Buscar
Mostrando ítems 1-10 de 14
Synaptic vesicle pool size, release probability and synaptic depression are sensitive to Ca2+ buffering capacity in the developing rat calyx of Held
(Associação Brasileira de Divulgação Científica, 2009)
The calyx of Held, a specialized synaptic terminal in the medial nucleus of the trapezoid body, undergoes a series of changes during postnatal development that prepares this synapse for reliable high frequency firing. These ...
Modulation of acid sensing ion channel dependent protonergic neurotransmission at the mouse calyx of Held
(Pergamon-Elsevier Science Ltd, 2020-07)
Acid-sensing ion channels (ASICs) regulate synaptic activities and play important roles in neurodegenerative diseases. It has been reported that homomeric ASIC-1a channels are expressed in neurons of the medial nucleus of ...
Acute modulation of calcium currents and synaptic transmission by gabapentinoids
(Landes Bioscience, 2010-12)
Gabapentin and pregabalin are anticonvulsant drugs that are extensively used for the treatment of several neurological and psychiatric disorders. Gabapentinoids (GBPs) are known to have a high affinity binding to α2 δ-1 ...
Pregabalin modulation of neurotransmitter release is mediated by change in intrinsic activation/inactivation properties of Cav2.1 calcium channels
(American Society for Pharmacology and Experimental Therapeutics, 2011-03)
In this work, we studied the effects of the anticonvulsant and analgesic drug pregabalin (PGB) on excitatory postsynaptic currents (EPSCs) at principal neurons of the mouse medial nucleus of the trapezoid body and on ...
Gain of function in FHM-1 Cav2.1 knock-in mice is related to the shape of the action potential
(American Physiological Society, 2010-07)
Familial hemiplegic migraine type-1 FHM-1 is caused by missense mutations in the CACNA1A gene that encodes the α1A pore-forming subunit of CaV2.1 Ca2+ channels. We used knock-in (KI) transgenic mice harboring the pathogenic ...
CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis
(Elsevier, 2011-11)
Studies on the genetic forms of epilepsy, chronic pain, and migraine caused by mutations in ion channels have given crucial insights into the molecular mechanisms, pathogenesis, and therapeutic approaches to complex ...
Acid-Sensing Ion Channels Activated by Evoked Released Protons Modulate Synaptic Transmission at the Mouse Calyx of Held Synapse
(Society for Neuroscience, 2017-03)
Acid-sensing ion channels (ASICs) regulate synaptic activities and play important roles in neurodegenerative diseases. We found that these channels can be activated in neurons of the medial nucleus of the trapezoid body ...
Synaptic Gain-of-Function Effects of Mutant Cav2.1 Channels in a Mouse Model of Familial Hemiplegic Migraine Are Due to Increased Basal [Ca2+]i
(Society for Neuroscience, 2014-05)
Specific missense mutations in the CACNA1A gene, which encodes a subunit of voltage-gated CaV2.1 channels, are associated with familial hemiplegic migraine type 1 (FHM1), a rare monogenic subtype of common migraine with ...
Presynaptic Cav2.1 calcium channels carrying a familial hemiplegic migraine mutation r192q allow faster recovery from syanptic depression in mouse calyx of held
(American Physiological Society, 2012-12)
CaV2.1 Ca2+ channels have a dominant and specific role in initiating fast synaptic transmission at central excitatory synapses, through a close association between release sites and calcium sensors. Familial hemiplegic ...
Interaction between facilitation and depression at a large CNS synapse reveals mechanisms of short-term plasticity
(Society for Neuroscience, 2010-02)
The two fundamental forms of short-term plasticity, short-term depression and facilitation, coexist at most synapses, but little is known about their interaction. Here, we studied the interplay between short-term depression ...