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PubMed1998

Alterations in Ca2+ storage and mobilization in submandibular acinar cells of reserpine-treated rats.

The present study investigated the effects of the catecholamine-depleting drug reserpine on cellular Ca2+ storage and mobilization in rat submandibular acinar cells. Adult rats received seven daily injections of reserpine (0.5 mg/kg) and inositol 1,4,5-trisphosphate (IP3) formation and Ca2+ mobilization were measured in isolated submandibular acinar cells. Ultrastructural analysis demonstrated a significant reduction in rough endoplasmic reticulum (ER) and a dramatic accumulation of secretory granules in the cells of treated animals. Reserpine reduced acetylcholine (ACh)-stimulated IP3 formation by 46% and the initial increase in cytosolic Ca2+ concentration ([Ca2+]i) in response to ACh or thapsigargin was reduced by 21 and 56%, respectively. While norepinephrine (NE) did not induce significant IP3 formation, the [Ca2+]i response to NE was increased 360% by reserpine treatment. Reserpine treatment also enhanced the sustained [Ca2+]i increase following these stimuli. After stimulation with ACh or NE, exposure to ionomycin caused a further elevation in [Ca2+]i which was significantly larger in the cells of treated animals. After exposure to agonist + ionomycin, addition of monensin induced a third increase in [Ca2+]i which was significantly larger in cells of reserpine-treated animals. While capacitative Ca2+ entry was not altered, NE-activated Ca2+ influx was abolished after reserpine treatment. Reserpine treatment therefore alters IP3-sensitive and insensitive Ca2+ stores, non-capacitative Ca2+ influx and active Ca2+ transport in submandibular acinar cells of rats.

Acetylcholine↗

PubMed1992

Effects of PAF on excitatory neuro-effector transmission in dog airways.

1. Effects of PAF on excitatory neuro-effector transmission in smooth muscle cells of mucosa-free trachea and epithelium-intact bronchiole of the dog were investigated, by isometric tension recording, microelectrode and double sucrose-gap methods. 2. PAF (10(-11)-10(-7) M) dose-dependently enhanced the amplitude of contraction evoked by repetitive field stimulations (10 stimuli at 20 Hz) in both tracheal and bronchiolar tissues. At higher concentrations PAF (> 10(-8) M) increased the amplitude of contraction to a greater extent in the bronchiole than in the trachea. 3. In both muscle tissues, in parallel to the amplitude of contraction, PAF markedly enhanced the amplitude of excitatory junction potentials (e.j.ps) evoked by a single field stimulation in a dose-dependent manner, with no change in the resting membrane potential or input membrane resistance of the smooth muscle cells. PAF (5 x 10(-7) M) enhanced the amplitude of e.j.p. to a greater extent in the bronchiole than in the trachealis. In contrast, lyso-PAF (10(-10)-10(-7) M) showed no effect on e.j.p. amplitude in bronchiolar tissues. At a high concentration (10(-7) M) lyso-PAF slightly enhanced the e.j.p. amplitude in tracheal tissue, however the lyso-PAF induced stimulation of e.j.p. amplitude in the trachea was small compared to that of PAF. 4. PAF (10(-7) M) had no effect on the membrane depolarization induced by acetylcholine (ACh, 10(-9)-10(-5) M) and carbachol (10(-9)-10(-5) M) in tracheal smooth muscle cells. 5. The PAF-antagonists CV3988 (5 x i0-7 M) or WEB2086 (5 x 10-7 M) significantly enhanced the e.j.p. amplitude themselves, PAF (5 x 10-8 M) further enhanced the ej.p. amplitude in the presence of WEB2086 (5 x l0-7 M) but not CV3988 (5 x 10-7 M). In contrast, the new PAF-antagonist, E 6123(5 x l0-8 M), did not affect the ej.p. amplitude itself, and completely inhibited the increase in ej.p. amplitude caused by 5 x 10-8 M PAF. On the other hand, in the presence of the Hi-antagonist,mepyramine, PAF (5 X 10-8 M) further enhanced the ej.p. amplitude.6. The leukotriene synthesis inhibitor AA-861 (10-6 M) or leukotriene antagonist ONO1078 (10-7 M)inhibited the increase in ej.p. amplitude caused by 5 X 10-8 M PAF, respectively.7. In the presence of AA-861 (10-6 M), leukotriene B4 (LTB4, 10-' M) or LTD4 (10-8 M) slightly, and LTC4 (10- M) markedly enhanced the ej.p. amplitude. In contrast, LTE4 (10-8 M) significantly suppressed the e.j.p. amplitude.8. PAF (5 x 10-8 M) attenuated the depression phenomena of ej.ps observed during double stimulus experiments at different time intervals (5-10 s), but had no effect on the summation of ej.ps during repetitive field stimulation at a high frequency (20 Hz) in the trachealis.9. These results indicate that PAF potentiates excitatory neuro-effector transmission mainly through stimulating the release of lipoxygenase products, mainly LTC4 in the dog airway smooth muscle tissues.

