PubMed Health⌕ Search

Biomedical subjects

S L Patterson

Publications and source records attributed to S L Patterson.

15 recordsLinked to original sources
PubMed2001

Some forms of cAMP-mediated long-lasting potentiation are associated with release of BDNF and nuclear translocation of phospho-MAP kinase.

Long-lasting forms of synaptic plasticity like the late phase of LTP (L-LTP) typically require an elevation of cAMP, the recruitment of the cAMP-dependent protein kinase (PKA), and ultimately the activation of transcription and translation; some forms also require brain-derived neurotrophic factor (BDNF). Both cAMP and BDNF can activate mitogen-activated protein kinase (MAPK/ERK), which also plays a role in LTP. However, little is known about the mechanisms whereby cAMP, BDNF, and MAPK interact. We find that increases in cAMP can rapidly activate the BDNF receptor TrkB and induce BDNF-dependent long-lasting potentiation at the Schaffer collateral-CA1 synapse in hippocampus. Surprisingly, in these BDNF-dependent forms of potentiation, which are also MAPK dependent, TrkB activation is not critical for the activation of MAPK but instead appears to modulate the subcellular distribution and nuclear translocation of the activated MAPK.

Active Transport, Cell Nucleus↗
PubMed2001

A novel transverse push-pull microprobe: in vitro characterization and in vivo demonstration of the enzymatic production of adenosine in the spinal cord dorsal horn.

Adenosine produces analgesia in the spinal cord and can be formed extracellularly through enzymatic conversion of adenine nucleotides. A transverse push-pull microprobe was developed and characterized to sample extracellular adenosine concentrations of the dorsal horn of the rat spinal cord. Samples collected via this sampling technique reveal that AMP is converted to adenosine in the dorsal horn. This conversion is decreased by the ecto-5'-nucleotidase inhibitor, alpha,beta-methylene ADP. Related behavioral studies demonstrate that AMP administered directly to the spinal cord can reverse the secondary mechanical hyperalgesia characteristic of the intradermal capsaicin model of inflammatory pain. The specific adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT) inhibits the antihyperalgesia produced by AMP. This research introduces a novel microprobe that can be used as an adjunct sampling technique to microdialysis and push-pull cannulas. Furthermore, we conclude that AMP is converted to adenosine in the dorsal horn of the spinal cord by ecto-5'-nucleotidase and subsequently may be one source of adenosine, acting through adenosine A(1) receptors in the dorsal horn of the spinal cord, which produce antihyperalgesia.

5'-Nucleotidase↗
PubMed1999

Ultrastructural localization of full-length trkB immunoreactivity in rat hippocampus suggests multiple roles in modulating activity-dependent synaptic plasticity.

Neurotrophins acting at the trkB receptor have been shown to be important modulators of activity-dependent plasticity in the hippocampus, but the mechanisms underlying these effects are not yet well understood. To identify the cellular and subcellular targets of trkB ligands in the adult rat hippocampal formation, full-length trkB receptor immunoreactivity (trkB-IR) was localized using electron microscopy. trkB-IR was present in the glutamatergic pyramidal and granule cells. Labeling in these neurons appeared as discrete clusters and was primarily in axons, excitatory-type axon terminals, and dendritic spines and to a lesser extent in somata and dendritic shafts. trkB-IR was commonly found on the plasma membrane of dendritic spines, whereas in other subcellular regions trkB-IR was often intracellular. Labeling was strikingly dense within axon initial segments, suggesting extensive receptor trafficking. trkB-IR was not confined to pyramidal and granule cells. Dense trkB-IR was found in occasional interneuron axon initial segments, some axon terminals forming inhibitory-type synapses onto somata and dendritic shafts, and excitatory-type terminals likely to originate extrahippocampally. This suggests that trkB is contained in some GABAergic interneurons, neuromodulatory (e.g., cholinergic, dopaminergic, and noradrenergic) afferents, and/or glutamatergic afferents. These data indicate that full-length trkB receptor activation may modulate glutamatergic pathways of the trisynaptic circuit both presynaptically at axon terminals and initial segments and postsynaptically at dendritic spines and shafts. Signaling via catalytic trkB may also presynaptically affect inhibitory and modulatory neurons. A pan-trkB antibody labeled the same neuronal populations as the full-length-specific trkB antiserum, but the labels differed in density at various subcellular sites. These findings provide an ultrastructural foundation for further examining the mechanisms through which neurotrophins acting at trkB receptors contribute to synaptic plasticity.

