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W X Shi

Publications and source records attributed to W X Shi.

At least 19 recordsLinked to original sources
PubMed2005

Identification of an HLA-B*07 allele variant (B*0740) in the Chinese Han population.

A novel HLA-B*07 allele, B*0740, has been identified by sequence-based typing (SBT) in the Chinese Han population. This new allele is identical to B*0705 and B*0706 for exons 2, 3, and 4, except for a single nucleotide at position 605 of codon 202 in exon 3 (AAG-->ATG) leading to an amino acid change from lysine to methionine. SBT was performed following allele separation using the Haploprep method. The serological equivalence of B*0740 to the B7 antigen did not change.

Alleles↗
PubMed2005

A novel HLA allele, DRB1*1609, identified in the Chinese Han population*.

A novel human leucocyte antigen-DRB1*16 (HLA-DRB1*16) allele (DRB1*1609) has been identified by sequencing-based typing (SBT) in Chinese Han population. This new allele has identical nucleotide sequence to DRB1*160101 in exon 2, except for a single-nucleotide substitution from A to T at position 127. This change leads to an amino acid change from tyrosine to phenylalanin at residue 47 (Y47F). SBT was performed for cloned DRB1*16-specific polymerase chain reaction fragment. The serological phenotype of DRB1*1609 is equivalent to DR16 antigen.

Alleles↗
PubMed2001

Dynamic modulation of NMDA-induced responses by ifenprodil in rat prefrontal cortex.

Ifenprodil is known to inhibit channel opening of NMDA receptors containing the NR2B subunit. However, it has also been shown to increase NMDA receptor affinity for glutamate-site agonists, including NMDA. The coexistence of the two opposing effects may explain why ifenprodil can either enhance or suppress an NMDA response depending on the level of NMDA binding and thus the NMDA concentration. Using whole cell recordings in rat prefrontal cortical slices, we report here that the effect of ifenprodil also depends on the speed and the direction of change of NMDA concentration. As shown previously, ifenprodil increased the inward current induced by low concentrations of NMDA applied through a local Y-tube perfusion system. However, the rising phase of the current was less enhanced compared to the falling phase. Increasing the speed of rising of NMDA concentration further reduced the enhancing effect of ifenprodil. When pressure ejection was used to produce even faster NMDA responses, the entire rising phase including the peak of the response was suppressed by ifenprodil, while the falling phase remained enhanced. These results are consistent with the suggestion that ifenprodil decreases both the association and dissociation rates of NMDA from NMDA receptors, and suggest that ifenprodil affects slow and fast NMDA responses in different manners. In particular, this study suggests that ifenprodil inhibits the rising phase of a fast NMDA response by suppressing both channel opening and the association of NMDA with NMDA receptors and that this inhibition can occur even when the level of NMDA binding is low.

Animals↗
PubMed2001

Anatomic basis of sequence-dependent predictability exhibited by nigral dopamine neuron firing patterns.

Interspike intervals (ISIs) of dopamine (DA) neurons recorded in the substantia nigra are predicted partially by their immediate prior history. This study was designed to assess neuroanatomic origins of these sequential relationships. ISI data recorded from three groups of nigral DA neurons were studied: 1) 16 neurons recorded in unlesioned animals, 2) 14 neurons recorded after forebrain hemisection, 3) 12 neurons recorded after partial forebrain hemisection that reproduced nonspecific effects of the surgical lesion while leaving forebrain connections intact. As predicted, DA neurons recorded after full forebrain hemisection yielded statistically significant reductions in sequential predictability relative to control neurons and neurons recorded following partial hemisection. These data support the hypothesis that the sequence-dependent behavior of DA neurons arise in part from interactions with forebrain structures. ISI sequences recorded from unlesioned rats demonstrated maximum predictability when an average of 3.7 prior events were incorporated into the forecasting algorithm, thereby suggesting a physiological process whose "depth" of history-dependence is approximately 600-800 msec. Additional studies examining the functional significance of sequence-dependent ISI structure exhibited by nigral DA neurons are indicated.

Action Potentials↗
PubMed2000

Dual effects of D-amphetamine on dopamine neurons mediated by dopamine and nondopamine receptors.

