Extracellular glutamate is not modulated by cannabinoid receptor activity.

Cannabinoid receptor activation has been proposed to trigger glutamate release from astrocytes located in cortical layer 2/3. Here, we measure the basal concentration of extracellular glutamate in layer 2/3 of mouse somatosensory cortex and find it to be 20-30 nM. We further examine the effect of cannabinoid receptor signaling on extracellular glutamate, and find no evidence for increased extracellular glutamate upon cannabinoid receptor agonist application.

Sigh generation in preBötzinger Complex.

We explored neural mechanisms underlying sighing. Photostimulation of parafacial (pF) neuromedin B (NMB) or gastrin releasing peptide (GRP), or preBötzinger Complex (preBötC) NMBR or GRPR neurons elicited ectopic sighs with latency inversely related to time from preceding endogenous sigh. Of particular note, ectopic sighs could be produced without involvement of these peptides or their receptors in preBötC.

Synaptotagmin 7 Sculpts Short-Term Plasticity at a High Probability Synapse.

Synapses with high release probability ( ) tend to exhibit short-term synaptic depression. According to the prevailing model, this reflects the temporary depletion of release-ready vesicles after an initial action potential (AP). At the high- layer 4 to layer 2/3 (L4-L2/3) synapse in rodent somatosensory cortex, short-term plasticity appears to contradict the depletion model: depression is absent at interstimulus intervals (ISIs) <50 ms and develops to a maximum at ∼200 ms.

Synaptic NMDA receptor activity at resting membrane potentials.

NMDA receptors (NMDARs) are crucial for glutamatergic synaptic signaling in the mammalian central nervous system. When activated by glutamate and glycine/D-serine, the NMDAR ion channel can open, but current flux is further regulated by voltage-dependent block conferred by extracellular Mg ions. The unique biophysical property of ligand- and voltage-dependence positions NMDARs as synaptic coincidence detectors, controlling a major source of synaptic Ca influx.

Extracellular Glutamate in the Nucleus Accumbens Is Nanomolar in Both Synaptic and Non-synaptic Compartments.

In the CNS, glutamate is both phasically and tonically released into the extracellular space and must be removed by excitatory amino acid transporters (EAATs) to prevent excitotoxic accumulation. There remains uncertainty, however, regarding the functional steady-state concentration, with estimates ranging from tens of nanomolar to tens of micromolar. Efforts to reconcile these disparate values have led to a hypothesis that the extracellular space comprises distinct compartments in which basal glutamate concentrations are maintained independently.

Ca(2+)-dependent enhancement of release by subthreshold somatic depolarization.

In many neurons, subthreshold somatic depolarization can spread electrotonically into the axon and modulate subsequent spike-evoked transmission. Although release probability is regulated by intracellular Ca(2+), the Ca(2+) dependence of this modulatory mechanism has been debated. Using paired recordings from synaptically connected molecular layer interneurons (MLIs) of the rat cerebellum, we observed Ca(2+)-mediated strengthening of release following brief subthreshold depolarization of the soma.