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PubMed1991

Potassium ion channels operated by receptor stimulation can be activated simply by raising temperature.

Application of either dopamine (DA), acetylcholine (ACh), or histamine (HA) to the identified ganglion cells of Aplysia elicits a K(+)-dependent slow hyperpolarization. When temperature of the bathing solution was raised from 22 to 32 degrees C, these cells were also hyperpolarized with a marked increase in K+ conductance. The warm- and transmitter-induced current responses recorded under voltage clamp were not blocked by either 1 mM Ba2+ or 10 mM TEA. Intracellularly injected guanosine 5'-O-(2-thiodiphosphate) (GDP beta S) depressed both warm- and transmitter-induced K+ responses immediately after the injection. Intracellular application of guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) caused a gradual, irreversible increase in K+ conductance of the plasma membrane and occluded both responses. Transmitter-induced response markedly decreased when the temperature was raised from 22 to 32 degrees C, suggesting that the response to transmitter was occluded during the warm-induced response. These results suggested that the G-protein regulating the receptor-operated K+ channels could be activated simply by raising temperature.

Acetylcholine↗
PubMed1991

Kinetics of the Ca(2+)-activated K+ channel in rat hippocampal neurons.

The kinetics of the large-conductance Ca(2+)-activated K+ channel (235 pS in symmetrical 150 mM K+) were examined in the inside-out mode of the patch clamp technique. The open probability of the channel increased when [Ca2+]i, [Sr2+]i, or [Ba2+]i was increased. The [Ca2+]i-response relation was fitted with a Hill coefficient of 2 and half-maximum concentrations of 185, 80, 14.5, and 5.5 microM at -40, -20, +20, and +40 mV, respectively. The channel was blocked by TEA or Ba2+. The open-time histogram showed a single exponential component and the closed-time histogram showed at least two exponential components at various [Ca2+]i. Increasing [Ca2+]i decreased the time constant of the slow component of the closed-time histogram. Cell-attached patch recording revealed activation of the large-conductance Ca(2+)-activated K+ channel (BK channel) during the action potential. The deactivation time course was consistent with the fast after-hyperpolarization. A minimum model of the channel, close(2)-close(1)-open, where the transition from close(2) to close(1) requires the binding of 2 Ca2+, reconstructed quick activation of the channel if [Ca2+]i of 40 microM was assumed.

Action Potentials↗
PubMed1994

A calcium-activated potassium channel in growth plate chondrocytes: regulation by protein kinase A.

Single channel K+ currents were recorded from inside-out patches of membrane obtained from cultured chicken growth plate chondrocytes. With a symmetrical 140 mM concentration of K+ across the cell membrane, a large conductance (211 pS), outward-rectifying, K+ channel was identified. Opening of this channel was dependent on the presence of internal Ca2+ with half maximal activation of the channel occurring with 3 microM Ca2+. The channel was blocked by internal application of tetraethylammonium (IC50 = 45 mM) and 1 mM Ba2+. Application of the catalytic subunit of protein kinase A to the cytosolic membrane resulted in over a three-fold increase in the open probability for the channel. Thus, growth plate chondrocytes contain a large-conductance, Ca(2+)-activated K+ channel which can be up-regulated during stimulation of protein kinase A.

Adenosine Triphosphate↗
PubMed1995

Multiple ion binding sites in Ih channels of rod photoreceptors from tiger salamanders.

The mechanism of ion permeation in K+/Na(+)-permeable Ih channels of tiger salamander rod photoreceptors was investigated using the whole-cell voltage-clamp technique. Ih channels showed features indicative of pores with multiple ion binding sites: in mixtures of K+ and thallium (T1+), the amplitude of the time-dependent current showed an anomalous mole fraction dependence, and K+ permeation was blocked by other permeant ions (with K0.5 values: T1+, 44 microM; Rb+, 220 microM and NH4+, 1100 microM) as well as by essentially impermeant ions (Cs+, 22 microM Ba2+, 9200 microM) which apparently block Ih by binding in the pore. In contrast, Na+ had little blocking action on K+ permeation. The block by all of these ions was sensitive to external K+ with the block by Cs+ being the least sensitive. Na+ was more effective than K+ in reducing the block by T1+, Rb+ and NH4+, but was less effective for the block by Cs+ and Ba2+. The blocking action of Cs+ and Ba2+ was non-competitive, suggesting that they block Ih channels at independent sites. Based on the efficacy of block by the different ions, the degree to which K+ and Na+ antagonize this block and the noncompetitive blocking action of Cs+ and Ba2+, the permeation pathway of Ih channels appears to contain at least three ion binding sites with at least two sites having a higher affinity for K+ over Na+ and another site with a higher affinity for Na+ over K+.

