SEARCH · PubMed Health

Results for “EXTRACELLULAR SPACE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

PubMed1996

Changes of extracellular space volume and tortuosity in the spinal cord of Lewis rats with experimental autoimmune encephalomyelitis.

Three diffusion parameters of nervous tissue, extracellular space (ECS) volume fraction (alpha), tortuosity (gamma) and non-specific uptake (k') of tetramethylammonium (TMA+), were studied in the spinal cord of rats during experimental autoimmune encephalomyelitis (EAE). The three parameters were determined in vivo from concentration-time profiles of TMA+ using ion-selective microelectrodes. EAE was induced by injection of guinea-pig myelin basic protein (MBP), which resulted in typical morphological changes in the CNS tissue, namely inflammatory reaction, astrogliosis, blood-brain barrier (BBB) damage and paralysis. EAE was accompanied by a statistically significant increase of alpha (mean +/- S.E.M.) in the dorsal horn from 0.21 +/- 0.01 to 0.28 +/- 0.02, in the intermediate region from 0.22 +/- 0.01 to 0.33 +/- 0.02, in the ventral horn from 0.23 +/- 0.01 to 0.47 +/- 0.02 and in white matter from 0.18 +/- 0.03 to 0.30 +/- 0.03. There were significant decreases in tortuosity in the dorsal horn and in the intermediate region and decreases in non-specific uptake in the intermediate region and in the ventral horn. Although the inflammatory reaction and the astrogliosis preceded and greatly outlasted the neurological symptoms, the BBB damage had a similar time course. Moreover, there was a close correlation between the changes in extracellular space diffusion parameters and the manifestation of neurological signs. We suggest that the expansion of the extracellular space alters the diffusion properties in the spinal cord. This may affect synaptic as well as non-synaptic transmission, intercellular communication and recovery from acute EAE, and may contribute to the manifestation of neurological signs in EAE rats.

Animals↗

PubMed1997

Adenine nucleotides undergo rapid, quantitative conversion to adenosine in the extracellular space in rat hippocampus.

There are multiple mechanisms by which adenine nucleotides can be released into the extracellular space in brain. Adenine nucleotides are converted extracellularly to adenosine, which then acts on adenosine receptors to elicit physiological responses, but the rate at which this conversion takes place is unknown. In the present experiments, adenine nucleotides were applied to individual hippocampal neurons, and the subsequent activation of a postsynaptic K+ conductance by adenosine A1 receptors was used to determine the rate of adenosine formation. None of the adenine nucleotides tested (cAMP, AMP, ADP, and ATP) activated A1 receptors directly at the concentrations tested (</=200 microM). AMP, ADP, and ATP were all rapidly converted to adenosine, with a T1/2 for ATP conversion to adenosine of approximately 200 msec, and the last step in this pathway (transformation of AMP to adenosine by 5'-nucleotidase) seems to be the rate-limiting step. As we have reported previously, cAMP is converted to adenosine as well, but on a much slower time scale than any of the other nucleotides tested. These experiments demonstrate that fast, localized release of AMP, ADP, or ATP can result in a transient activation of adenosine receptors but that this is unlikely to occur with cAMP. The existence of a highly active ecto-nucleotidase pathway in brain provides a mechanism for the rapid generation of adenosine after the release of adenine nucleotides into the extracellular space.

Adenine Nucleotides↗

PubMed1979

Discrepancies in the extracellular space of sympathetic ganglia measured using different isotopes of mannitol and sucrose.

The extracellular space of rat superior cervical ganglia in vitro was measured using mannitol and sucrose labelled with tritium and carbon-14. The volumes of distribution of the 3H-labelled derivatives, especially [3H]mannitol, exceeded those of the 14C-derivatives. The divergence increased with increasing lengths of incubation. Thus, after 30 min incubation, 'spaces' (ml . g-1) were: [14Cu]mannitol, 0.407; [3H]mannitol 0.447; [14C]mannitol, 0.458; [3H]mannitol, 0.645; [14C]sucrose, 0.430; [3H]sucrose, 0.497. Using thin layer chromatography, it was shown that an average of 22% of the label in ganglia incubated for 120 min with [3H]mannitol, but only 4% with [14C]mannitol, was not associated with the parent compound. Both [3H]- and [14C]sucrose appeared to be metabolized by 11%. It is concluded that mannitol and sucrose can be metabolized in isolated ganglia and that this may lead to substantial errors in estimating the extracellular space, particularly when [3H]markers are used.