By increasing dopamine (DA) release and activating feedback mechanisms, amphetamine and related psychostimulants are known to inhibit DA cell firing. Here, we report that D-amphetamine also has an excitatory effect on DA cells, which under control conditions, is masked by the inhibitory effect of D-amphetamine and is revealed when D2-like receptors are blocked. Thus, using in vivo single-unit recording in rats, we found that the selective D2 antagonist raclopride not only blocked the inhibition induced by D-amphetamine but also enabled D-amphetamine to excite DA cells. The excitation, expressed as an increase in both firing rate and bursting, persisted when both D1- and D2-like receptors were blocked by SCH23390 and eticlopride, suggesting that it is not mediated by DA receptors. The norepinephrine uptake blocker nisoxetine mimicked the effect of D-amphetamine, especially the increase in bursting, whereas the 5-HT uptake blocker fluoxetine produced no significant effect. Adrenergic alpha1 antagonists prazosin and WB4101 and the nonselective alpha antagonist phenoxybenzamine completely blocked increase in bursting induced by D-amphetamine and partially blocked the increase in firing rate. The alpha2 antagonist idazoxan and the beta antagonist propranolole, however, failed to prevent D-amphetamine from producing the excitation. Thus, revising the traditional concept, this study suggests that D-amphetamine has two effects on DA cells, a DA-mediated inhibition and a non-DA-mediated excitation. The latter is mediated in part through adrenergic alpha1 receptors.

Action Potentials↗
PubMed2000

Endogenous DA-mediated feedback inhibition of DA neurons: involvement of both D(1)- and D(2)-like receptors.

To investigate the role of D(1)-like receptors in endogenous dopamine (DA)-mediated feedback control of DA neurons in vivo, single unit recordings were made from rat nigral DA cells using low cerveau isolé preparations. The D(2) antagonist raclopride, but not the D(1) antagonist SCH23390, increased baseline activity of DA neurons, suggesting that spontaneously released DA acts primarily through D(2)-like receptors to inhibit DA cells. However, feedback inhibition induced by an increased DA release by D-amphetamine (1 mg/kg, i.v.) was partially reversed by SCH23390. The same inhibition, on the other hand, was always completely reversed by raclopride, suggesting that the D(1)-mediated portion of the inhibition depends upon co-activation of D(2)-like receptors. In rats with forebrain hemitransections, D-amphetamine-induced inhibition was markedly decreased and the remaining inhibition was not blocked by SCH23390, supporting the suggestion that D(1)-D(2) co-activation-induced inhibition is mediated through long feedback pathways. In chloral hydrate-anesthetized rats, D-amphetamine-induced inhibition was also insensitive to SCH23390; however, the degree of the inhibition was not reduced. Combined with previous studies, these data suggest that chloral hydrate not only inactivates the D(1) feedback pathway but also enables the D(2) feedback pathway to operate independently of D(1)-like receptors. Conversely, in parkinsonian animals D(1) receptor activation alone has been reported to inhibit DA cells. Taken together, these results suggest that a major portion of endogenous DA-mediated feedback inhibition is due to concurrent activation of D(1)- and D(2)-like receptors. However, this D(1)-D(2) interdependence may alter under certain conditions and may play a role in the pathophysiology of Parkinson's disease.

Animals↗
PubMed2000

Enhancement of NMDA-induced current by the putative NR2B selective antagonist ifenprodil.

Ifenprodil has been widely used as an antagonist selective for NMDA receptors containing the NR2B subunit. Evidence suggests, however, that ifenprodil also increases NMDA receptor affinity. Using rat brain slices, we found that ifenprodil enhanced NMDA-induced current in both cortical and subcortical areas examined. To test whether the effect is due to an increase in NMDA receptor affinity, we compared the effect of ifenprodil on currents induced by different concentrations of NMDA. Consistent with the hypothesis, the enhancing effect (percent increase) was relatively constant at low NMDA concentrations. As NMDA concentration increased, however, the effect decreased. To test whether the effect is blocked when NMDA binding sites are saturated with NMDA, high concentrations of NMDA were applied. To partially block Ca(2+) influx and prevent cells from deteriorating, the experiments were performed in the presence of either MK801 or kynurenate, two noncompetitive antagonists. Under such conditions, ifenprodil not only failed to potentiate NMDA currents, but consistently suppressed the current. When the same concentration of NMDA was applied in the presence of the competitive antagonist CGP37849, ifenprodil regained its ability to potentiate NMDA currents. Furthermore, the higher the concentration of CGP37849 the more the NMDA current was potentiated by ifenprodil. These results, combined with previous studies, suggest that the enhancing effect is due to an increase in NMDA receptor affinity and is specific for responses induced by low NMDA concentrations. As NMDA concentration increases, the affinity-enhancing effect decreases. Consequently, the channel-suppressing effect becomes more prominent.