Amino Acid Sequence↗
PubMed1996

Recombinant BDNF rescues deficits in basal synaptic transmission and hippocampal LTP in BDNF knockout mice.

Brain-derived neurotrophic factor (BDNF) is expressed at high levels in hippocampal neurons, and its expression is modulated by neural activity. Knockout mice can be used to study the roles of molecules like BDNF in synaptic plasticity with more molecular specificity than is possible using pharmacological approaches. Because in conventional knockouts the disrupted gene product is absent in all tissues throughout the life of the animal, developmental effects may complicate the interpretation of deficits in the adult. Rescue experiments can help to distinguish between developmental and acute requirements for the missing gene product. We here demonstrate that treatment of hippocampal slices from BDNF knockout mice with recombinant BDNF completely reverses deficits in long-term potentiation and significantly improves deficits in basal synaptic transmission at the Schaffer collateral-CA1 synapse. Thus, BDNF has an acute role in hippocampal synaptic function.

Animals↗
PubMed1996

Microbiologic assessment of the transabdominal ultrasound transducer head.

The objectives of this study were to determine (1) the rate of bacterial isolation from the abdomen of women having obstetric ultrasonography, (2) the rate of bacterial transmission to the transducer head, and (3) the eradication rate after routine wiping of the transducer head. A total of 191 obstetric patients participated in this study. At the start of each day, the transducer head and the coupling gel were cultured. Aerobic cultures were obtained from each patient's periumbilical and suprapubic areas before the transabdominal scan and from the transducer head before and after wiping off the gel with a dry cloth. Daily transducer head and gel cultures were negative. Of the abdominal skin cultures, 175 (92%) were positive; 35 (18%) were positive for serious organisms, and 140 (74%) were positive for organisms of low virulence. Sixty percent of the transducer head cultures from women with abdominal skin pathogens were positive before the gel was wiped off. None of the cultures from the transducer head were positive after removal of the gel. We conclude that many women carry potentially virulent pathogens on the abdominal skin and that transmission of these organisms to the transducer head commonly occurs. Physical removal of the gel from the transducer head effectively eradicates these microorganisms, minimizing patient-to-patient transmission.

Abdomen↗
PubMed1993

Nerve growth factor and a fibroblast growth factor-like neurotrophic activity in cerebrospinal fluid of brain injured human patients.

We report here the presence of nerve growth factor (NGF) in the cerebrospinal fluid (CSF) of some brain-injured human patients soon after injury. The NGF was quantified against a recombinant human NGF standard in a two-site enzyme-linked immunoabsorbent assay using antibodies against murine B NGF. None of the samples collected more than 2 days after injury contained detectable levels of NGF. When the CSF was assayed for the ability to promote neurite outgrowth from PC12 cells, neurite outgrowth was reduced, but not completely blocked, by antibodies to B NGF, suggesting that there were other biologically active factors present. Fibroblast growth factor (FGF) also promotes neurite outgrowth in PC12 cells. In an initial screening for the presence of FGF, we employed PC12 cells and NR119 cells, PC12 variants in which recombinant human B NGF, but not recombinant human basic FGF, promotes neurite outgrowth. CSF from brain injury patients promoted greater neurite outgrowth from PC12 cells than from NR119 cells, suggesting that some of the biological activity associated with the injury CSF may be due a FGF. This possibility is further supported by the observation that the biological activity of the injury CSF significantly reduced by batch absorption with heparin Sepharose, suggesting the presence of a heparin binding neurotrophic factor. Neurotrophic factors appear in CSF as a consequence of diverse types of brain injury, including head trauma, intracerebral hemorrhage and subarachnoid hemorrhage. The appearance of these factors may reflect important common elements in the complex series of cellular changes occurring in response to acute brain injury.

