Biomedical subjects

Thanos Tzounopoulos

Publications and source records attributed to Thanos Tzounopoulos.

3 recordsLinked to original sources

PubMed2004

Cell-specific, spike timing-dependent plasticities in the dorsal cochlear nucleus.

In the dorsal cochlear nucleus, long-term synaptic plasticity can be induced at the parallel fiber inputs that synapse onto both fusiform principal neurons and cartwheel feedforward inhibitory interneurons. Here we report that in mouse fusiform cells, spikes evoked 5 ms after parallel-fiber excitatory postsynaptic potentials (EPSPs) led to long-term potentiation (LTP), whereas spikes evoked 5 ms before EPSPs led to long-term depression (LTD) of the synapse. The EPSP-spike protocol led to LTD in cartwheel cells, but no synaptic changes resulted from the reverse sequence (spike-EPSP). Plasticity in fusiform and cartwheel cells therefore followed Hebbian and anti-Hebbian learning rules, respectively. Similarly, spikes generated by summing EPSPs from different groups of parallel fibers produced LTP in fusiform cells, and LTD in cartwheel cells. LTD could also be induced in glutamatergic inputs of cartwheel cells by pairing parallel-fiber EPSPs with depolarizing glycinergic PSPs from neighboring cartwheel cells. Thus, synaptic learning rules vary with the postsynaptic cell, and may require the interaction of different transmitter systems.

Animals↗

PubMed2003

Enhancing synaptic plasticity and memory: a role for small-conductance Ca(2+)-activated K+ channels.

Calcium-activated potassium (K+) channels are distributed throughout the central nervous system as well as many other peripheral tissues and comprise three distinct classes of K+ channels: small conductance (SK), intermediate conductance, and large conductance. This update focuses on SK channels. Increases in cytosolic calcium in response to depolarization activate SK channels. Activation of these channels decreases neuronal excitability. In this review, the authors discuss the role of SK channels in the induction of synaptic plasticity and their influence on learning and memory. A testable model that synthesizes the current literature is offered, suggesting that SK channels represent an important regulator of synaptic plasticity and memory.

Animals↗

PubMed2002

Small conductance Ca2+-activated K+ channels modulate synaptic plasticity and memory encoding.

Activity-dependent changes in neuronal excitability and synaptic strength are thought to underlie memory encoding. In hippocampal CA1 neurons, small conductance Ca2+-activated K+ (SK) channels contribute to the afterhyperpolarization, affecting neuronal excitability. In the present study, we examined the effect of apamin-sensitive SK channels on the induction of hippocampal synaptic plasticity in response to a range of stimulation frequencies. In addition, the role of apamin-sensitive SK channels on hippocampal-dependent memory encoding and retention was also tested. The results show that blocking SK channels with apamin increased the excitability of hippocampal neurons and facilitated the induction of synaptic plasticity by shifting the modification threshold to lower frequencies. This facilitation was NMDA receptor (NMDAR) dependent and appeared to be postsynaptic. Mice treated with apamin demonstrated accelerated hippocampal-dependent spatial and nonspatial memory encoding. They required fewer trials to learn the location of a hidden platform in the Morris water maze and less time to encode object memory in an object-recognition task compared with saline-treated mice. Apamin did not influence long-term retention of spatial or nonspatial memory. These data support a role for SK channels in the modulation of hippocampal synaptic plasticity and hippocampal-dependent memory encoding.

Action Potentials↗