Ambystoma↗
PubMed1988

Opioids excite rather than inhibit sensory neurons after chronic opioid exposure of spinal cord-ganglion cultures.

Tests were carried out to determine if the tolerance that develops in dorsal-horn network responses of mouse dorsal root ganglion (DRG)-spinal cord explants after chronic exposure to opioids could be accounted for by alterations in the excitability and pharmacologic properties of the afferent DRG cells. Intracellular recordings were made from DRG neurons in organotypic DRG-cord explants after chronic treatment with 1 microM D-Ala2-D-Leu5-enkephalin (DADLE) for greater than 4 days in vitro. Acute application of 10 microM DADLE shortened the duration of the Ca2+ component of the somatic action potential (APD) in only 5% of the treated neurons (4 out of 79 cells), in contrast to about 50% of the cells in naive explants (36 out of 74). Thus many DRG neuron perikarya became tolerant to the APD-shortening effects of DADLE. Furthermore, 77% of the treated DRG cells (61 out of 79) showed prolongation of the APD in response to an acute increase in DADLE concentration vs 34% in naive explants (25 out of 74). However, when the DADLE responsivity tests were carried out in the presence of multiple K+ channel blockers, only 20% of the treated DRG neurons showed APD prolongation (3 out of 15 cells), whereas 73% showed APD-shortening responses (11 out of 15 cells). The results suggest that: (1) DADLE-induced APD prolongation of the treated DRG neurons is mediated by opioid receptor subtypes that decrease a voltage-sensitive K+ conductance; (2) the DADLE-induced APD-shortening effects which are unmasked during more complete K+ channel blockade are mediated by opioid-receptor subtypes in the same neuron that reduce a voltage-sensitive Ca2+ conductance (resembling kappa receptors). DRG neurons did not become tolerant to either of these two opioid effects after chronic exposure to DADLE. Opioid shortening of the APD of DRG neuron perikarya has been generally accepted to be a model of opioid inhibition of calcium influx and transmitter release at presynaptic DRG terminals6,52,53,65,75,76. It is postulated that the opioid-induced APD prolongation observed in the present study provides evidence that opioids can also evoke direct excitatory effects on neurons. The enhancement of DADLE-induced excitatory responses and attenuation of DADLE-induced inhibitory responses of DRG neurons after chronic exposure to this opioid show striking similarities to the effects of forskolin or pertussis toxin treatment. These in vitro studies may provide clues to compensatory mechanisms underlying physiologic expression of tolerance to opioid analgesic effects in primary afferent synaptic networks.

Action Potentials↗
PubMed1991

Functional characterization of a minimal K+ channel expressed from a synthetic gene.

A gene for a slowly activating, voltage-dependent K(+) -selective channel was designed and synthesized on the basis of its known amino acid sequence. The synthetic gene was cloned into a transcription vector, and in vitro transcribed mRNA was injected into Xenopus oocytes for electrophysiological assay of the resulting ionic currents. The currents are voltage-dependent and highly selective for K+ over Na+. The selectivity among monovalent cations follows a familiar K(+)- channel sequence: K+ greater than Rb+ greater than NH4+ greater than Cs+ much greater than Na+, Li+. The currents are inhibited by Ba2+, Cs+, and tetraethylammonium (TEA), common pore blockers of K+ channels. Open-channel blockade by Cs+ (but not by Ba2+ or TEA) depends on applied voltage. The major inhibitory effect of Ba2+ is to alter channel gating by favoring the closed state; this effect is specific for Ba2+ and is relieved by external K+. The results argue that although the polypeptide expressed is very small for a eukaryotic ion channel, 130 amino acid residues in length, the ionic currents observed are indeed mediated by a genuine K(+) -channel protein. This synthetic gene is therefore well suited for a molecular analysis of the basic mechanisms of K(+) -channel function.

Amino Acid Sequence↗
PubMed1997

Improvement in specificity of [14C]d-xylose breath test for bacterial overgrowth.

