both the baseline excitability state of Aplysia tail sensory neurons (SNs) as well as the excitability induced by the neuromodulator serotonin (5HT). First, we examined the effects of increasing and decreasing tyrosine kinase activity in the SNs. We found that tyrosine kinase inhibitors decreasebaseline SN excitability in addition to attenuating the increase in excitability induced by 5HT. Conversely, functionally increasing cellular tyrosine kinase activity in the SNs by either inhibiting opposing tyrosine phosphatase activity or by direct injection of an active tyrosine kinase (Src) induces increases in SN excitability in the absence of 5HT. Second, we examined the interaction between protein kinase A (PKA), which is known to mediate5HT-induced excitability changes in the SNs, and tyrosine kinases, in the enhancement of SN excitability. We found that the tyrosine kinases functiondownstream of PKA activation since tyrosine kinase inhibitors reduce excitability induced by activators of PKA. Finally, we examined the role of tyrosine kinases in other forms of 5HT-induced plasticity in the SNs. We found that while tyrosine kinase inhibitors attenuate excitability produced by 5HT, they have no effect on short-term facilitation (STF) of the SN-motor neuron (MN) synapse induced by 5HT. Thus tyrosine kinases modulate different forms of SN plasticity independently. Such differential modulation would have important consequences for activity-dependent plasticity in a variety of neural circuits.

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Documento generato il 05/12/20 alle ore 22:19:42