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PubMed2006

Nociceptive threshold and analgesic response to morphine in aged and young adult rats as determined by thermal radiation and intracerebral electrical stimulation.

The present experiment compared the nociceptive threshold and analgesic response to morphine in young (4-5 months) and aged (24 months) rats using peripheral thermal stimulation and intracerebral electrical stimulation. Responses to thermal stimuli were assessed using both the classical tail-flick procedure in which latency of response is the dependent variable and a new method in which threshold in calories of heat is the dependent variable. In the intracerebral nociceptive threshold procedure, electrical stimuli were delivered via an electrode implanted in the mesencephalic reticular formation (MRF), a pain pathway, and the animals were trained to terminate the stimulation by turning a cylindrical manipulandum embedded in one wall of the experimental chamber. For the classical tail-flick method, the aged rats required a greater intensity of stimulation to produce a basal response latency that was between 2.5 and 3.5 s. Using the new psychophysical method for determining the tail-flick threshold, the aged rats' basal thresholds were significantly higher than that of the young rats. However, the basal thresholds obtained by direct stimulation of the MRF failed to show a significant age effect, suggesting that the registration of pain is not different between young and aged rats. These age-related differences in baseline tail-flick response may be due to changes in the spinal reflex associated with aging. Although, there was no difference in the analgesic effects of morphine between young and aged rats using the latency of the tail-flick response, evidence for decreased analgesic response was seen using the tail-flick threshold measure and the intracerebral stimulation threshold method.

Analgesics, Opioid↗

PubMed2001

Influence of transcranial magnetic stimulation on pupil size.

In 22 healthy subjects, painless repetitive transcranial magnetic stimulation (rTMS) was used to investigate the role of the cortex in the regulation of pupil size and the influence of TMS on the central autonomic nervous system. RTMS was performed over three brain regions of each hemisphere (frontal, central, parieto-occipital), over cervical nerve roots and in front of the ear (sham stimulation) while the size of the pupil was measured by infrared oculography. rTMS always elicited a dilatation of both pupils, with its maximum after approximately 1.5 s and without significant R-L difference in latency or amplitude of pupillary response. No differential effects were observed for stimulation over different cortex regions of one hemisphere, but stimulation over the right central region evoked a larger dilatation of the pupil than stimulation over the left. Pupillary dilatation was larger for cervical nerve root stimulation (+13.2+/-8.3% (S.D.) of baseline) than for suprathreshold cortex stimulation (+8.4+/-4.5%, five 10-Hz stimuli). Pupillary dilatation in response to magnetic cortex stimulation appears to reflect a mainly unspecific activation of the sympathetic system rather than an activation of a cortical pupillomotor centre. Sympathetic activation following rTMS of the cortex does not limit its experimental and therapeutic application.

Adult↗

PubMed2001

The behavioural importance of dynamically activated descending inhibition from the nucleus reticularis gigantocellularis pars alpha.

