Vadim Y. Bolshakov

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Long-term depression (LTD) is an activity-dependent decrease in synaptic efficacy that together with its counterpart, long-term potentiation, is thought to be an important cellular mechanism for learning and memory in the mammalian brain. The induction of LTD in hippocampal CA1 pyramidal neurons in neonatal rats is shown to depend on postsynaptic calcium(More)
Developmental changes in rat hippocampal transmitter release and synaptic plasticity were investigated. Recordings from pairs of pyramidal neurons in slices showed that an action potential in a CA3 neuron released only a single quantum of transmitter onto a CA1 neuron. Failures of synaptic transmission reflected probabilistic transmitter release. The(More)
Auditory information critical for fear conditioning, a model of emotional learning, is conveyed to the lateral nucleus of the amygdala via two routes: directly from the medial geniculate nucleus and indirectly from the auditory cortex. Here we show in the cortico-amygdala pathway that learned fear occludes electrically induced long-term potentiation (LTP).(More)
The small GTP-binding protein Rab3A is a Rab family member that is abundant in brain synaptic vesicles. Here we show that mice in which the rab3A gene has been mutated by homologous recombination do not express Rab3A but are viable and fertile. Electrophysiological recordings in hippocampal CA1 pyramidal cells indicate that most of their synaptic parameters(More)
Although the function of the p42/p44 mitogen-activated protein (MAP) kinase pathway in long-term potentiation at hippocampal CA3-CA1 synapses has been well described, relatively little is known about the importance of the p38 MAP kinase pathway in synaptic plasticity. Here we show that the p38 MAP kinase pathway, a parallel signaling cascade activated by(More)
Long-term potentiation at CA3-CA1 hippocampal synapses exhibits an early phase and a late phase, which can be distinguished by their underlying molecular mechanisms. Unlike the early phase, the late phase is dependent on both cAMP and protein synthesis. Quantal analysis of unitary synaptic transmission between a single presynaptic CA3 neuron and a single(More)
We identified the Grp gene, encoding gastrin-releasing peptide, as being highly expressed both in the lateral nucleus of the amygdala, the nucleus where associations for Pavlovian learned fear are formed, and in the regions that convey fearful auditory information to the lateral nucleus. Moreover, we found that GRP receptor (GRPR) is expressed in GABAergic(More)
Retrieval of fear extinction memory is associated with increased firing of neurons in the medial prefrontal cortex (mPFC). It is unknown, however, how extinction learning-induced changes in mPFC activity are relayed to target structures in the amygdala, resulting in diminished fear responses. Here, we show that fear extinction decreases the efficacy of(More)
We have generated mice lacking synaptogyrin I and synaptophysin I to explore the functions of these abundant tyrosine-phosphorylated proteins of synaptic vesicles. Single and double knockout mice were alive and fertile without significant morphological or biochemical changes. Electrophysiological recordings in the hippocampal CA1 region revealed that(More)
Presenilins play essential roles in memory formation, synaptic function, and neuronal survival. Mutations in the Presenilin-1 (PSEN1) gene are the major cause of familial Alzheimer's disease (FAD). How PSEN1 mutations cause FAD is unclear, and pathogenic mechanisms based on gain or loss of function have been proposed. Here, we generated Psen1 knockin (KI)(More)