Acetylcholine↗

PubMed1989

Effects of verapamil on reoxygenation and programmed electrical stimulation-induced ventricular arrhythmias in the isolated heart.

The antiarrhythmic effect of verapamil was tested on spontaneous ventricular arrhythmias during reoxygenation after 15 min of glucose-free hypoxia and on programmed electrical stimulation-(8 stimuli + 1 or 2 extrastimuli) induced ventricular fibrillation in isolated Langendorff perfused guinea pig hearts. Verapamil (1 mg/l) added during hypoxia and reoxygenation significantly reduced, during reoxygenation, the incidence of arrhythmias (46%, N = 13 vs. controls 87%, N = 30; P less than 0.01), of ventricular fibrillation (0%, N = 13 vs. controls 70%, N = 30; P less than 0.001) and of programmed stimulation-induced ventricular fibrillation (0%, N = 10 vs. controls 100%, N = 16). No effect was observed on programmed stimulation-induced ventricular fibrillation during hypoxia (90%, N = 10 vs. controls 100%, N = 10). Verapamil added during reoxygenation reduced the incidence of reoxygenation arrhythmias and ventricular fibrillation (47% and 29%, N = 17, P less than 0.01 and P less than 0.05 vs. controls, respectively) but it had no effect on programmed stimulation-induced ventricular fibrillation (100%, N = 10). It is likely that verapamil exerts its antiarrhythmic effect by preventing cellular calcium overload during hypoxia and reoxygenation.

Animals↗

PubMed1987

Field sampling of unfed adults of Amblyomma hebraeum Koch.

No methods have previously been available for the field sampling of unfed adults of Amblyomma hebraeum. We released 2000 unfed adults into a 5-m2 area in mopane woodland in southeastern Zimbabwe. The ticks sought shelter beneath the debris on the soil surface but emerged and became active in host seeking when stimulated. Effective stimuli were the odours of cattle and sheep and high concentrations of carbon dioxide from dry ice. The ticks did not respond to low concentrations of carbon dioxide, vibrations generated by stamping the ground with poles, or two volatile components of ox breath known to attract tsetse flies. The presence of humans in the release area also had little or no effect in stimulating the ticks. As adults of A. hebraeum are large and conspicuous they can easily be collected from the soil surface, either manually or using a vacuum device, after stimulation by cattle or the release of high concentrations of carbon dioxide.

Animals↗

PubMed2004

Decreased sensory neuropeptide release in isolated bronchi of rats with cisplatin-induced neuropathy.

We studied if attenuated neurogenic bronchoconstriction was associated with a change in sensory neuropeptide release in preparations from rats with cisplatin-induced neuropathy. Electrical field stimulation (100 stimuli, 20 V, 0.1 ms, 20 Hz) induced an increase in the release of somatostatin, calcitonin gene-related peptide (CGRP) and substance P determined by radioimmunoassay from baseline 0.18+/-0.01, 0.17+/-0.01 and 0.86+/-0.02, to 0.59+/-0.02, 1.77+/-0.04 and 5.96 fmol/mg wet tissue weight, respectively, in organ fluid of tracheal tubes from rats. This was significantly attenuated to post-stimulation values of 0.36+/-0.02, 0.45+/-0.02, 4.68+/-0.24 fmol/mg wet tissue weight for somatostatin, CGRP, and substance P, respectively, with a significant decrease in field stimulation-induced contraction of bronchial preparations from animals 11 days after a 5-day treatment period with cisplatin (1.5 mg/kg i.p. once a day). The cisplatin-treated animals developed sensory neuropathy characterized by a 40% decrease in femoral nerve conduction velocity. The results show that a decrease in tracheo-bronchial sensory neuropeptide release associates with feeble bronchomotor responses in rats with cisplatin-induced sensory neuropathy.