The aim of the study was to determine whether the specificity of the [14C]d-xylose breath test could be improved, by excluding false-positive tests due to premature colonic metabolism of the [14C]d-xylose caused by rapid colonic transit. Forty-seven patients with suspected small bowel bacterial overgrowth were investigated by (1) aspiration and culture of duodenal fluid and (2) a [14C]d-xylose breath test. Those with either a positive duodenal culture or breath test had a repeat [14C]d-xylose breath test given with one of three transit markers (barium, Gastrografin or 99mTc-labeled tin colloid) to determine if the site of metabolism was in the small bowel or colon. Fourteen patients had positive duodenal cultures, four of whom had a negative [14C]d-xylose breath test, 15 patients had a positive [14C]d-xylose breath test, three of which were due to colonic metabolism of the xylose. Where transit markers were used, 14C was detectable in the breath and serum before barium had entered the small bowel, thus the barium did not comigrate with the xylose. Gastrografin accelerated small bowel transit, leading to malabsorption of the xylose in the small intestine and subsequent colonic metabolism of the xylose. 99mTc-labeled tin colloid had no obvious disadvantages and appeared to be the marker of choice. The use of a transit marker increased the specificity of the [14C]d-xylose breath test from 85% to 94%. The specificity of the [14C]d-xylose breath test for the detection of small bowel bacterial overgrowth is improved to greater than 90% by the use of an appropriate transit marker.

Bacteria↗
PubMed1994

Evidence that the S6 segment of the Shaker voltage-gated K+ channel comprises part of the pore.

Potassium channels are highly selective and allow the rapid flux of potassium ions through their pore. Several studies have implicated the H5 (P or SS1-SS2) segment as part of the pore in voltage-gated ion channels. The proposal that H5 spans at least 80% of the electric potential drop across the K+ channel pore is based on altered internal tetraethylammonium sensitivity arising from mutations of H5 residues that are 100% conserved among K+ channels having differing sensitivity to tetraethylammonium. Here we report that the S6 segment is also involved in K+ ion permeation and in governing the sensitivity to internal tetraethylammonium and barium. Transplanting the S6 segment of NGK2 into Shaker causes this S6 chimaera to adopt the single-channel conductance and sensitivity to internal tetraethylammonium and barium ions from the NGK2 channel. The differences between NGK2 and Shaker in external tetraethylammonium sensitivity, but not single-channel conductance, can be attributed to the differences in their H5 sequences. Three nonconserved S6 residues have been found to affect either single-channel conductance or internal tetraethylammonium sensitivity.

Amino Acid Sequence↗
PubMed2005

Emissions of organic compounds and trace metals in fine particulate matter from motor vehicles: a tunnel study in Houston, Texas.

Fine particulate matter (PM) samples collected in a highway tunnel in Houston, TX, were analyzed to quantify the concentrations of 14 n-alkanes, 12 polycyclic aromatic hydrocarbons, and nine petroleum biomarkers, as well as 21 metals, with the ultimate aim of identifying appropriate tracers for diesel engines. First, an exploratory multivariate dimensionality reduction technique called principal component analysis (PCA) was employed to identify all potential candidates for tracers. Next, emission indices were calculated to interpret PCA results physically. Emission indices of n-heneicosane, n-docosane, n-tricosane, n-tetracosane, n-pentacosane, fluoranthene, and pyrene were correlated highly and increased strongly with percentage carbon present in the tunnel emanating from diesel vehicles. This suggests that these organic compounds are useful molecular markers to separate emissions from diesel and gasoline engines. Additionally, the results are the first quantification of the metal composition of PM with aerodynamic diameters smaller than 2.5 microm (PM2.5) emissions from mobile sources in Houston. PCA of trace metal concentrations followed by emission index calculations revealed that barium in fine airborne particles can be linked quantitatively to diesel engine emissions, demonstrating its role as an elemental tracer for heavy-duty trucks.

Air Pollutants↗
PubMed1993

Different responses to acetylcholine in the presence of nitric oxide inhibitor in rat aortae and mesenteric arteries.

