Aβ1-16 controls synaptic vesicle pools at excitatory synapses via cholinergic modulation of synapsin phosphorylation.

Amyloid beta (Aβ) is linked to the pathology of Alzheimer's disease (AD). At physiological concentrations, Aβ was proposed to enhance neuroplasticity and memory formation by increasing the neurotransmitter release from presynapse. However, the exact mechanisms underlying this presynaptic effect as well as specific contribution of endogenously occurring Aβ isoforms remain unclear.

Mobility of calcium channels in the presynaptic membrane.

Unravelling principles underlying neurotransmitter release are key to understand neural signaling. Here, we describe how surface mobility of voltage-dependent calcium channels (VDCCs) modulates release probabilities (P(r)) of synaptic vesicles (SVs). Coupling distances of <10 to >100 nm have been reported for SVs and VDCCs in different synapses.

Intracellular Ca²⁺ and not the extracellular matrix determines surface dynamics of AMPA-type glutamate receptors on aspiny neurons.

The perisynaptic extracellular matrix (ECM) contributes to the control of the lateral mobility of AMPA-type glutamate receptors (AMPARs) at spine synapses of principal hippocampal neurons. Here, we have studied the effect of the ECM on the lateral mobility of AMPARs at shaft synapses of aspiny interneurons. Single particle tracking experiments revealed that the removal of the hyaluronan-based ECM with hyaluronidase does not affect lateral receptor mobility on the timescale of seconds.

Bassoon specifically controls presynaptic P/Q-type Ca(2+) channels via RIM-binding protein.

Voltage-dependent Ca(2+) channels (CaVs) represent the principal source of Ca(2+) ions that trigger evoked neurotransmitter release from presynaptic boutons. Ca(2+) influx is mediated mainly via CaV2.1 (P/Q-type) and CaV2.

Hyperpolarization-activated cation current contributes to spontaneous network activity in developing neocortical cultures.

The mechanisms underlying spontaneous burst activity (SBA), appearing in networks of embryonic cortical neurons at the end of the first week in vitro, remain elusive. Here we investigated the contribution of the hyperpolarization-activated cation current (I(h)) to SBA in cortical cultures of GAD67-GFP mice. I(h) current could be detected in GFP-positive large GABAergic interneurons (L-INs) and glutamatergic principal neurons (PNs) as early as DIV 5.

Developmental downregulation of GABAergic drive parallels formation of functional synapses in cultured mouse neocortical networks.

Networks of cortical neurons in vitro spontaneously develop synchronous oscillatory electrical activity at around the second week in culture. However, the underlying mechanisms and in particular the role of GABAergic interneurons in initiation and synchronization of oscillatory activity in developing cortical networks remain elusive. Here, we examined the intrinsic properties and the development of GABAergic and glutamatergic input onto presumed projection neurons (PNs) and large interneurons (L-INs) in cortical cultures of GAD67-GFP mice.

Synaptic and non-synaptic mechanisms of amygdala recruitment into temporolimbic epileptiform activities.

Lateral amygdala (LA) activity during synchronized-epileptiform discharges in temporolimbic circuits was investigated in rat horizontal slices containing the amygdala, hippocampus (Hip), perirhinal (Prh) and lateral entorhinal (LEnt) cortex, through multiple-site extra- and intracellular recording techniques and measurement of the extracellular K+ concentration. Application of 4-aminopyridine (50 microm) induced epileptiform discharges in all regions under study. Slow interictal-like burst discharges persisted in the Prh/LEnt/LA after disconnection of the Hip, seemed to originate in the Prh as shown from time delay analyses, and often preceded the onset of ictal-like activity.