Animals↗

PubMed1992

Spontaneous and evoked activity of the caudate neurons to central and peripheral stimuli after brain lesions.

The involvement of the cerebral cortex, commissural fibers and thalamus on caudate-caudate relations was studied in locally anesthetized, paralysed and artificially ventilated cats. This type of experimental preparation was necessary since a complete suppression of spontaneous and evoked activity is produced by subanesthetic doses of general anesthesia. Two types of caudate action potentials were encountered on the basis of their waveform characteristics: biphasic and triphasic spikes, the former being the largest population (80%). These waveforms were independent of the microelectrode resistance and the distance to recorded neurons. However, their responses were very similar to both central and peripheral stimuli. Caudate stimulation depressed the spontaneous discharges of the majority of the responsive units recorded within the opposite nucleus, while striatal neurons were activated by stimulation of the contralateral cortex. Decortication, thalamic lesion (motor nuclei and massa intermedia) and section of the corpus callosum decrease the firing rates of caudate neurons with biphasic spikes, while the discharges of the neurons with triphasic action potentials remained unchanged. Bilateral ablation of the cerebral cortex decreased the responsiveness of striatal neurons to contralateral nucleus and sciatic nerve and reduced the number of spontaneously active cells per recording tract. Section of the commissural fibers also depressed the caudate responses to the contralateral nucleus, and to the opposite precruciate cortex, although thalamic lesion did not affect the responsiveness of caudate cells to both central and peripheral stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed2000

[Physiology and methods for studying the baroreceptor reflex].

The baroreflex is of major importance for the moment-to-moment maintenance of arterial pressure particularly during orthostatic stress. Blood pressure increase stimulates the receptors e.g. in the carotid sinuses and the aortic arch, and rapidly increases the receptor discharge rate. Blood pressure decrease induces arrest of impulse transmission to the nucleus of the solitary tract. The impulses are modulated by the nucleus ambiguous, the rostral ventrolateral medulla, the dorsal nucleus of the vagus nerve, parabrachial and paraventricular nuclei and other central structures. Blood pressure increase induces an increase of cardiovagal activity resulting in cardiodeceleration and a decrease of sympathetic peripheral vasoconstrictor outflow. The receptor firing rates show adaptation and resetting to longer lasting blood pressure changes, hysteresis, i.e. firing rates that are higher with rapid blood pressure increase than during the return to baseline pressure. The receptors interact with respiration, chemoreceptor stimulation, central stimuli, exercise and sleep, etc. Baroreceptor function and interaction e.g. with chemoreceptors is compromised in diseases such as diabetic autonomic neuropathy. Guillain-Barré syndrome, arterial hypertension, heart failure and probably in most stroke patients. Fatal complications may result from baroreceptor malfunction. Subtle analysis of the baroreflex is therefore crucial for a refined pathophysiological understanding of these diseases. Pharmacological testing and "neck chamber" negative pressure stimulation of the receptors are as useful as the non-invasive computerized analysis of the interaction of spontaneous blood pressure and heart rate fluctuations.

Aorta, Thoracic↗

PubMed1999

Hemodynamics evoked by microelectrical direct stimulation in rat somatosensory cortex.

