PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “IONTOPHORESIS”

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 685 records · Page 38Linked to original sources
PubMed1975

Iontophoresis of cyclic AMP.

The design, calibration, and operation of a source of controlled amounts of cyclic AMP (c-AMP) are described. Typically, 1.5 s pulses containing 10(10)-10(-12) molecules of c-AMP can be delivered to a region about 10 mum in diameter on an agar plate. The resulting concentration profiles are given as functions of distance and time. The diffusion coefficient of c-AMP in agar was measured to be 0.97 times 10(-5) cm2-s-1 at 21 degrees C.

Agar↗
PubMed1976

Characterization of drug iontophoresis with a fast microassay technique.

The iontophoretic release of drugs from micropipettes into free (Ringer's) solution was described using an ion-selective microelectrode assay method. This characterization, with a temporal resolution of 20 ms, showed that the equilibrium rate of drug transport was not linearly proportional to release current; the departure from linearity was increased by backing current and the result was demonstrated with analytically derived drug release functions. The general relation between the drug transport rate and release current was independent of the specific drug or pipette resistance; no functional relation was observed that might quantitatively predict this dependence without prior use of the assay. The diffusion coefficients at 25 degrees C in frog Ringer's of the drugs used in this study, all neuromuscular agonists, were determined: all values X 10(6) cm2/s; acetylcholine 6.11 +/- 0.30; carbamylcholine 7.44 +/- 0.34; 3-(m-hydroxyphenyl) prophyltrimethyl ammonium 5.79 +/- 0.13.

Acetylcholine↗
PubMed2002

Iontophoresis of lithium antagonizes noradrenergic action on prefrontal neurons of the rat.

Various lithium (Li(+)) compounds have been proven to be effective in the therapy of bipolar affective disorder, but their mechanism of pharmacological action is not clearly defined. In our present in vivo electrophysiological study we tested the action of microiontophoretically applied Li(+) and NE on the maintained firing activity of prefrontal cortical neurons of the rat. Target cells were located in the prelimbic cortical projection region (PrL) of the ascending norepinephrinergic pathway. Our data, collected from single unit activity of 59 PrL neurons, demonstrate that lithium can (1) suppress maintained discharge activity, or (2) antagonize both the inhibitory and excitatory modulation of firing activity elicited by NE. These effects of Li(+) were not replicable with GABA-initiated inhibition or glutamate analogue-initiated excitation of discharge activity. Our findings suggest that the action of Li(+) mainly targets the NE-coupled receptor mechanisms and, therefore, it may play an important role in stabilizing the modulation of discharge activity in the PFC caused by different extracellular levels of NE.

Adrenergic alpha-Agonists↗
PubMed1999

Modulation of striatal neuronal activity by glutamate and GABA: iontophoresis in awake, unrestrained rats.

To examine the effects of glutamate (GLU) and gamma-aminobutyric acid (GABA) and their interactions in the striatum under behaviorally relevant conditions, single-unit recording was combined with microiontophoresis in awake, unrestrained rats. Iontophoretically applied GLU (0-40 nA, 20 s) excited all spontaneously active neurons in dorsal (caudate-putamen) and ventral (accumbens, core) striatum; phasic GLU-induced excitations (mean threshold 19.7 nA) were dose-dependent, inversely correlated with rate of basal activity (excitation limit approximately 65 imp/s), and highly stable during repeated GLU applications. GLU also excited silent and sporadically active units, which greatly outnumbered spontaneously active cells, and enhanced neuronal excitations associated with movement. Both spontaneously active and GLU-stimulated striatal neurons were highly sensitive to GABA (0-40 nA, 20 s); most showed short-latency inhibitions during GABA diffusion from the pipette (0 nA) and the response quickly progressed to complete silence with a small increase in current. The GABA-induced inhibition was current-dependent, equally strong on spontaneously active and GLU-stimulated units, and independent of neuronal discharge rate, but less stable than the GLU-induced excitation during repeated drug applications. Prolonged GABA application (0-20 nA, 2-4 min) reduced basal impulse activity, but was less effective in attenuating the neuronal excitations induced by GLU or associated with movement. Our data support the role of GLU afferents in the phasic activation of striatal neurons and suggest that the effects of GLU strongly depend on the level of ongoing neuronal activity. The ability of GABA to modulate both basal and GLU-evoked activity suggests that GABA, released from efferent collaterals and interneurons, plays a critical role in regulating neuronal activity and responsiveness to phasic changes in excitatory input.