Animals↗

PubMed1999

Modulation of AV nodal and Hisian conduction by changes in extracellular space.

Previous studies have demonstrated that the extracellular space (ECS) component of the atrioventricular (AV) node and His bundle region is larger than the ECS in adjacent contractile myocardium. The potential physiological significance of this observation was examined in a canine blood-perfused AV nodal preparation. Mannitol, an ECS osmotic expander, was infused directly into either the AV node or His bundle region. This resulted in a significant dose-dependent increase in the AV nodal or His-ventricular conduction time and in the AV nodal effective refractory period. Mannitol infusion eventually resulted in Wenckebach block (n = 6), which reversed with mannitol washout. The ratio of AV nodal to left ventricular ECS in tissue frozen immediately on the development of heart block (n = 8) was significantly higher in the region of block (4.53 +/- 0.61) compared with that in control preparations (2.23 +/- 0.35, n = 6, P < 0.01) and donor dog hearts (2.45 +/- 0.18, n = 11, P < 0.01) not exposed to mannitol. With lower mannitol rates (10% of total blood flow), AV nodal conduction times increased by 5-10% and the AV node became supersensitive to adenosine, acetylcholine, and carbachol, but not to norepinephrine. We conclude that mannitol-induced changes in AV node and His bundle ECS markedly alter conduction system electrophysiology and the sensitivity of conductive tissues to purinergic and cholinergic agonists.

Acetylcholine↗

PubMed2006

Ceramide/sphingosine/sphingosine 1-phosphate metabolism on the cell surface and in the extracellular space.

Sphingolipid metabolites, ceramide, sphingosine, and sphingosine 1-phosphate, have emerged as a new class of lipid biomodulators of various cell functions. These metabolites are known to function not only as intracellular second messengers, but also in the extracellular space. Sphingosine 1-phosphate especially has numerous functions as an important extracellular mediator that binds to cell surface S1P receptors. Recent studies have also shown that sphingolipid-metabolizing enzymes function not only in intracellular organelles but also in the extracellular spaces, including the outer leaflet of the plasma membrane. This review focuses on the metabolic enzymes (acid and alkaline sphingomyelinases, neutral ceramidase, and sphingosine kinase) that are involved in the production of the sphingolipid metabolites in these extracellular spaces, and on the metabolic pathway itself.

Amidohydrolases↗

PubMed1980

Access of horseradish peroxidase (HRP) to the extracellular spaces of the maturation zone of the rat incisor enamel organ.

Adult rats received a single dose of HRP intravenously and were killed from 10 min to 6 hr after injection. Following fixation with glutaraldehyde, the enamel organs were treated with a Graham-Karnovsky-type procedure for peroxidase activity, post-osmicated, and embedded in plastic. Sections were studied with light and electron microscopes. Ten minutes after injection, reaction product was found in all extracellular spaces of the enamel organ, at the enamel-ameloblast interface over smooth-ended and intermediate ameloblasts, and in apical surface invaginations and vesicles of the latter cell types. The enamel-ameloblast interface over the ruffle-ended aemloblasts and the extracellular spaces within the ruffled border were free of reaction product and remained so for up to 6 hr. The apical terminal bars of the ruffle-ended ameloblasts functioned as a barrier to HRP. The basal terminal bars of the smooth-ended ameloblasts likewise seemed to prevent the passage of the HRP. Possibly, HRP flows in a lateral direction from groups of ruffle-ended into groups of smooth-ended ameloblasts. Between 10 min and 6 hr, HRP was cleared more rapidly from the extracellular spaces of the papillary layer than from those of the ameloblast layer, and there was little backflow of tracer from the ameloblast into the papillary layer. Eventually, tracer was cleared also from the extracellular spaces of the ameloblast layer, probably mainly through micropinocytosis by the ameloblasts. A working model is proposed regarding the handling of large molecules by the enamel organ in the maturation zone.

Ameloblasts↗

PubMed1980

Albumin shifts across the extracellular space secondary to experimental infections.