The aim of this study was to estimate the timing (latency) of the increase in red blood cell (RBC) velocity and RBC concentration, and the magnitude of response in local cerebral blood flow (LCBF) for neuronal activation. We measured LCBF change during activation of the somatosensory cortex by direct microelectrical stimulation. Electrical stimuli of 5, 10 and 50 Hz of 1 ms pulse with 10-15 microA, were given for 5 s. LCBF, RBC velocity and RBC concentration were monitored by laser-Doppler flowmetry (LDF) in alpha-chloralose anesthetized rats (n = 7). LCBF, RBC velocity and RBC concentration increased nearly proportionally to stimulus frequency, i.e. neuronal activity. LCBF rose approximately 0.5 s after the onset of stimulation, and there was no significant time lag of the latencies among LCBF, RBC velocity and RBC concentration at the same stimulus frequency. We interpret these results to mean that the onset of LCBF increase on cortical activation is reflected by a rapid change in arteriole (resistance vessel) dilation and capillary volume. The data also elucidate the linear relationship between LCBF increase and cortical activity.

Animals↗

PubMed1992

Involvement of cyclic GMP in non-adrenergic, non-cholinergic inhibitory neurotransmission in dog proximal colon.

1. Nitric oxide (NO) may serve as a non-adrenergic, non-cholinergic (NANC) neurotransmitter released from enteric inhibitory nerves in the gastrointestinal tract. We tested whether guanosine 3':5'-cyclic monophosphate (cyclic GMP) may serve as a second messenger in transducing the NO signal into inhibitory junction potentials (i.j.ps) and relaxation in the canine proximal colon. 2. The membrane permeable analogue of cyclic GMP, 8-bromo cyclic GMP (8-Br-cyclic GMP) mimicked the effects of NO by hyperpolarizing cells near the myenteric border of the circular muscle layer and shortening slow waves in cells near the submucosal surface of the circular muscle layer. 8-Br-cGMP also inhibited spontaneous phasic contractions. 3. The specific cyclic GMP phosphodiesterase inhibitor, M&B 22948, hyperpolarized cells near the myenteric border and prolonged the duration of i.j.ps. M&B 22948 also inhibited phasic contractile activity. 4. Methylene blue failed to reduce significantly the amplitude and duration of i.j.ps and had variable effects on contractions. 5. Cyclic GMP levels were assayed in unstimulated muscles and in muscles exposed to exogenous NO and electrical field stimulation. Both stimuli hyperpolarized membrane potential, inhibited contractions, and elevated cyclic GMP levels. 6. Treatment of muscles with L-NG-nitroarginine methyl ester (L-NAME) increased spontaneous contractile activity and lowered cyclic GMP levels. The inhibitory effect of M&B 22948 on contractions was greatly reduced after muscles were treated with L-NAME. 7. These data support the concept that the effects of NANC nerve stimulation and NO (which may be one of the enteric inhibitory transmitters) may be mediated by cyclic GMP.

3',5'-Cyclic-GMP Phosphodiesterases↗

PubMed1999

Implanted functional electrical stimulation system for mobility in paraplegia: a follow-up case report.

A 16-channel functional electrical stimulation (FES) system has been implanted in a person with T10 paraplegia for over a year. The system consists of two eight-channel radio frequency controlled receiver-stimulators delivering stimuli through a network of 14 epimysial and two intramuscular electrodes. Using this system and a walker for support, the subject was able to stand up for 8 min and walk regularly for 20 m. The standing duration was limited by arm fatigue since upper extremities supported an average of 25% of body weight. This was due to suboptimal hip extension and some undesired recruitment of rectus femoris and sartorius with stimulation of quadriceps electrodes. The left quadriceps exhibited rapid fatigue that limited walking distance and duration. The metabolic energy requirements were well within the aerobic limits of the sedentary paraplegic population. At one-year follow-up evaluation all electrodes are functional except one intramuscular electrode. The implant caused no adverse physiological effects and the individual reported health benefits such as increased energy and overall fitness as a result of the FES system use. With further improvements in muscle response through innovative surgical techniques, the 16-channel implanted FES system can be a viable addition to exercise and mobility function in persons with paraplegia.

Adult↗

PubMed1989

Catecholaminergic projections to tuberoinfundibular neurones of the paraventricular nucleus: I. Effects of stimulation of A1, A2, A6 and C2 cell groups.