2-Amino-5-phosphonovalerate↗
PubMed1999

Opposite modulation of cortical N-methyl-D-aspartate receptor-mediated responses by low and high concentrations of dopamine.

To examine whether dopamine modulates cortical N-methyl-D-aspartate receptor-mediated glutamate transmission, whole-cell recordings were made from identified pyramidal cells located in layers V and VI of the medial prefrontal cortex of the rat using a slice preparation. In the presence of tetrodotoxin and the absence of Mg2+, a brief local application of N-methyl-D-aspartate evoked an inward current which was blocked by the N-methyl-D-aspartate antagonist dizocilpine maleate but not affected by the non-N-methyl-D-aspartate antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline, suggesting that the observed current is mediated by N-methyl-D-aspartate receptors located on recorded cells. Bath application of dopamine produced opposite effects on the N-methyl-D-aspartate current depending on the concentrations of dopamine applied. At low concentrations (<50 microM), dopamine enhanced the N-methyl-D-aspartate current, whereas at higher concentrations, dopamine suppressed the current. The same concentrations of dopamine did not significantly affect the inward current induced by the non-N-methyl-D-aspartate agonist alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid. The enhancing effect of dopamine on the N-methyl-D-aspartate response was mimicked by the D1 agonist SKF38393 and blocked by the D1 antagonist SCH31966, whereas the suppressing effect was mimicked by the D2 agonist quinpirole and blocked by the D2 antagonist eticlopride. The above results suggest that dopamine at low concentrations acts preferentially on D1-like receptors to promote N-methyl-D-aspartate receptor-mediated transmission, while at high concentrations dopamine also activates D2-like receptors, leading to a suppression of the N-methyl-D-aspartate function. This differential modulation of N-methyl-D-aspartate function may have significant implications for understanding behaviors and disorders involving both cortical dopamine- and glutamate-mediated neurotransmission.

1-Methyl-3-isobutylxanthine↗
PubMed1999

Dendritic glutamate-induced bursting in prefrontal pyramidal cells: role of NMDA and non-NMDA receptors.

AIM: To investigate whether in the prefrontal cortical (PFC) pyramidal cells, focal glutamate application to the apical dendrite induces bursting and whether the effect of glutamate involves activation of both NMDA and non-NMDA receptors. METHODS: Pyramidal cells in layers V and VI of the PFC were visualized in rat brain slices using infrared videomicroscopy and recorded with whole-cell electrodes. Glutamate and its agonists were focally applied to the apical dendrite and the soma using microiontophoresis. RESULTS: Dendritic glutamate application (0-20 nA, 10 mmol/L) induced repetitive bursts in most cells tested (12/17). In the same cells, somatic glutamate (5-20 nA, 10 mmol/L) induced only regular spiking. The bursting effect is likely to be direct since applications 5 microns away from the dendrite resulted in either a much reduced effect or no effect. Both CGP 37849 1 mumol/L and NBQX 1 mumol/L reduced the effect, suggesting an involvement of both NMDA and non-NMDA receptors. However, when non-NMDA receptors were selectively activated using AMPA (2-50 nA, 10 mmol/L), only regular spiking was observed. In contrast, selective NMDA receptor activation (NMDA 1.3-25 nA, 100 mmol/L) reliably induced bursting. CONCLUSION: In most PFC pyramidal cells tested, dendritic glutamate application induces repetitive bursting, whereas somatic glutamate application induces only regular spiking. Both NMDA and non-NMDA receptors are activated during dendritic glutamate application. However, bursting is primarily mediated by NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1998

Induction of sialic acid 9-O-acetylation by diverse gene products: implications for the expression cloning of sialic acid O-acetyltransferases.