The pathway across tissue spaces of intravenously injected 125I albumin was studied in five dogs before and after the injection of Escherichia coli endotoxin by the use of perforated plastic capsules placed in the subcutaneous tissue. The already negative extracellular space pressure became less so after the endotoxin injection, when albumin was detected shifting from the intravascular space into the extracellular space compartment and then into the intralymphatic space. The injection of endotoxin produced a marked increase in the thoracic duct lymph flow, while, at the same time, erythrocytes entered the lymphatic stream. Results of this study suggest that experimental canine endotoxemia is associated with an increased passage of albumin into the extravascular compartment and explains, in part, the fall in serum levels of this protein during clinical and experimental sepsis.

Animals↗

PubMed2000

Changes in brain cell shape create residual extracellular space volume and explain tortuosity behavior during osmotic challenge.

Diffusion of molecules in brain extracellular space is constrained by two macroscopic parameters, tortuosity factor lambda and volume fraction alpha. Recent studies in brain slices show that when osmolarity is reduced, lambda increases while alpha decreases. In contrast, with increased osmolarity, alpha increases, but lambda attains a plateau. Using homogenization theory and a variety of lattice models, we found that the plateau behavior of lambda can be explained if the shape of brain cells changes nonuniformly during the shrinking or swelling induced by osmotic challenge. The nonuniform cellular shrinkage creates residual extracellular space that temporarily traps diffusing molecules, thus impeding the macroscopic diffusion. The paper also discusses the definition of tortuosity and its independence of the measurement frame of reference.

Animals↗

PubMed1995

Evidence that stratum corneum chymotryptic enzyme is transported to the stratum corneum extracellular space via lamellar bodies.

Stratum corneum chymotryptic enzyme (SCCE) is a recently discovered human serine proteinase that may be specific for keratinizing squamous epithelia. SCCE has properties compatible with a function in the degradation of intercellular cohesive structures during stratum corneum turnover and desquamation. SCCE is expressed in suprabasal keratinocytes. In this study, we demonstrate the subcellular localization of SCCE in the upper granular layer, in the stratum corneum of normal non-palmoplantar skin, and in cohesive parts of hypertrophic plantar stratum corneum, using immunoelectron microscopy of ultrathin cryosections labeled with SCCE-specific monoclonal antibodies detected with gold-labeled secondary antibodies. A narrow zone close to the transition between the granular and cornified layers showed positive SCCE staining after fixation. By means of immunoelectron microscopy, SCCE was found in association with structures resembling intracellular lamellar bodies in the uppermost granular cells and in similar structures undergoing extrusion to the extracellular space between the uppermost granular cells and the lowermost cornified cells. In the stratum corneum, the detected SCCE was confined to the extracellular space and was found in association with intact and partially degraded desmosomes, as well as in the parts of the extracellular space devoid of desmosomes. We conclude that SCCE may be stored in lamellar bodies in the stratum granulosum and transported via these structures to the stratum corneum extracellular space. The results further support the idea that the physiologic function of SCCE may be to catalyze the degradation of desmosomes in the stratum corneum during remodeling of the deeper layers of this tissue, and at a later stage serve as a prerequisite for desquamation.

Adult↗

PubMed2003

Diffusion parameters of the extracellular space in human gliomas.

Tumor cell migration through the extracellular space (ECS) might be affected by its pore size and extracellular matrix molecule content. ECS volume fraction alpha (alpha = ECS volume/total tissue volume), tortuosity lambda (lambda(2) = free/apparent diffusion coefficient) and nonspecific uptake k' were studied by the real-time tetramethylammonium method in acute slices of human tissue. The diffusion parameters in temporal cortical tissue resected during surgical treatment of temporal lobe epilepsy (control) were compared with those in brain tumors. Subsequently, tumor slices were histopathologically classified according to the grading system of the World Health Organization (WHO), and proliferative activity was assessed. The average values of alpha, lambda, and k' in control cortex were 0.24, 1.55, and 3.66 x 10(-3)s(-1), respectively. Values of alpha, lambda, and k' in oligodendrogliomas did not significantly differ from controls. In pilocytic astrogliomas (WHO grade I) as well as in ependymomas (WHO grade II), alpha was significantly higher, while lambda and k' were unchanged. Higher values of alpha as well as lambda were found in low-grade diffuse astrocytomas (WHO grade II). In cellular regions of high-grade astrocytomas (WHO grade III and IV), alpha and lambda were further increased, and k' was significantly larger than in controls. Classic medulloblastomas (WHO grade IV) had an increased alpha, but not lambda or k', while in the desmoplastic type alpha and k' remained unchanged, but lambda was greatly increased. Tumor malignancy grade strongly corresponds to an increase in ECS volume, which is accompanied by a change in ECS structure manifested by an increase in diffusion barriers for small molecules.