1. This study compared the relaxation induced by acetylcholine (ACh) in aortic and mesenteric arterial rings from Sprague-Dawley (SD) rats in the presence and absence of inhibitors of the known endothelium-derived relaxing factors. 2. ACh-induced relaxations were completely blocked by methylene blue and N omega-nitro-L-arginine (LNNA) in aortae, whereas these were only partially attenuated by methylene blue and LNNA in mesenteric arteries. 3. This methylene blue-resistant relaxation of ACh was partly attenuated by potassium channel blockers (tetraethylammonium and barium) but not affected by LNNA, indomethacin and calcium-free solution. 4. These results suggest that there may be another endothelial relaxing factor which is not nitric oxide (NO), prostanoids or endothelium-derived hyperpolarizing factor (EDHF) in mesenteric arteries but not in aortae. This unknown factor seems to be extracellular calcium ([Ca2+]0)-independent.

Acetylcholine↗
PubMed1991

Muscarinic receptor is coupled with a cation channel through a GTP-binding protein in guinea-pig chromaffin cells.

1. The ionic current evoked by muscarinic receptor agonists was investigated in dispersed chromaffin cells of the guinea-pig adrenal medulla using the whole-cell version of the patch-clamp procedure. 2. Muscarine or oxotremorine (0.03-10 microns) produced an inward current associated with an increase in current noise at a holding potential of -40 mV. The relationship between current and oxotremorine concentration fitted well to a rectangular hyperbole with an apparent dissociation constant (KA) of 0.23 micron. 3. The muscarinic antagonists pirenzepine (0.1 micronM) and AF-DX 116 (0.3 microM) shifted the dose-response curve to the right in a parallel manner. Dissociation constants (KB) for pirenzepine and AF-DX 116 were estimated to be 50 and 70 nM, respectively. 4. The current-voltage relation for the current induced by muscarine had a negative slope below -30 or -20 mV, and the current reversed its polarity at 0.4 +/- 0.8 mV (n = 4) in standard salt solution. Removal of Mg2+ or Ca2+ from the perfusate did not modify the muscarinic current-voltage relationship. 5. When Na+ in the bath solution was replaced with Tris, the muscarinic current-voltage relationship shifted to the left (the hyperpolarizing direction); the current reversed its polarity at -18.7 +/- 1.2 mV in a solution containing 72 mM-Na+ (three cells) and at -57.5 +/- 2.7 mV in nominally Na(+)-free solution (three cells). When Ca2+ was replaced by Mg2+, in Na(+)-free solution, an inward current was not evoked by muscarinic stimulation. 6. Tetraethylammonium (TEA; 0.03-3 mM) reduced the muscarinic current at -40 mV, and the KD value was 0.34 mM with a Hill coefficient of 1. Barium (4 mM) reduced the current to 0.69 +/- 0.06 of control (n = 3). 7. When the recording electrodes contained guanosine-5'-O-(3-thiophosphate) (GTP gamma S, 100 microM), an inward current developed at -55 mV during the first few minutes after breaking into the cell interior. This inward current was associated with an increase in noise and was not larger at -70 mV than at -55 mV; it reached a peak value about 3-4 min after breaking into the cell interior and then declined over the next 2-3 min. 8. Muscarinic agonists had no effect in those cells in which intracellular GTP gamma S had first evoked a transient inward current. The inward current caused by nicotine was unaffected by intracellular GTP gamma S.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Medulla↗
PubMed1995

Characterization of single potassium channels in mouse pancreatic acinar cells.

1. Single K(+)-selective channels with a conductance of about 48 pS (pipette, 145 mM KCl; bath, 140 mM NaCl + 4.7 mM KCl) were recorded in the patch-clamp whole-cell configuration in isolated mouse pancreatic acinar cells. 2. Neither application of the secretagogues acetylcholine (second messenger, inositol 1,4,5-trisphosphate) or secretin (second messenger, cAMP), nor addition of the catalytic subunit of protein kinase A to the pipette solution changed the activity of the 48 pS K+ channel. 3. Intracellular acidification with sodium propionate (20 mM) diminished activity of the 48 pS channel, whereas channel open probability was increased by cytosolic alkalization with 20 mM NH4Cl. 4. BaCl2 (5 mM), TEA (10 mM) or apamin (1 microM) added to the bath solution had no obvious effect on the kinetics of the 48 pS channel. Similarly, glibenclamide and diazoxide failed to influence the channel activity. 5. When extracellular NaCl was replaced by KCl, whole-cell recordings revealed an inwardly rectifying K+ current carried by a 17 pS K+ channel. 6. The inwardly rectifying K+ current was not pH dependent and could largely be blocked by Ba2+ but not by TEA. 7. Since the 48 pS K+ channel is neither Ca2+ nor cAMP regulated, we suggest that this channel could play a role in the maintenance of the negative cell resting potential.