Sialic acids can be modified by O-acetyl esters at the 7- and/or 9-position, altering recognition by antibodies, lectins and viruses. 9(7)-O-acetylation is mediated by a sialic acid-specific O-acetyltransferase, which has proven difficult to purify. Two groups have recently isolated cDNAs possibly encoding this enzyme, by expression cloning of human melanoma libraries in COS cells expressing the substrate ganglioside GD3. Pursuing a similar approach, we have isolated additional clones that can induce 9-O-acetylation. One clone present in a melanoma library encodes a fusion protein between a bacterial tetracycline resistance gene repressor and a sequence reported to be part of the P3 plasmid. Expression of the open reading frame is necessary for inducing 9-O-acetylation, indicating that this is not a reaction to the introduction of bacterial DNA. Another clone from a rat liver cDNA library induced 9-O-acetylation on COS cells expressing alpha2-6-linked sialic acids, and encodes an open reading frame identical to the Vitamin D binding protein. However, truncation at the 5' end eliminates the amino-terminal hydrophobic signal sequence, predicting cytosolic hyperexpression of a truncated protein. Thus, diverse types of cDNAs can indirectly induce sialic acid 9-O-acetylation in the COS cell system, raising the possibility that the real enzyme may be composed of multiple subunits which would not be amenable to expression cloning. Importantly, the cDNAs we isolated are highly specific in their ability to induce 9-O-acetylation either on alpha2-6-linked sialic acids of glycoproteins (truncated vitamin D binding protein) or on the alpha2-8-linked sialic acids of gangliosides (Tetrfusion protein). These data confirm our prior suggestion that a family of O-acetyltransferases with distinctive substrate specificities exists in mammalian systems.

Acetylation↗
PubMed1997

D1-D2 interaction in feedback control of midbrain dopamine neurons.

Dopamine (DA) D1-like receptors are present in pathways implicated in feedback control of midbrain DA neurons. However, stimulation of these receptors either produces no effect on DA cells, or the effect is inconsistent. It is possible that the expression of a D1 feedback effect requires co-activation of D2-like receptors. To test this hypothesis, we recorded extracellularly the spontaneous activity of nigral DA cells in a low cerveau isolé rat preparation. SKF38393 and dyhydrexidine, two D1 agonists, were administered systemically to animals pretreated with different doses of the D2 agonist quinpirole. Supporting the hypothesis, the two D1 agonists consistently inhibited DA cells in animals given high doses of quinpirole (>/=40 microg/kg, i.v.). However, no significant D1 effect was observed in animals pretreated with only low doses (</=20 microg/kg) of quinpirole. Because low doses of D2 agonists preferentially act on DA autoreceptors, and because the D1 inhibition persisted in animals whose DA autoreceptors were blocked by intranigral application of raclopride, our results suggest that the expression of D1 feedback inhibition requires co-activation of D2-like receptors on DA target neurons, instead of DA neurons themselves. These results, together with the finding that chloral hydrate completely blocked the D1 inhibition, may explain why previous studies have failed to show a consistent D1 effect on DA cells and suggest that drugs designed to act specifically on one subtype of DA receptor may, via feedback pathways, influence the action of endogenous DA on other DA receptor subtypes as well.

Anesthetics, Intravenous↗
PubMed1997

Characterization of dopamine-induced depolarization of prefrontal cortical neurons.

Dopamine (DA) has been reported to depolarize neurons in the prefrontal cortex (PFC). To further characterize this effect of DA, we made whole cell recordings from PFC pyramidal cells in rat brain slices. As reported previously, DA depolarized most PFC cells tested. This effect of DA was concentration-dependent and persisted in the presence of synaptic blockade, indicating a direct effect of DA on the recorded cell. During DA-induced depolarization, PFC neurons consistently showed an increase in excitability, suggesting that the depolarization is not directly related to DA-induced inhibition of PFC neurons previously observed in vivo. Surprisingly, the effect of DA was not mimicked or blocked by several commonly used DA agonists and DA antagonists. The alpha and beta antagonists phentolamine and alprenolol and the atypical antipsychotic drug clozapine also showed no significant effect on DA-induced depolarization. These results suggest that DA-induced depolarization may be mediated by a nonspecific mechanism. However, it remains possible that there exists a new type of DA receptors in the PFC not sensitive to classical DA agonists and antagonists, particularly given the fact that DA applied in the same manner depolarized only PFC neurons but not those in the striatum or the substantia nigra.

Animals↗
PubMed1996

Regulation of sialic acid 9-O-acetylation during the growth and differentiation of murine erythroleukemia cells.

