Previous studies have reported the presence of migrating and dividing neuronal progenitors in the subventricular zone (SVZ) and rostral migratory stream (RMS) of the postnatal mammalian brain. Although the behaviour of these progenitors is thought to be influenced by local signals, the nature and mode of action of the local signals are largely unknown. One of the signalling molecules known to affect the behaviour of embryonic neurons is the neurotransmitter GABA. In order to determine whether GABA affects neuronal progenitors via the activation of specific receptors, we performed cell‐attached, whole‐cell and gramicidin perforated patch‐clamp recordings of progenitors in postnatal mouse brain slices containing either the SVZ or the RMS. Recorded cells displayed a morphology typical of migrating neuronal progenitors had depolarized zero‐current resting potentials, and lacked action potentials. A subset of progenitors contained GABA and stained positive for glutamic acid decarboxylase 67 (GAD‐67) as shown by immunohistochemistry. In addition, every neuronal progenitor responded to GABA via picrotoxin‐sensitive GABAA receptor (GABAAR) activation. GABAARs displayed an ATP‐dependent rundown and a low sensitivity to Zn2+. GABA responses were sensitive to benzodiazepine agonists, an inverse agonist, as well as a barbiturate agonist. While GABA was hyperpolarizing at the zero‐current resting potentials, it was depolarizing at the cell resting potentials estimated from the reversal potential of K+ currents through a cell‐attached patch. Thus, our study demonstrates that neuronal progenitors of the SVZ/RMS contain GABA and are depolarized by GABA, which may constitute the basis for a paracrine signal among neuronal progenitors to dynamically regulate their proliferation and/or migration.

Study of the different stages of postnatal neurogenesis relies on using antigenic markers and transgenic mice. In particular, neural stem cells that express GFAP are studied using mice expressing GFP under the human GFAP promoter (GFAP-GFP). However, it remains unclear whether GFP and the commonly used progenitor markers label different cell populations in the neurogenic subventricular zone (SVZ) and its rostral extension into the olfactory bulb (i.e. rostral migratory stream, RMS). Here, we found that all GFP-fluorescent cells express GFAP, the radial glia marker brain lipid-binding protein (BLBP), Lewis X (LeX), and the astrocytic marker GLAST. Faint GFP fluorescence could be detected in a few cells expressing EGF receptors (EGFRs), Olig2, or S100, suggesting that GFAP-GFP cells generate these diverse cell types. GFP-fluorescent cells were slowly cycling, as shown by their long-term retention of BrdU, and less than 10% expressed the proliferative markers Ki67 and Mcm2. The majority of EGFR-expressing cells and Olig2-expressing cells were cycling. NG2 and EGFR identified distinct progenitor populations while Olig2 labeled a subset of EGFR-expressing cells. The entire neurogenic zone contained a mosaic of different cell types and was ensheathed by processes of GFAP-expressing cells and NG2 cells. Finally, using time-lapse imaging in acute slices, we show that GFP-fluorescent cells are stationary within the SVZ. Our findings collectively highlight the cellular mosaic of the neurogenic niche, show that the slowly-cycling GFAP-expressing cells are stationary and generate distinct intermediate progenitors.

Taurine uptake is essential for the maintenance of millimolar intracellular concentrations of taurine, which is released during ischaemia and is thought to be neuroprotective. To determine whether Bergmann glia express functional transporters that can mediate both taurine uptake and efflux, whole‐cell patch‐clamp recordings were obtained from these cells in rat cerebellar slices. Taurine‐induced inward currents can be pharmacologically separated into GABAA receptor and taurine transporter currents. In the presence of GABA receptor blockers, residual taurine currents averaged −28 pA at −70 mV and were strictly inwardly rectifying between −70 and +50 mV. These residual currents were also abolished by external Na+ removal and diminished by reduction of external Cl−, consistent with transport currents. Taurine transport currents were reduced by a taurine transporter inhibitor, guanidinoethyl sulphonate (GES). Other classical inhibitors reduced taurine transport currents with an order of potency (hypotaurine > β‐alanine > GES > GABA) similar to that reported for cloned rat taurine transporters. Following intracellular taurine perfusion during the recording, a progressively developing outward current could be observed at −50 mV but not at −70 mV. Intracellular perfusion of taurine also decreased taurine‐induced inward currents at both holding potentials. Outward currents induced by intracellular taurine increased in amplitude with depolarization, activated near −50 mV, and were affected by GES. For the first time, these results demonstrate that taurine activates both GABAA receptors and Na+/Cl−‐dependent taurine transporters in Bergmann glia in slices. In addition, our data show that taurine transporters can work in reverse and can probably mediate taurine efflux under ischaemic conditions.

Previous studies have reported that mature oligodendrocytes (OLGs) in vitro display various voltage-dependent K+ currents while in situ OLGs show only voltage-independent K+ currents. Given this discrepancy and the lack of information on myelinating OLG ion channel expression in situ, we characterized mature OLG currents in myelinating corpus callosum slices from 17 to 36-day old rats. OLGs were recorded in cell-attached and whole-cell patch-clamp configurations, displayed morphology typical of mature OLGs, and stained positive for myelin basic protein. OLGs displayed large voltage-independent currents that decayed during the voltage pulse and small voltage-activated outward currents. The latter were blocked by TEA, activated between -40 and -50 mV, and decayed slowly. The former were composed of large voltage-independent, time-dependent Ba2+ (1 mM)-sensitive currents, and voltage-dependent Cs+ (5 mM) and Ba2+ (100 mM)-sensitive currents that reversed near the K+ equilibrium potential and inactivated at hyperpolarized potentials, identifying them as inwardly rectifying K+ currents. Inwardly rectifying single-channel K+currents could be recorded in the cell-attached configuration. The estimated single-channel slope conductance was 30 pS. The steady-state open probability was voltage-dependent and declined from 0.9 to 0.5 between -80 and -150 mV. Overall, mature OLGs in situ possess time- and also voltage-dependent K+ currents, which may facilitate clearance of K+ released during axonal firing.