The neurotransmitter GABA is present around the central canal and is known to affect cells within other postnatal neurogenic niches

The neurotransmitter GABA is present around the central canal and is known to affect cells within other postnatal neurogenic niches. depolarised all ependymal cells tested; the partial antagonism of this response by bicuculline and gabazine indicates that GABAA receptors contribute to this response. A lack of effect by baclofen suggests that GABAB receptors do not contribute to the GABAergic response. The ability of ependymal cells to respond to GABA suggests that GABA Alvimopan (ADL 8-2698) could be capable of influencing the proliferation and differentiation of cells within the neurogenic niche of the postnatal spinal cord. (2, 6)?=?0.310, (3)?=?3.685, (2, 4)?=?2.601, (2, 4)?=?1.449, em P /em ?=?0.366; Fig. 2D). 4.?Discussion This study provides an electrophysiological characterisation of ependymal cells surrounding the CC and is the first study to demonstrate that ependymal cells in this area within the postnatal mammalian spinal cord respond to GABA. Ependymal cells displayed typical characteristics of glial cells, with no spontaneous or evoked activity, indicating a lack of voltage-gated channels. Dye coupling with Neurobiotin following intracellular loading confirmed reports that ependymal cells are coupled and the gap junction blocker 18-glycrrhetinic acid established that this coupling was mediated by gap junctions. Ependymal cells consistently depolarised to GABA, an effect partially antagonised by GABAA receptor antagonists, bicuculline and gabazine, but the remainder of the response was not decreased by GABA transporter blockers, nor was the response mimicked by the GABAB agonist baclofen. The ability of these cells, which are considered to be neural stem cells, to respond to GABA is extremely pertinent and highlights the need for further studies investigating how GABA affects the proliferation and differentiation of these cells. The input resistance of 96?M in ependymal cells is slightly lower than that previously determined for ependymal cells in the rat spinal cord, 124?M [16]. As connexin expression is known to increase steadily from P0 to adulthood in other CNS areas [10], the lower input resistance here may be due to the older animals used (P11CP21) Alvimopan (ADL 8-2698) compared to that of Marichal et al. ([16] P0CP5). The lack of spontaneous or evoked activity and the linear voltageCcurrent relationship agrees with previous studies of rat and turtle spinal cord ependymal cells [15,16,21] and suggests that ependymal Alvimopan (ADL 8-2698) cells lack voltage-gated ion channels. 4.1. The relevance of gap junction coupling This study confirmed previous reports that gap junction coupling occurs between ependymal cells of the rat spinal cord [16]. As 18-GA is a nonselective gap junction blocker, the specific identity of the connexin subunits forming the gap junctions was not identified, however, immunohistochemistry implies that either connexin 43 [16,19] and/or connexin 45 [4] form the gap junctions between ependymal cells. The strong correlation between the change in input resistance and the change in membrane potential in response to 18-GA indicates that the depolarisation is a direct effect of gap junction blockade rather Alvimopan (ADL 8-2698) than a non-gap junction specific effect of 18-GA. This effect is similar to that observed in progenitor cells surrounding the turtle CC [20]. A possible reason for ependymal cells to form gap junctions is to allow the control of cellular proliferation, as seen in the embryonic neocortex and in the adult SVZ [3,11] 4.2. Could GABA influence ependymal cells? The depolarisation of ependymal cells observed following bath or focal application of GABA resembles that observed in progenitor cells surrounding the CC of the turtle spinal cord [20] and in the postnatal neurogenic niches of the brain [12,23]. Given that EGABA is predominantly Ppia influenced by em E /em Cl?, which was ?103?mV in this study, a hyperpolarisation rather than a depolarisation would have been expected. Although the presence of the Na+CK+C2Cl? co-transporter (NKCC1) in ependymal cells would not generally be enough to overcome the low intracellular Cl? concentration imposed by the intracellular solution within the patch pipette, if the NKCC1 channels were expressed in close proximity to GABAA receptors in the.

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