Adolescent↗

PubMed2002

Certain forms of matrix metalloproteinase-9 accumulate in the extracellular space after microdialysis probe implantation and middle cerebral artery occlusion/reperfusion.

Matrix metalloproteinases (MMPs) are activated in focal cerebral ischemia. The activation of MMP-9 is involved in blood-brain barrier breakdown and tissue remodeling. The MMPs are released to the extracellular space, but the form and fate of secreted enzymes in brain are unknown. Using microdialysis in vivo, the authors studied whether ischemia-induced MMP-9 in brain tissue was related to free MMP-9 in the extracellular fluid. A microdialysis probe was placed into the right striatum and microdialysis was initiated 24 hours later in controls (n = 7). One hour prior to microdialysis, a group of rats (n = 7) was subjected to 1-hour occlusion of the right middle cerebral artery, followed by reperfusion. Dialysates were collected at discrete time points up to 24 hours, and subjected to zymography and Western blot analysis. The MMP-9 was released after ischemia and accumulated in the extracellular space at 24 hours (P < 0.05). Free MMP-9 forms include mainly the 95-kd proform, and, to a lesser extent, dimers and cleaved active forms (70 kd), but not the 88-kd form found in tissue. Probe implantation and microdialysis increased free MMP-9 in the dialysate. This increase was concomitant with neutrophil infiltration after the mechanical lesion, as myeloperoxidase was found by means of Western blot analysis in the brain hemisphere subjected to microdialysis (P < 0.005), and immunohistochemistry revealed the presence of myeloperoxidase stain surrounding the site of probe implantation. The results suggest that certain forms of MMP-9 are released and accumulate in the extracellular space after brain injury, and that vascular alterations and neutrophil recruitment elicit MMP-9 activation in the brain after focal ischemia and trauma.

Animals↗

PubMed1993

External Ca effect on water permeability, regulatory volume decrease, and extracellular space in barnacle muscle cells.

The effect of extracellular Ca2+ (Cao) on sarcolemmal hydraulic water permeability (L'p), regulatory volume decrease (RVD), and extracellular space (ECS) was studied in barnacle muscle cells. Absence or presence of Cao had no effect on L'p [0 Cao = 2.762 +/- 0.098 x 10(-5), and 11 mM Cao = 2.720 +/- 0.222 x 10(-5) cm.kg.s-1 x osmol x 1-kgH2O-1]. Likewise, cells exposed to anisosmotic media (for < 30 min) behaved as osmometers in 0 and 11 mM Cao, showing similar slopes and intercepts in van't Hoff plots. At longer incubation times, however, hyposmotic conditions promoted a Cao-dependent RVD. The relationship between Cao and the percentage of cells responding with RVD to a hyposmotic challenge was sigmoidal (half-maximal Cao = 4.83 mM). The mean rate of RVD (40 nl/min) was independent of the level of swelling in response to hyposmotic challenges. However, the magnitude of RVD increased with larger hyposmotic challenges. Both the presence of Cao and hypotonicity reduced the "apparent" ECS by 47 +/- 6 and 39 +/- 6%, respectively. Three-dimensional reconstruction of autoradiographs of the cells was made to interpret these results.

Animals↗

PubMed1995

Analysis of ceftriaxone and ceftazidime distribution in cerebrospinal fluid of and cerebral extracellular space in awake rats by in vivo microdialysis.

