NMDA receptor-dependent afterdepolarizations are curtailed by carbonic anhydrase 14: regulation of a short-term postsynaptic potentiation.

In the hippocampus, extracellular carbonic anhydrase (Car) speeds the buffering of an activity-generated rise in extracellular pH that impacts H(+)-sensitive NMDA receptors (NMDARs). We studied the role of Car14 in this brain structure, in which it is expressed solely on neurons. Current-clamp responses were recorded from CA1 pyramidal neurons in wild-type (WT) versus Car14 knock-out (KO) mice 2 s before (control) and after (test) a 10 pulse, 100 Hz afferent train.

Preemptive regulation of intracellular pH in hippocampal neurons by a dual mechanism of depolarization-induced alkalinization.

Numerous studies have documented the mechanisms that regulate intracellular pH (pH(i)) in hippocampal neurons in response to an acid load. Here, we studied the response of pH(i) to depolarization in cultured hippocampal neurons. Elevation of external K+ (6-30 mm) elicited an acid transient followed by a large net alkaline shift.

Functional demonstration of surface carbonic anhydrase IV activity on rat astrocytes.

Buffering of the brain extracellular fluid is catalyzed by carbonic anhydrase (CA) activity. Whereas the extracellular isoform CA XIV has been localized exclusively to neurons in the brain, and to glial cells in the retina, there has been uncertainty regarding the form or forms of CA on the surface of brain astrocytes. We addressed this issue using physiological methods on cultured and acutely dissociated rat astrocytes.

Beta-amyloid-induced reactive astrocytes display altered ability to support dendrite and axon growth from mouse cerebral cortical neurons in vitro.

Objectives: The presence of beta-amyloid (betaA) deposition, induction of reactive gliosis and dystrophic neurites, is a characteristic feature of neuritic plaques in Alzheimer's disease. In vitro, betaA-exposed astrocytes become reactive, similar to astrocytes in contact with betaA plaques in vivo. How betaA-exposed reactive astrocytes support neuron process growth, however, is not well defined.

BMP-7 and excess glutamate: opposing effects on dendrite growth from cerebral cortical neurons in vitro.

Glutamate is an important regulator of dendrite development. During cerebral ischemia, however, there is massive release of glutamate reaching millimolar concentrations in the extracellular space. An early consequence of this excess glutamate is reduced dendrite growth.

Astrocytes mediate cerebral cortical neuronal axon and dendrite growth, in part, by release of fibroblast growth factor.

Astrocytes occupy a central role in central nervous system (CNS) function. In particular astyrocytes can support neurite growth, in part, by release of diffusable factors. We therefore performed biochemical analysis of astrocyte conditioned medium to examine possible mechanisms of astrocyte mediated axon and dendrite growth in the mammalian CNS.