Topic: paired-pulse depression

One of the most fundamental tenets in neuroscience is that information is stored in the strength of synapses, and that learning relies on changes in synaptic strength. Here we aim to extend this tenet into the temporal domain by proposing that synapses not only learn to strengthen or weaken, but can learn when to be weak or strong on the subsecond scale. It has been known for more than half a century that synapses exhibit short-term synaptic plasticity (STP): a form of presynaptic, use-dependent, plasticity in which consecutive spikes can elicit progressively depressing (short-term depression/

Hypoinsulinemia is a pathological consequence of diabetes mellitus that can stimulate the development of neurodegenerative processes in the brain due to dysfunction of insulin signaling cascades into neurons and impaired synaptic plasticity properties. We used the whole-cell patch-clamp recording of evoked glutamatergic excitatory postsynaptic currents (eEPSCs) with the local stimulation of presynaptic axon to investigate the insulin (100 nM) effect on the paired-pulse plasticity at cultured hippocampal neurons under hypoinsulinemia (4 days insulin-free media incubation).At control normoinsuli

Recent data show that a significant fraction of cortical pyramidal neurons has an axon originating from a basal dendrite (axon-carrying dendrite, AcD) rather than from the soma. In the rodent hippocampus, these AcD cells convey privileged synaptic excitation especially in network states with strong perisomatic inhibition (Hodapp et al., 2022). We have recently shown that hippocampal AcD cells receive stronger commissural input than neurons with somatic axon origin (non-AcD) (Stevens et al., 2023).AcD cells are also present in the neocortex, though seemingly less frequent than in the hippocampu