Acetylcholine↗
PubMed2004

Visceral periadventitial adipose tissue regulates arterial tone of mesenteric arteries.

Periadventitial adipose tissue produces vasoactive substances that influence vascular contraction. Earlier studies addressed this issue in aorta, a vessel that does not contribute to peripheral vascular resistance. We tested the hypothesis that periadventitial adipose tissue modulates contraction of smaller arteries more relevant to blood pressure regulation. We studied mesenteric artery rings surrounded by periadventitial adipose tissue from adult male Sprague-Dawley rats. The contractile response to serotonin, phenylephrine, and endothelin I was markedly reduced in intact vessels compared with vessels without periadventitial fat. The contractile response to U46619 or depolarizing high K+-containing solutions (60 mmol/L) was similar in vessels with and without periadventitial fat. The K+ channel opener cromakalim induced relaxation of vessels precontracted by serotonin but not by U46619 or high K+-containing solutions (60 mmol/L), suggesting that K+ channels are involved. The intracellular membrane potential of smooth muscle cells was more hyperpolarized in intact vessels than in vessels without periadventitial fat. Both the anticontractile effect and membrane hyperpolarization of periadventitial fat were abolished by inhibition of delayed-rectifier K+ (K(v)) channels with 4-aminopyridine (2 mmol/L) or 3,4-diaminopyridine (1 mmol/L). Blocking other K+ channels with glibenclamide (3 micromol/L), apamin (1 micromol/L), iberiotoxin (100 nmol/L), tetraethylammonium ions (1 mmol/L), tetrapentylammonium ions (10 micromol/L), or Ba2+ (3 micromol/L) had no effect. Longitudinal removal of half the perivascular tissue reduced the anticontractile effect of fat by almost 50%, whereas removal of the endothelium had no effect. We suggest that visceral periadventitial adipose tissue controls mesenteric arterial tone by inducing vasorelaxation via K(v) channel activation in vascular smooth muscle cells.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

MR imaging of the gastrointestinal tract with i.v., gadolinium and diluted barium oral contrast media compared with unenhanced MR imaging and CT.

OBJECTIVE: To determine an optimal MR imaging technique and pulse sequence for evaluating mural and serosal disease of the gastrointestinal tract, we administered 2% oral barium sulfate and obtained fat-suppressed gadolinium-enhanced breath-hold fast multiplanar spoiled gradient-recalled (FMPSPGR) MR images. We then compared these images with spin-echo T1-weighted and T2-weighted fast spin-echo MR images and with CT images. SUBJECTS AND METHODS: Thirty-one patients with suspected diseases of the gastrointestinal tract were imaged with spin-echo T1-weighted, fast spin-echo T2-weighted, and fat-saturated gadolinium-enhanced FMPSPGR MR imaging. Before undergoing MR imaging, all patients received 1350 ml of 2% barium sulfate oral contrast media. For CT scans, patients received 120 ml of iodinated i.v. contrast material and 2% barium sulfate oral contrast material. CT and MR images were retrospectively and independently reviewed by two radiologists for ability to see normal bowel wall, for the presence of abnormal gastrointestinal tract mural thickening or enhancement, and for overall gastrointestinal tract visualization. Findings were correlated with surgical findings, endoscopy, and barium studies. RESULTS: Ten patients had benign disease, 16 had malignant gastrointestinal tract disease, and five had no gastrointestinal tract abnormalities. In 94% of patients, the gadolinium- and barium-enhanced FMPSPGR MR images were superior to CT and spin-echo MR sequences for depicting the wall of the normal bowel (p < .001). For the two observers, the FMPSPGR MR images with i.v. and oral contrast material were seen as revealing 94% and 95% of bowel segments with malignant or inflammatory mural thickening or serosal tumor. In comparison, CT revealed 64% and 72% (p < .01 and p < .0001, respectively), fast spin-echo T2-weighted MR images revealed 21% and 28% (p < .0001), and T1-weighted MR images revealed 17% and 18% (p < .0001). The gadolinium- and barium-enhanced MR images were preferred for overall gastrointestinal tract visualization in 65% of patients compared with 1% for CT scans (p < .001). In 32% of patients, the enhanced MR images were equivalent to CT images. CONCLUSION: MR evaluation of the gastrointestinal tract requires bowel distention with oral contrast material as well as motion reduction techniques, including glucagon and rapid gradient-echo pulses that allow breath-hold imaging. Fat-suppressed gadolinium-enhanced FMPSPGR MR imaging with diluted barium oral contrast media is effective for imaging benign and malignant mural and serosal abnormalities of the gastrointestinal tract.