Sialic acids are typically found at the terminal position on vertebrate oligosaccharides. They are sometimes modified by an O-acetyl ester at the 9-position, potentially altering recognition of sialic acid by antibodies, lectins, and viruses. 9-O-Acetylation is known to be selectively expressed on gangliosides in melanoma cells and on N-linked chains in hepatocytes. Using a recently developed probe, we show here that in murine erythroleukemia cells, this modification is selectively expressed on another class of oligosaccharides, O-linked chains carried on cell surface sialomucins. These cells also express 9-O-acetylation on the ganglioside GD3, but this modification appears to be undetectable on the cell surface. Increasing cell density in culture is associated with a decrease in cell surface 9-O-acetylation of sialomucins. This change correlates with the spontaneous differentiation toward a mature erythroid phenotype. This down-regulation upon differentiation and entry into the G0/G1 stage of the cell cycle is confirmed by differentiation-inducing agents. In contrast, cells arrested in G2/M by the microtubule depolymerizing agent nocodazole show increased expression of cell surface 9-O-acetylated sialomucins (but not the 9-O-acetylated ganglioside). However, the microtubule stabilizer taxol does not induce this increase, showing that the nocodazole effect is independent of cell cycle stage. Indeed, direct analysis showed no correlation of 9-O-acetylation with cell cycle stage in rapidly growing cells, and shorter treatments with nocodazole also increased expression. Western blots of cell extracts confirmed that changes caused by differentiation and nocodazole are not due to redistribution of molecules from the cell surface. Indeed, following selective removal of 9-O-acetyl groups from the cell surface by a specific esterase, the recovery of expression is mediated by new synthesis rather than by redistribution from an internal pool. Thus, 9-O-acetylation on these sialomucins appears to be primarily regulated by the rate of synthesis, and the increase with nocodazole treatment is likely due to the inhibition of turnover of cell surface molecules. These data show that 9-O-acetylation of sialic acids in murine erythroleukemia cells is a highly regulated modification, being selectively expressed in a cell type-specific manner on certain classes of oligosaccharides and differentially regulated with regard to subcellular localization and to the state of cellular differentiation.

Acetylation↗
PubMed1996

Sialic acid 9-O-acetylation on murine erythroleukemia cells affects complement activation, binding to I-type lectins, and tissue homing.

O-Acetylation of the 9-hydroxyl group of sialic acids has been suggested to modify various recognition phenomena involving these molecules, but direct proof has been lacking in most situations. In the accompanying paper (Shi, W.-X., Chammas, R., and Varki, A. (1996) J. Biol. Chem. 261, 31517-31525), we report that the extent of 9-O-acetylation of cell surface sialic acids on murine erythroleukemia (MEL) cells can be modified by various manipulations, including differentiation, nocodazole treatment, and 9-O-acetyl esterase treatment. We have used this system to explore the putative roles of 9-O-acetylation in modulating alternative pathway complement activation, I-type lectin binding, and tissue homing. MEL cells are shown to be sensitive to lysis in vitro by the alternative pathway of human complement. Induced differentiation of the MEL cells causes resistance to lysis, and this correlates directly with extent of decrease in 9-O-acetylation. A similar resistance to alternative pathway lysis can be obtained by selective enzymatic removal of 9-O-acetyl groups from sialic acids. Conversely, the increase in cell surface 9-O-acetylation caused by nocodazole treatment correlates with increased sensitivity to alternative pathway lysis. Thus, a 9-O-acetyl group added to the side chain of cell surface sialic acids may abrogate its normal function in restricting alternative pathway activation. Indeed, the binding of human complement factor H, a negative regulator of the alternative pathway, is shown to be blocked by O-acetylation of the sialic acids on MEL cells. MEL cells are also shown to have cell surface ligands for the I-type lectins sialoadhesin and CD22. Sialoadhesin (but not CD22) binding is selectively enhanced by differentiation-induced loss of cell surface 9-O-acetylation and by direct enzymatic removal of the ester groups. Thus, some sialoadhesin ligands are masked by 9-O-acetylation, presumably because the side chain is required for recognition. Since sialoadhesin is expressed on some macrophages in vivo, we reasoned that tissue homing of MEL cells might be affected by O-acetylation. Indeed, enzymatic removal of cell surface 9-O-acetyl groups alters the tissue distribution of intravenously injected cells. In particular, de-O-acetylation caused significant increase in homing to the liver and spleen. These data demonstrate that cell surface 9-O-acetylation can affect a variety of biological recognition phenomena and provide a system for further exploration of the specific molecular mechanisms involved.

Acetylation↗
PubMed1996

Chronic morphine induces visible changes in the morphology of mesolimbic dopamine neurons.