In vivo microdialysis was used to estimate the extracellular concentrations of ceftazidime and ceftriaxone, two expanded-spectrum cephalosporins commonly used in the treatment of bacterial meningitis, in two brain regions (the right corpus striatum and the left lateral ventricle_ of awake, freely moving rats. Antibiotics were administered by constant intravenous infusion at 18 mg/h until steady-state levels were reached. Ceftriaxone levels measured at the steady state in the extracellular space of the corpus striatum (0.80 +/- 0.17 micrograms/ml) were statistically equivalent to those obtained in the cerebrospinal fluid of the lateral ventricle (0.71 +/- 0.15 micrograms/ml). The ratios of these levels in the brain to the steady-state levels in plasma were 0.5 +/- 0.1% for both regions. The postinfusion concentrations of ceftriaxone in the brain declined monoexponentially, with an elimination half-life similar to that obtained in plasma. However, the mean antibiotic concentration of ceftazidime in the striatum (2.2 +/- 0.4 micrograms/ml) was lower (P < 0.001) than that in the lateral ventricle (3.8 +/- 0.5% and 4.0 +/- 1.8%, respectively) were higher than those obtained with ceftriaxone. Moreover, the half-life of ceftazidime elimination from plasma was lower than that obtained in the two brain regions. It was concluded that the in vivo microdialysis technique yields useful data on antibiotic distribution in the extracellular space of the brain, that the distribution may not be homogeneous, and that the decay of postinfusion concentrations in the brain may be different from the decay of postinfusion concentrations in plasma.

Animals↗

PubMed2004

Use of magnetic resonance to measure molecular diffusion within the brain extracellular space.

Ion-selective microelectrode measurements of molecular diffusion have provided unique information about the structural characteristics of the extracellular compartment of brain tissue. Magnetic resonance (MR) techniques can also be used to perform diffusion measurements in living tissue in situ. In MR applications, the challenge to study a particular physiological compartment lies in achieving the appropriate specificity in the experimentally-observed MR signal, and many strategies have been used to provide measurements that reflect molecular diffusion within the extracellular space. This review describes how magnetic resonance and microelectrode diffusion measurements are performed, and applications using the MR technique are summarized. Comparisons of experimental results obtained from the two techniques indicate that their use in combination may further augment what is known about extracellular space structure.

Animals↗

PubMed1986

The chronology of lesion repair in the developing rat brain: biological significance of the pre-existing extracellular space.

We observed the histological peculiarities of the repair process in a destructive lesion of the developing rat brain during neurogenesis. Degeneration was induced selectively in certain cells of the proliferating phase in the rat fetal neopallium on embryonic day 16 by transplacental administration of ethylnitrosourea. Successive elimination of necrotic cells and the restoration process were observed. The repair process was divided into the following steps: elimination of individually affected cells by phagocytes in the pre-existing extracellular space; successive restoration of the disintegrated area by cells which differentiated from remaining matrix cells. No reactive gliosis, fibrosis, abnormal vascularization or infiltration of granulocytes and lymphocytes was observed at any time. The thinned neopallium on postnatal day 21 revealed only a small number and abnormal distribution of the cortical neurons. It may be assumed that the fetal brain owes its unique repair features to the presence of a vast extracellular space under normal conditions. In this pre-existing extracellular space, every kind of cell seems to exist separately without the intracellular adhesions characteristic of the adult brain. When degeneration occurs in certain cells the phagocytes would be able to eliminate the degenerate cells completely in this space without having to break intercellular adhesions. As a result, after the completion of cell elimination, the injured brain is restored to its original state with no cell reaction, giving the appearance of a small brain with normal-looking histological architecture, save only for the sparseness of cells.

Animals↗

PubMed1992

Clearance of brain edema and macromolecules through the cortical extracellular space.

The transit routes of fluid and particulate matter through brain tissue remain unclear. The object of this study was to examine the movement of macromolecules through brain tissue to further clarify the clearance pathways of edema proteins as they migrate toward the cortex. For this purpose, albumin solution (20 microliters rat albumin diluted to 65 mg/ml with mock cerebrospinal fluid (CSF)) was intracerebrally infused into the caudate putamen, and the migration through brain tissue as well as through the ultrastructure of the cortical surfaces was explored using an immunocytochemical technique. The authors observed immunoreactive product on the glial limitans and pial lining as well as in the extracellular space of the cortical neuropil at 24 hours postinfusion, confirming that the protein had reached the cortical surface. To confirm the efflux of macromolecules into the subarachnoid CSF, 71,200 D fluorescein isothiocyanate-dextran (FITC-dextran 71,200) was infused; cortical surfaces of brains removed en bloc as well as coronal sections were macroscopically observed under ultraviolet illumination at 15 minutes and 24 hours postinfusion. It was observed that infused FITC-dextran 71,200 mainly localized in the cortical white matter and caudate putamen of the infusion site at 15 minutes postinfusion and by 24 hours was distributed in the entire cortex of the infused hemisphere. However, the dynamics of lower-molecular-weight substances was completely different. The spatial distribution of FITC-dextran 4400 diverged upward toward the cortical surface and spread more extensively than FITC-dextran 71,200. These observations were consistent with a diffusion process as the spread of the tracer was dependent upon molecular size. These studies provide compelling evidence that a process other than bulk flow was involved in the spread of macromolecules through the extracellular space of the normal cortical neuropil to sink into the subarachnoid space. It was concluded that the CSF pathway via the extracellular space of the cortical neuropil is a primary route for clearance of extracellular edema proteins to the subarachnoid space and that diffusion is involved in this process.