Administration, Oral↗
PubMed1984

Regulation of cytosolic free calcium in rabbit proximal renal tubules.

The relative role of various Ca2+ transport systems in the regulation of Ca2+ cytosolic free Ca2+ concentration was evaluated using rabbit renal proximal tubules. Intracellular compartmentation was evaluated through Ca2+ releases induced by carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), A23187, and ruthenium red (RR) alone and in combination. In a Ca2+-free solution after 1 h of incubation, FCCP released 43 +/- 4%, A23187 54 +/- 3%, and RR 29 +/- 5% of total cellular Ca2+; in addition, RR inhibited the rate of FCCP-induced release, confirming its mitochondrial origin. In 1 mM Ca2+, the releases were 57 +/- 9%, 70 +/- 5%, and 34 +/- 10%, respectively. Therefore, the mitochondrial Ca2+ content is 20-60 nmol/mg of mitochondrial protein, sufficiently large to effectively buffer cell Ca2+. To evaluate the role of the plasma membrane Na:Ca exchanger, 10(-4) M ouabain was added and caused a slight decline in total cell Ca2+ content and no change in ionized Ca2+ measured by the null-point method, suggesting that the plasmalemmal Na+:Ca2+ exchanger does not play an important role in Ca2+ extrusion. Cytosolic free Ca2+ increased when 100 mM sodium was replaced with equimolar choline or tetramethylammonium. However, tetramethylammonium replacement released 55% of the mitochondrial Ca2+ content by increasing mitochondrial Ca2+ efflux without affecting the Ca2+ influx pathway. These results suggest that Na+ replacements in this tissue increase ionized Ca2+ by increasing mitochondrial Ca2+ efflux and not by inhibition of Na+:Ca2+ exchange at the plasma membrane.

Adenosine Triphosphate↗
PubMed1994

Developmental regulation of voltage-gated K+ channel and GABAA receptor expression in Bergmann glial cells.

Bergmann glial cells are closely associated with neurons: during development they provide guiding structures for migrating granule cells and in the adult cerebellum they display intimate interactions with Purkinje cells. In this study, we have addressed the question of whether such changes in neuronal-glial interactions during development are accompanied by variations in the membrane properties of Bergmann glial cells. We used a mouse cerebellum slice preparation to study membrane currents of the Bergmann glial cells at various stages of development in situ using the patch-clamp technique. The distinct morphology of Bergmann glial cells was revealed by Lucifer yellow injections during recording. While Bergmann glial cells in mice of postnatal day 20 (P20) to P30 have thick processes with arborized, irregularly shaped leaf-like appendages, the processes of cells from younger mice (P5-P7) are thinner and smoother. This morphological maturation is accompanied by a variation in voltage-gated currents. In cells from P5 to P7, delayed outward- and inward-rectifying K+ currents were recorded, while older Bergmann glial cells were characterized by, large, voltage- and time-independent K+ currents. In addition, application of GABA induces two effects, a rapid activation of a Cl- conductance and a longer-lasting decrease in the (resting) K+ conductance. Both effects were mediated by benzodiazepine-insensitive GABAA receptors. Responses in cells of P5-P7 mice were large as compared to the small or even undetectable responses in P20-P30 cells. These GABAA receptors were characterized immunohistochemically in mice and rat brain sections with five subunit-specific antibodies. Bergmann glial cells exhibit a distinct but transient immunoreactivity for the GABAA receptor alpha 2-, alpha 3-, and delta-subunits. Staining is maximal between P7 and P10 and decreases gradually thereafter. In contrast, antibodies to the alpha 1- and beta 2,3-subunits fail to decorate Bergmann glial cells, although they yield a prominent staining of both the Purkinje cells and the granule cells. These changes in the Bergmann glial cell membrane properties and GABAA receptor expression suggest a transition between functional states during development of the Bergmann glial cells.

Aging↗