Extracellular electrical activity was recorded from 203 paraventricular nucleus (PVN) neurones antidromically identified as projecting to the median eminence. Spontaneous activity and the effects of stimulation of the A1, A2, A6 and C2 catecholaminergic cell groups upon the PVN neurones were examined. Cells were located at a mean height 2.29 +/- 0.03 mm above the base of the brain, corresponding with the corticotropin-releasing factor (CRF) rich component of the nucleus. The mean firing rate was 3.2 +/- 0.3 Hz and antidromic invasion latency was 9.9 +/- 0.3 msec. Seventy-six % of cells tested were activated by painful somatosensory stimuli. Electrical stimulation of the A1 or A2 region evoked excitatory responses from the majority of cells tested (76% and 85%, respectively), whilst stimulation of the A6 and C2 regions evoked more inhibitory responses (43% and 59%, respectively). Most responses (56%), whether excitatory or inhibitory, were not clearly defined in terms of latency, and were only observed following delivery of 5-10 single shocks at 0.5 Hz. Excitation recorded following A1 and A2 stimulation suggests a facilitatory role for noradrenaline in the regulation of PVN activity. Inhibitory responses following C2 stimulation indicate that adrenaline may serve to inhibit such activity, whilst the more mixed responses following A6 stimulation suggest that the projections of this region differ in some way from those of the A1 and A2 cells. Response reversals were observed, after delivery of higher frequency stimulation, for a substantial proportion (20%) of the cells tested.

Action Potentials↗

PubMed2001

Influence of fear conditioning on elicited ponto-geniculo-occipital waves and rapid eye movement sleep.

The amygdala plays a central role in fear conditioning, a model of anticipatory anxiety. It has massive projections to brainstem regions involved in rapid eye movement sleep (REM) and ponto-geniculo-occipital (PGO) wave generation. PGO waves occur spontaneously in REM or in response to stimuli. Electrical stimulation of the central nucleus of the amygdala enhances spontaneous PGO wave activity during REM and the amplitude of both the acoustic startle response and the elicited PGO wave (PGOE), a neural marker of alerting. This study examined the effects of fear conditioning on REM and on PGOE. On conditioning days, the number of REM episodes, the average REM duration and the REM percentage were decreased while REM latency was increased. The presentation of auditory stimuli in the presence of a light conditioned stimulus produced PGOE of greater amplitudes. The results suggest that fear, most likely involving the amygdala, can influence REM and brainstem alerting mechanisms.

Amygdala↗

PubMed2000

Effects of caloric stimulation on respiratory frequency and heart rate and blood pressure variability.

Heart rate variability (HRV), blood pressure variability (BPV) and respiratory frequency were measured by power spectrum techniques in six normal humans (25-34 years old) and one labyrinthine-defective patient (33 years old) during cold (30 degrees ) vestibular caloric stimulation. Caloric stimuli were delivered intermittently for 2 min, under two different breathing conditions: (1) spontaneous breathing and (2) breathing paced with a metronome (0.25 Hz). During the spontaneous breathing condition, in the normal subjects, the caloric stimuli induced a significant increase in the absolute magnitude of the power spectrum density of the high frequency component (0.15-0. 40 Hz) of HRV and the total bandwidth (0.04-0.4 Hz) of mean BPV. These responses were related to a shift in the weighted average of the respiration frequency on the respiration spectrum, from a median value of 0.27 Hz (range, 0.17-0.29 Hz) during baseline to 0.31 Hz (0. 26-0.31 Hz) following caloric stimulation. This change was not observed in the labyrinthine-defective patient, who had weighted averages of 0.37 Hz and 0.34 Hz, respectively. No significant changes in the normalised units of the low frequency component (0. 04-0.15 Hz) or the high frequency component (0.04-0.4 Hz) of HRV and BPV were observed. During the paced breathing condition, no consistent effect on HRV or BPV was evident. For both breathing conditions, the proportions of HRV and BPV power linearly independent from respiration did not show any caloric-induced change. This study shows that caloric vestibular stimulation produces changes in HRV and BPV by modifying the respiratory pattern.