Albumins↗

PubMed1989

Role of extracellular space in hyperosmotic suppression of potassium-induced electrographic seizures.

1. Focal electrographic seizures arose in the CA1 region of rat hippocampal slices bathed in elevated (8.5 mM) external potassium [( K+]o). High [K+]o also induced spontaneous interictal bursts that originated in area CA3 and propagated to CA1. To examine the contribution to electrographic seizure initiation of excitatory mechanisms that are influenced by extracellular volume, we studied the effect of hyperosmotic expansion of interstitial volume on seizure occurrence, interictal bursts, and excitatory synaptic transmission. The tissue electrical resistance was also measured leading up to and during seizures. 2. Media made 5-30 mosmol/kg hyperosmotic by addition of agents restricted to the extracellular space (mannitol, sucrose, raffinose, L-glucose, dextran) rapidly and reversibly abolished [K+]o-induced spontaneous CA1 seizures in 86% of slices tested. However, similar increases in osmolality effected by agents that access the intracellular compartment (D-glucose, glycerol) did not influence electrographic seizure occurrence. Hyperosmotic changes with plasma membrane impermeable compounds, but not permeable compounds, produced significant concentration-dependent decreases (1-10%) in the electrical resistance of CA1 stratum pyramidale. Because tissue resistance is proportional to extracellular volume, these results suggest that hyperosmotic suppression of electrographic seizures is associated with expansion of the extracellular space in hippocampal slices. 3. Measurement of electrical resistance of the CA1 stratum pyramidale during spreading depression and electrographic seizure revealed an increase in tissue resistance to 122% and 108% of control, respectively. Furthermore, a slight (approximately 2%) but significant increase in electrical resistance gradually occurred over the 20 s immediately preceding seizure generation. The observed increase in tissue resistance suggests extracellular space is decreased during these events. 4. Hyperosmolality did not alter CA3 interictal burst frequency. However, burst intensity, estimated from the total length of the burst waveform, was significantly reduced in both the CA3 (83% control) and CA1 region (67% control) when osmotic changes were imposed by plasma membrane impermeant compounds. Additionally, media made hypoosmotic by removal of 7.5 mM NaCl reversibly increased burst intensity. 5. High [K+]o potentiated excitatory synaptic transmission and excitatory postsynaptic potential (EPSP) spike coupling.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2004

L-Glutamate in the extracellular space regulates endogenous D-aspartate homeostasis in rat pheochromocytoma MPT1 cells.

In previous studies [FEBS Lett. 434 (1998) 231, Arch. Biochem. Biophys. 404 (2002) 92], we demonstrated for the first time that D-aspartate (D-Asp) is synthesized in cultured mammalian cell lines, such as pheochromocytoma 12 (PC12) and its subclone, MPT1. Our current focus is analysis of the dynamics of D-Asp homeostasis in these cells. In this communication, we show that L-glutamate (Glu) and L-Glu transporter substrates in the extracellular space regulate the homeostasis of endogenous D-Asp in MPT1 cells. D-Asp is apparently in dynamic homeostasis, whereby endogenous D-Asp is constantly released into the extracellular space by an undefined mechanism, and continuously and intensively taken up into cells by an L-Glu transporter. Under these conditions, L-Glu and its transporter substrates in the medium may competitively inhibit the uptake of D-Asp via the transporter, resulting in accumulation of the amino acid in the extracellular space. We additionally demonstrate that DL-TBOA, a well-established L-Glu transporter inhibitor, is taken up by the transporter during long time intervals, but not on a short time-scale.

Amino Acid Transport System X-AG↗