The mesolimbic dopamine system, which arises in the ventral tegmental area (VTA), is an important neural substrate for opiate reinforcement and addiction. Chronic exposure to opiates is known to produce biochemical adaptations in this brain region. We now show that these adaptations are associated with structural changes in VTA dopamine neurons. Individual VTA neurons in paraformaldehyde-fixed brain sections from control or morphine-treated rats were injected with the fluorescent dye Lucifer yellow. The identity of the injected cells as dopaminergic or nondopaminergic was determined by immunohistochemical labeling of the sections for tyrosine hydroxylase. Chronic morphine treatment resulted in a mean approximately 25% reduction in the area and perimeter of VTA dopamine neurons. This reduction in cell size was prevented by concomitant treatment of rats with naltrexone, an opioid receptor antagonist, as well as by intra-VTA infusion of brain-derived neurotrophic factor. In contrast, chronic morphine treatment did not alter the size of nondopaminergic neurons in the VTA, nor did it affect the total number of dopaminergic neurons in this brain region. The results of these studies provide direct evidence for structural alterations in VTA dopamine neurons as a consequence of chronic opiate exposure, which could contribute to changes in mesolimbic dopamine function associated with addiction.

Animals↗
PubMed1996

Linkage-specific action of endogenous sialic acid O-acetyltransferase in Chinese hamster ovary cells.

9-O-Acetylation of sialic acids shows cell type-specific and developmentally regulated expression in various systems. In a given cell type, O-acetylation can also be specific to a particular type of glycoconjugate. It is assumed that this regulation is achieved by control of expression of specific 9-O-acetyltransferases. However, it has been difficult to test this hypothesis, as these enzymes have so far proven intractable to purification or molecular cloning. During a cloning attempt, we discovered that while polyoma T antigen-positive Chinese hamster ovary cells (CHO-Tag cells) do not normally express cell-surface 9-O-acetylation, they do so when transiently transfected with a cDNA encoding the lactosamine-specific alpha2-6-sialyltransferase (Galbeta1-4GlcNAc:alpha2-6-sialyltransferase (ST6Gal I); formerly ST6N). This phenomenon is reproducible by stable expression of ST6Gal I in parental CHO cells, but not upon transfection of the competing lactosamine-specific alpha2-3-sialyltransferase (Galbeta1-(3)4GlcNAc:alpha2-3-sialyltransferase; (ST6Gal III) formerly ST3N) into either cell type. Further analyses of stably transfected parental CHO-K1 cells indicated that expression of the ST6Gal I gene causes selective 9-O-acetylation of alpha2-6-linked sialic acid residues on N-linked oligosaccharides. In a similar manner, while the alpha2-3-linked sialic acid residue of the endogenous GM3 ganglioside of CHO cells is not O-acetylated, transfection of an alpha2-8-sialyltransferase (GM3:alpha2-8-sialyltransferase (ST8Sia I); formerly GD3 synthase) caused expression of 9-O-acetylation of the alpha2-8-linked sialic acid residues of newly synthesized GD3. These data indicate either that linkage-specific sialic acid O-acetyltransferase(s) are constitutively expressed in CHO cells or that expression of these enzymes is secondarily induced upon expression of certain sialyltransferases. The former explanation is supported by a low level of background 9-O-acetylation found in parental CHO-K1 cells and by the finding that O-acetylation is not induced when the ST6Gal I or ST8Sia I cDNAs are overexpressed in SV40 T antigen-expressing primate (COS) cells. Taken together, these results indicate that expression of sialic acid 9-O-acetylation can be regulated by the action of specific sialyltransferases that alter the predominant linkage of the terminal sialic acids found on specific classes of glycoconjugates.

Acetyltransferases↗
PubMed1996

Effects of lesions in the medial prefrontal cortex on the activity of midbrain dopamine neurons.

To determine whether lesions in the prefrontal cortex (PFC) alter the activity of midbrain dopamine (DA) neurons, single unit recordings were made from DA neurons in control and lesioned rats. PFC lesions, obtained by local injection of ibotenic acid into the medial PFC, had no effect on either firing rate or bursting activity of DA neurons in the ventral tegmental area (VTA). However, the number of spontaneously active DA neurons in the VTA was significantly decreased. In the substantia nigra (SN), the same lesions increased the firing rate and had no effect on either the bursting activity of the number of active DA cells. These results suggest that PFC lesions alter the activity of DA neurons. However, VTA and SN DA neurons may respond differently to PFC lesions.

Animals↗