Adult↗

PubMed1995

Effects of electrical stimulation of the central nucleus of the amygdala on the in vivo electrophysiological activity of rat nigral dopaminergic neurons.

The central nucleus of the amygdala (CeA) receives a dopaminergic (DA) innervation from the midbrain. Among its many efferent projections, the CeA innervates the substantia nigra. The possibility that the CeA influences the activity of nigral DA neurons was evaluated. The effects of electrical stimulation of the CeA on the firing rate and pattern of nigral DA neurons were investigated in anesthetized rats. Poststimulus time histograms revealed that nigral DA cells were either inhibited (N = 15), excited (N = 13), or unresponsive (N = 17) to CeA stimulation (250 stimuli at 0.5 Hz). The mean (+/- SEM) latency to inhibition (24 +/- 9 msec) was significantly shorter than that for excitation (65 +/- 10 msec); the duration of inhibition (200 +/- 29 msec) was also significantly greater than the duration of excitation (86 +/- 11 msec) (P < 0.01 for both). DA cells that were excited had basal firing rates significantly lower than those of the inhibited or unresponsive cells (P < 0.05). Preliminary data suggest that DA cell burst-firing increases or decreases, respectively, in association with stimulation-evoked increases or decreases in firing rate. The relatively long latencies for stimulation-evoked responses suggest that CeA projection neurons indirectly affect nigral DA neurons via polysynaptic pathways. These results demonstrate that the CeA has the ability to influence the activity of nigral DA neurons, consistent with the putative role of the CeA as an interface between the limbic and extrapyramidal systems. Given the crucial role of the amygdala in anxiety states, these findings suggest that DA cell function may also be affected in such disorders.

Action Potentials↗

PubMed1990

[Hormonal control of lactation].

We studied the mechanism of normal lactation, especially the roles of prolactin (PRL) and oxytocin (OXT) in the initiation of lactation, the lactation in the women complicated with endocrinological disorders, and medical therapies for stimulation and suppression of lactation. The level of serum PRL increases as pregnancy progresses, and reaches to a peak on the day of delivery. Despite high PRL level, milk secretion does not appear during pregnancy, because the sex steroid hormones suppress binding of PRL to the receptor in the mammary gland. The initiation of milk secretion in puerperal women seems to be closely related to an increase in PRL levels induced by adequate suckling. In the mechanism of suckling-induced PRL increase, OXT from posterior pituitary seems to have an important role. Furthermore, the poor response of PRL to suckling was due to insufficient stimulation to the nipples by suckling because the size of nipples were relatively small in these mothers. The other mechanism involved in lactation is suckling-induced OXT secretion. OXT stimulates milk ejection. Anxiety or fear may inhibit the OXT release. We demonstrated that the number of pulsatile release of OXT by nursing was significantly decreased by the psychological stress induced by mental calculation. In the puerperal women with prolactinomas after surgery, the serum PRL level did not increase during pregnancy and milk secretion in puerperium was poor. In the puerperal women with diabetes mellitus, milk secretion was also poor. One of the causes may be related to the low PRL response to suckling stimuli. PRL stimulates milk yield in the mammary gland, but is not commercially available.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗

PubMed1985

Visceral nociception: peripheral and central aspects of visceral nociceptive systems.

