Thus, when there is a breakdown in the blood-retinal barrier, this glycerophospholipid may be one of the serum-derived molecules that regulates ion channel activity in Müller cells.įreshly dissociated human and bovine Müller cells were prepared as detailed previously ( Kusaka, Dabin, Barnstable & Puro, 1996). We also found that lysophosphatidic acid (LPA), a component of serum, induces currents similar to those activated by whole serum. In addition, the electroretinograms (ERGs) from isolated retinas exposed to serum showed changes consistent with the idea that the serum-induced changes in the activity of ion channels reduces the role of Müller cells in the redistribution of K +. Another motivation for studying retinal cells is that a breakdown of the blood-retinal barrier is a frequently occurring, sight-threatening pathophysiological process ( Gass, 1997).īased on perforated-patch recordings from fresh bovine and human Müller cells, we now report that serum causes these glial cells to depolarize as a non-specific cation current and an outwardly rectifying K + current are activated. The extensive information concerning K + siphoning via Müller cells facilitates attempts to relate changes in ion channel activity to the function of these cells in regulating o. By a specialized mechanism of K + spatial buffering, termed K + siphoning (Newman, Frambach & Odette, 1994), K + enters a Müller cell where o is high and exits where o is lower. A reason for selecting these glial cells is that their role in K + redistribution has been particularly well studied ( Newman, 1995). To identify and characterize the effects of serum on glial channels, we chose to study Müller cells, the predominant glia of the retina. This redistribution via glial cells serves to limit wide swings in o which can alter neuronal excitability.
Glial K + channels are pathways for the redistribution of excess potassium. We focused our study on the activity of ion channels, since they are involved in important glial functions such as the maintenance of K + homeostasis ( Newman & Reichenbach, 1996). One reason the glia are of interest is that serum leaking from the vascular system would almost certainly contact these cells, since they ensheath the blood vessels of the nervous system. In this study, we examined the effect of serum on the activity of ion channels in glial cells. We hypothesize that serum-derived molecules enter the nervous system, induce receptor-mediated changes in cell function and thereby alter the activity of neural circuits. Whilst gross tissue swelling and distortion due to an influx of fluid from the vascular compartment can cause damage, knowledge of more subtle mechanisms by which a breakdown of this barrier alters function is limited. If you identify information that you believe to be incorrect or outdated, let us know.When there is a breakdown of the barrier between the circulatory and nervous systems, the function of the CNS is compromised. While CNN has attempted to clean this data, it may still contain errors. Employee totals, which the SBA refers to as “jobs retained,” refers to the number of employees as reported by the borrower and may not necessarily reflect the number of workers kept employed with PPP funds. Data for those and cancelled loans is not included in this database.īecause the SBA released loan amounts in ranges, date, business type, industry, state and county totals represent minimum estimates. Dollar amounts represent loan amounts approved by lenders and not necessarily the amount of money disbursed to businesses.įor loans worth less than $150,000, the SBA released anonymized data by state. This data represents about 13% of the 4.8 million loans and about 73% of the $521 billion approved under the PPP to date. The data in this database was published by the Small Business Administration (SBA) on Jand includes all approved, active Paycheck Protection Program (PPP) loans worth $150,000 or more. Email or, if you need to reach us securely, visit cnn.com/tips.
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