Calmodulin as a major calcium buffer shaping vesicular release and short-term synaptic plasticity: facilitation through buffer dislocation

نویسندگان

  • Yulia Timofeeva
  • Kirill E. Volynski
چکیده

Action potential-dependent release of synaptic vesicles and short-term synaptic plasticity are dynamically regulated by the endogenous Ca(2+) buffers that shape [Ca(2+)] profiles within a presynaptic bouton. Calmodulin is one of the most abundant presynaptic proteins and it binds Ca(2+) faster than any other characterized endogenous neuronal Ca(2+) buffer. Direct effects of calmodulin on fast presynaptic Ca(2+) dynamics and vesicular release however have not been studied in detail. Using experimentally constrained three-dimensional diffusion modeling of Ca(2+) influx-exocytosis coupling at small excitatory synapses we show that, at physiologically relevant concentrations, Ca(2+) buffering by calmodulin plays a dominant role in inhibiting vesicular release and in modulating short-term synaptic plasticity. We also propose a novel and potentially powerful mechanism for short-term facilitation based on Ca(2+)-dependent dynamic dislocation of calmodulin molecules from the plasma membrane within the active zone.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Calcium channels and short-term synaptic plasticity.

Voltage-gated Ca(2+) channels in presynaptic nerve terminals initiate neurotransmitter release in response to depolarization by action potentials from the nerve axon. The strength of synaptic transmission is dependent on the third to fourth power of Ca(2+) entry, placing the Ca(2+) channels in a unique position for regulation of synaptic strength. Short-term synaptic plasticity regulates the st...

متن کامل

Fine-tuning synaptic plasticity by modulation of Ca(V)2.1 channels with Ca2+ sensor proteins.

Modulation of P/Q-type Ca(2+) currents through presynaptic voltage-gated calcium channels (Ca(V)2.1) by binding of Ca(2+)/calmodulin contributes to short-term synaptic plasticity. Ca(2+)-binding protein-1 (CaBP1) and Visinin-like protein-2 (VILIP-2) are neurospecific calmodulin-like Ca(2+) sensor proteins that differentially modulate Ca(V)2.1 channels, but how they contribute to short-term syna...

متن کامل

Role of the calcium-binding protein parvalbumin in short-term synaptic plasticity.

GABAergic (GABA = gamma-aminobutyric acid) neurons from different brain regions contain high levels of parvalbumin, both in their soma and in their neurites. Parvalbumin is a slow Ca(2+) buffer that may affect the amplitude and time course of intracellular Ca(2+) transients in terminals after an action potential, and hence may regulate short-term synaptic plasticity. To test this possibility, w...

متن کامل

A use-dependent increase in release sites drives facilitation at calretinin-deficient cerebellar parallel-fiber synapses

Endogenous Ca(2+)-binding proteins affect synaptic transmitter release and short-term plasticity (STP) by buffering presynaptic Ca(2+) signals. At parallel-fiber (PF)-to-Purkinje neuron (PN) synapses in the cerebellar cortex loss of calretinin (CR), the major buffer at PF terminals, results in increased presynaptic Ca(2+) transients and an almost doubling of the initial vesicular releases proba...

متن کامل

P26: Long-Term Potentiation: The Mechanisms of CaMKII in Lerarning and Memory

Long-term potentiation (LTP) is a form of activity dependent plasticity that induced by high-frequency stimulation or theta burst stimulation and results in synaptic transmission. Several Studies have been shown that LTP is one of the most important processes in the CNS that plays an important role in learning and memory formation. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a major...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره 9  شماره 

صفحات  -

تاریخ انتشار 2015