Adolescent↗
PubMed1992

Neurotrophin expression in rat hippocampal slices: a stimulus paradigm inducing LTP in CA1 evokes increases in BDNF and NT-3 mRNAs.

We report that stimulation inducing long-term potentiation (LTP) in the CA1 pyramidal cell layer of the hippocampus evokes significant increases in both BDNF and NT-3 mRNAs in CA1 neurons. No changes in BDNF or NT-3 mRNA levels were seen in the nonstimulated regions of the pyramidal cell layer or the dentate. No change was seen in the levels of NGF mRNA at the time point examined. These results suggest that relatively normal levels of activity may regulate region-specific neurotrophin levels in the hippocampus. Given that known effects of NGF (and presumably of BDNF and NT-3) include elevation of neurotransmitter levels, elevation of sodium channels, and promotion of axonal terminal sprouting, activity-associated changes in neurotrophin levels may play a role in regulating neural connections in the adult as well as the developing nervous system.

Animals↗
PubMed1991

Nerve growth factor receptor expression in the young and adult rat olfactory system.

Nerve growth factor (NGF) and its receptor (NGFR) are proteins that have a role in the normal development and survival of neurons in the peripheral and central nervous systems. During development, NGF is necessary for outgrowth of axons and establishment of synapses, and NGFR is the transmembrane protein that binds NGF and brings it into the cell. NGF and NGFR expression in the rat olfactory system have been studied previously, and age differences in NGFR are explored further in this study, using immunocytochemistry and immunoelectron microscopy to determine the changes in two different ages: postnatal day 5 and the adult. Dramatic differences were found in the distribution of NGFR immunoreactivity in the olfactory system of each of the two ages studied. Electron microscopy revealed that glial cells were responsible for this immunoreactivity.

Animals↗
PubMed1991

Universal precautions are not universally followed.

Adherence to universal blood and body fluid precautions was studied in surgical patient care areas of a university hospital in an effort to identify potentially hazardous health care personnel practices. Surgical teams of an 18-unit operating room, three surgical ward patient care teams, and patient care personnel in a 16-bed surgical intensive care unit were observed during routine patient care activities before (study 1) and after (study 2) specific educational programs were held to improve universal precaution compliance. Overall, infractions occurred in 57% of 549 observed procedures in study 1 and in 58% of 616 observed procedures in study 2. In study 1, infractions occurred in 75% of operating room procedures, 30% of surgical ward procedures, and 75% of surgical intensive care unit procedures. Study 2 procedure infraction rates were 81%, 32%, and 40%, respectively. Only surgical intensive care unit compliance significantly improved. Noncompliance with universal precautions occurs frequently during the care of patients who have undergone surgery, with the type of infraction and specific offender varying according to patient locale. These violations appear unamenable to one-time educational efforts. Substantial overall improvement may arise from ongoing educational programs directed at specific personnel who care for patients who have undergone surgery.

Blood↗
PubMed1991

Expression of nerve growth factor (NGF) receptors in the developing inner ear of chick and rat.