Action Potentials↗
PubMed1987

Quantification of angiotensin iontophoresis.

A method of value for studying the effects of angiotensin II (AII) and angiotensin III (AIII) on the brain is microiontophoresis combined with single unit recording. The purpose of this study was to quantitate the release of angiotensins under various experimental conditions thus providing a firm basis for the iontophoretic application of angiotensins. Quantification of release was accomplished by adding the appropriate [3H]angiotensin to 1 X 10(-3) M solutions of AII and AIII and then measuring the counts released from the tip of the microiontophoretic pipette in vitro into a small volume of Ringer solution. Although both AII and AIII were released by diffusion from micropipettes, this release could all but be eliminated with a retaining current of 20 nA. The release of AII and AIII was linear with respect to the amount of ejecting current applied up to 60 nA, the highest current examined. Angiotensin II at pH 4.5 and AIII at pH 3.5 were released at similar rates of 41.5 and 45.1 fmol/min/nA respectively. Raising the pH of the AII solution to 4.5 reduced the rate of release to 17.9 fmol/min/nA. Transport numbers were determined as follows: AII pH 3.5-0.115; AII pH 4.5-0.035, and AIII pH 4.5-0.145. It can be concluded that angiotensins are readily released by microiontophoresis, the response is linear with respect to application current, and that with the use of the appropriate pH the rate of release of AII and AIII are comparable.

Angiotensin II↗
PubMed1999

Structural parameters involved in the permeation of propranolol HCl by iontophoresis and enhancers.

The purpose of this work was to study the effect of iontophoretic transport of Propranolol hydrochloride on the lipidic organization of the stratum corneum pretreated under passive or iontophoretic conditions by two model penetration enhancers, sodium lauryl sulfate and hexadecyl trimethylammonium bromide. Characterization of human stratum corneum was performed by X-ray diffraction, attenuated total reflectance-Fourier transform infrared (ATR-FTIR) spectroscopy and differential scanning calorimetry (DSC). The structural properties were compared with the iontophoretic permeability of propranolol hydrochloride on human stratum corneum. The iontophoretic fluxes of propranolol hydrochloride were effectively increased by two-fold in stratum corneum pretreated with sodium lauryl sulfate. In contrast, they were halved in stratum corneum pretreated with hexadecyl trimethylammonium bromide. These results could be related to changes in the electrical and structural properties of the stratum corneum after incorporation of these enhancers.

Adrenergic beta-Antagonists↗
PubMed2002

Kinetics of the temperature rise within human stratum corneum during electroporation and pulsed high-voltage iontophoresis.

Electroporation is believed to be a nonthermal phenomenon at the membrane level. However, the effects of associated processes, such as Joule heating, should be considered. Because electroporation of skin, specifically the stratum corneum (SC), occurs at highly localized sites, the heating is expected to conform locally to the sites of electroporation. Significant localized heating was found to be strongly dependent on the voltage and duration of the high-voltage pulses. Specifically, a localized temperature rise was predicted theoretically and confirmed by experiments, with only a small rise (about 17 degrees C) for short, large pulses (1 ms, 100 V across the SC), but was increased (about 54 degrees C) for long, large pulses (300 ms, 60 V across the SC). The latter case appears to result in irreversible structural changes like vesicularization of the lipid lattice. These results support the hypothesis that electroporation occurs within the SC and that additional processes, such as localized heating, may be important.

Electrochemistry↗