Discomfort and pain are the sensations most commonly evoked from viscera. Most nociceptive signals that originate from visceral organs reach the central nervous system (c.n.s.) via afferent fibres in sympathetic nerves, whereas parasympathetic nerves contain mainly those visceral afferent fibres concerned with the non-sensory aspects of visceral afferent function. Noxious stimulation of viscera activates a variety of specific and non-specific receptors, the vast majority of which are connected to unmyelinated afferent fibres. Studies on the mechanisms of visceral sensation can thus provide information on the more general functions of unmyelinated afferent fibres. Specific visceral nociceptors have been found in the heart, lungs, testes and biliary system, whereas noxious stimulation of the gastro-intestinal tract appears to be detected mainly by non-specific visceral receptors that use an intensity-encoding mechanism. Visceral nociceptive messages are conveyed to the spinal cord by relatively few visceral afferent fibres which activate many central neurons by extensive functional divergence through polysynaptic pathways. Impulses in visceral afferent fibres excite spinal cord neurons also driven by somatic inputs from the corresponding dermatome (viscero-somatic neurons). Noxious intensities of visceral stimulation are needed to activate viscero-somatic neurons, most of which can also be excited by noxious stimulation of their somatic receptive fields. The visceral input to some viscero-somatic neurons in the spinal cord can be mediated via long supraspinal loops. Pathways of projection of viscero-somatic neurons include the spino-reticular and spino-thalamic tracts. All these findings give experimental support to the 'convergence-projection' theory of referred visceral pain. Visceral pain is the consequence of the diffuse activation of somato-sensory nociceptive systems in a manner that prevents accurate spatial discrimination or localization of the stimuli. Noxious stimulation of visceral receptors triggers general reactions of alertness and arousal and evokes unpleasant and poorly localized sensory experiences. This type of response may be a feature of sensory systems dominated by unmyelinated afferent inputs.

Abdomen↗

PubMed1987

Biochemical correlates of short-term sensitization in Aplysia: temporal analysis of adenylate cyclase stimulation in a perfused-membrane preparation.

During short-term sensitization, a simple form of nonassociative learning in Aplysia, the presentation of a single brief noxious stimulus results in enhancement of the defensive withdrawal reflex lasting minutes to tens of minutes. This behavioral plasticity involves presynaptic facilitation of synaptic transmission from the mechanosensory neurons that mediate the reflex to their central target cells. This facilitation is due to cAMP-dependent protein phosphorylation. To determine whether the time course of presynaptic facilitation might be due to a persistent increase in activity of adenylate cyclase (EC 4.6.1.1) itself, persistence of the transmitter, or yet other processes, we developed a perfused-membrane method to analyze the time course of activation of adenylate cyclase by transient stimuli. After stimulation by a pulse of stimulatory transmitter, activation of adenylate cyclase decayed within 60 sec. This finding indicates that the enzyme does not remain persistently active in the absence of transmitter and suggests that short-term retention is likely to be due to other mechanisms. Possible additional mechanisms include continued activation of the cyclase by transmitter, cellular factors extrinsic to the cyclase that prolong the time course of its activation, and persistence of processes downstream from the cyclase.

Adenylyl Cyclases↗

PubMed1981

Effect of various stimulus parameters on electrically-induced catecholamine secretion by thin slices of bovine adrenal medulla.

We examined the role of various stimulus parameters in electrically-induced catecholamine secretion by thin slices of bovine adrenal medulla. The stimulus parameters examined were voltage, duration, pulse width, and frequency for square-wave monophasic pulses. As each was examined it was held constant at a selected value for the evaluation of subsequent stimulus characteristics. For 16 mm2 tissue slices, catecholamine secretion was approximately linearly related to stimulus voltage over the range 20--80 volts, with a threshold of 20 V. Increasing the voltage beyond 80 V did not enhance secretion. Similarly, catecholamine secretion was dependent upon the frequency of stimulation. For stimuli delivered at 50 V for a 10-sec interval there was a four-fold increase in secretion over the frequency range 10--100/sec. Increasing pulse width at a constant voltage (50 V) over the range 0.4--2.0 msec resulted in a four-fold increase in catecholamine secretion. For pulses of 50 V, 50/sec and 0.8 msec pulse width, secretion was dependent upon the duration of the stimulus. Enhanced secretion was evident for times as short as 2 sec; between 5 and 15 sec of stimulation catecholamine secretion was linearly related to stimulus duration. Over the range 2--15 sec there was a five-fold enhancement of secretion. Electrically-induced catecholamine secretion by slices was markedly dependent upon stimulus parameters. In general, it was enhanced by increasing voltage, stimulus duration, pulse width and frequency. For most experiments a good choice of stimulus parameters appears to be 50 V 10 sec duration, 0.8 msec pulse width delivered at a frequency of 50/sec. Maximizing all stimulus parameters resulted in a 17-fold enhancement of secretion.

Adrenal Medulla↗