The expression of nerve growth factor receptors (NGFRs) was studied in the developing inner ear with in situ hybridization in chick embryos and with immunocytochemistry in rat embryos to determine sites of possible functions of NGF or NGF-like molecules in inner ear development. NGFR expression in the chick otocyst and acoustic ganglion is compared with epithelial differentiation and the onset of afferent innervation as determined with fluorescent carbocyanine tracers. In the inner ear of the chick embryo, NGFR mRNA expression shows an alternating pattern in mesenchymal and epithelial tissues. NGFR mRNA is heavily expressed in the mesenchyme surrounding the otocyst (E2-3), ceases at E3-5, and reappears in a thin layer of mesenchymal cells surrounding the membraneous epithelia (E5-13). In the otocyst epithelium, NGFR mRNA expression develops in one anterior and one posterior focus at E3-4.5. NGFR mRNA is expressed in the primordia of the ampullary cristae (E5-7) and possibly the anlage of the utricle; label transiently concentrates in the planum semilunatum of the cristae ampullares and in superior portions of the semicircular canals at E9, but is not seen in differentiating hair cells. In the acoustic ganglion, NGFR mRNA expression begins at E4; at the same time, the first peripheral acoustic nerve processes penetrate the otic epithelium (E4-4.5). The acoustic ganglia remain weakly NGFR mRNA-labeled in the posthatch animal. In the rat embryo, NGFR immunoreactivity is present in the auditory placode at E9, in the periotic mesenchyme at E9-10, and in the medial half of the otocyst at E10-11. At E12, epithelial NGFR expression becomes restricted anteriorly and posteriorly in a pattern similar to that of the chick otocyst and ceases at E13. NGFR immunoreactivity appears transiently in pillar cells of the cochlea in the third week of gestation. NGFR and NGFR mRNA is expressed after E11 in the acoustic ganglia. While NGFR transcripts are expressed in the cochlear ganglion cell bodies, NGFR protein becomes restricted to neuronal processes by the third week of gestation. The vestibular, but not the cochlear (spiral) ganglia remain NGFR-labeled in the adult rat. Onset of NGFR mRNA expression in the acoustic ganglion during the period of afferent fiber ingrowth into the otocyst epithelium is consistent with the hypothesis that NGF-like molecules may have a neurotrophic function for acoustic ganglion cells. Transient expression of NGFRs in secretory cells of the vestibular endorgan and pillar cells in the organ of Corti implicate a role for neurotrophins in the differentiation of these epithelial cell types.

Animals↗
PubMed1989

Thermoregulation in hypergravity-acclimated rats.

To determine the effect of hypergravity acclimation on thermoregulation, core temperature (Tc), tail temperature (Tt), and O2 consumption (VO2) were measured in control rats (raised at 1 G) and in rats acclimated to 2.1 G. When the animals were exposed to a low ambient temperature of 9 degrees C, concurrently with a hypergravic field of 2.1 G, Tc of rats raised at 1 G fell markedly by approximately 6 degrees C (to 30.8 +/- 0.6 degrees C) while that of the rats raised at 2.1 G remained relatively constant (falling only approximately 1 degree C to 36.4 +/- 0.3 degrees C). Thus prior acclimation to a 2.1-G field enabled rats to maintain Tc when cold exposed in a 2.1-G field. To maintain Tc, thermogenic mechanisms were successfully activated in the 2.1-G-acclimated rats as shown by measurements of VO2. In contrast, VO2 measurements showed that rats reared at 1 G and then cold exposed at 2.1 G did not activate thermogenic mechanisms sufficiently to prevent a fall in Tc. In other experiments, rats acclimated to either 1 or 2.1 G were found to lack the ability to maintain their Tc when exposed to a 5.8-G field or when exposed to prolonged cold exposure at 1 G. Results are interpreted as showing that when placed in a 2.1-G field, rats acclimated to 2.1 G can more closely maintain their Tc near 37 degrees C when cold exposed than can rats acclimated to 1 G. However, this enhanced regulatory ability of 2.1-G-acclimated rats over 1.0-G-acclimated rats is restricted to 2.1-G fields and is not observed in 1.0- and 5.8-G fields.

Adaptation, Physiological↗
PubMed1984

Hypnotic susceptibility and performance on various attention-specific cognitive tasks.

We conducted two experiments to investigate cognitive performance as related to level of hypnotic susceptibility. In Experiment 1 time-to-location of a target in a visual search task was assessed. For this task the letter Z was embedded either within straight-form or round-form letters. Results indicated that high-hypnotic-susceptibility subjects (highs) were significantly faster than low-susceptibility-subjects (lows) in locating the embedded letter. Experiment 2 investigated performance on single- and double-digit arithmetic (addition) problems as a function of hypnotic susceptibility level. Subjects were presented with arithmetic problems and were asked to complete them within a 60-s time period. Highs completed a significantly greater number of double-digit problems but not single-digit problems within this time frame than did lows. The results of the two experiments are explained in terms of the application of differing strategies or operations by highs and lows in the performance of cognitive tasks.

Attention↗