We have recently demonstrated (J Physiol 506 (1998) 459) that the dynamic activation of descending inhibition of the nociceptive response of spinal multireceptive cells occurs in the nucleus reticularis gigantocellularis pars alpha (GiA). In the same paper we have shown that Lamina I dorsal horn cells are responsible for activating this inhibition via a pathway which runs in the contralateral dorsolateral funiculus. The effects of dynamically activating this system by noxious stimulation on behavioural responses to noxious stimuli have not been established. Here we demonstrate the effects of GiA on the behavioural response during application of standardized noxious stimuli. As this system is activated in response to noxious stimulation (J Physiol 506 (1998) 459), it is possible that chronic pain states may also activate GiA. We have therefore investigated this possibility in animals following partial sciatic nerve ligation (an animal model of chronic pain; Pain 43 (1990) 205). Male Wistar rats (280-310 g) were anaesthetized with halothane (0.5-2% in O(2)). Guide cannulae for microinjections were stereotaxically placed above GiA. In one group of animals the sciatic nerve was partially ligated. Animals were allowed to recover for 4-6 days. The responses of each animal during the formalin test (Pain 4 (1977) 161) and the tail flick test (Pain 12 (1982) 229) were recorded on different days. Microinjections (0.5 microl) of either gamma-aminobutyric acid (GABA, 200 mM), D-L homocysteic acid (DLH, 25 mM) or 0.9% saline (as control) into GiA were performed during these tests in a randomized, blind manner. In animals without sciatic nerve ligation, microinjection of GABA to GiA did not significantly affect the animal's response during the tail flick test. However microinjection of DLH significantly increased the latency of tail flick from 6.2 +/- 0.8 to 8.4 +/- 0.5 s for up to 15 min (n = 7, P < 0.01, Mann-Whitney U-test). Microinjection of GABA to GiA increased the behavioural response to formalin between 10 and 20 min post-injection, while microinjection of DLH reduced this response at all time points except 10 min post-injection (n = 8, P < 0.05, Mann-Whitney U-test). In animals with sciatic nerve ligation, microinjections (0.5 microl) of either GABA (200 mM), or saline (as control) into GiA contralateral to the partial sciatic ligation were performed during these tests in a randomized, blind manner. Partial sciatic ligation significantly reduced the behavioural response to contralaterally applied formalin from 15 min post-injection onwards, compared to controls without sciatic nerve ligation. Microinjection of GABA to GiA significantly increased the behavioural response to formalin from 20 to 50 min post-injection. The inactivation of GiA only causes behavioural effects in nociceptive tests of a long enough duration to activate the system (i.e. the formalin test but not the tail flick test). Chemical activation of the system affects both tests. These data strongly support the concept of an important analgesic system which is activated in response to noxious stimulation, and subsequently acts to reduce behavioural responses to noxious stimuli.

Animals↗

PubMed2003

Imaging of central itch modulation in the human brain using positron emission tomography.

The unpleasantness of itching is reduced by cooling. Although previous research suggests the presence of a central itch modulation system, there is little documentation about the modulation system in the brain. In the present study, we investigated the modulating system of the itching sensation in human brains using positron emission tomography and H(2) (15)O. The significant increases of regional cerebral blood flow caused by histamine stimuli using iontophoresis were observed in the anterior cingulate cortex (BA24), the thalamus, the parietal cortex (BA40 and BA7), the dorsolateral prefrontal cortex (BA46) and the premotor cortex (BA6). We did not observe any changes in the secondary somatosensory cortex (S2) during the itching stimulus, corresponding to the previous imaging studies concerning itching. Activation in these areas related to itching stimuli was decreased by a simultaneous stimulation of itching and cold pain (the dual stimuli), as compared to itching alone. Interestingly, the midbrain, including periaqueductal gray matter (PAG), was only activated during the dual stimuli. PAG is well known to be a modulating noxious stimulus. Here we hypothesize that the activation of PAG may also be related to the itch modulation. These findings indicate that the modified brain activities in the PAG, the cingulate, the frontal and the parietal cortex might be associated with the itch modulation in the central nervous system and that the S2 might not be primarily involved in processing the itching perception in the brain since the activity of S2 was not observed in any concentration of itching stimuli.

Adult↗

PubMed1992

Retention of habituation in PC12 cells.

The time course of habituation and recovery of neurotransmitter release was measured in neuronally differentiated PC12 cells stimulated with either acetylcholine or ATP. The release of norepinephrine in response to either stimulant declined exponentially with repeated presentation of that stimulant. When the stimulus was withheld, the cells' ability to respond recovered to initial levels with an exponential time course. The rate of response recovery depended on the stimulant used and, in the case of stimulation with acetylcholine, on the number of previous stimuli. After habituation and recovery, or partial recovery, of norepinephrine release, the response to a second series of repetitive stimuli declined more rapidly than in the naive case. This increase in habituation rate was dependent on the number of previous stimuli and, in the case of stimulation with acetylcholine, was stable with time for at least 90 min after stimulation. These phenomena are analogous to characteristics of short- and long-term memories of habituative learning observed in behavioral studies. Kinetic equations based on a putative reversible stimulation-dependent inactivation of the cellular response mechanism were used to analyze the rates of habituation and response recovery.

Acetylcholine↗

PubMed1997

Responses of cortical EEG-related basal forebrain neurons to brainstem and sensory stimulation in urethane-anaesthetized rats.

The basal forebrain can be considered to be a rostral extension of the ascending reticular activating system. A large number of neurons in the basal forebrain have been shown to display higher firing rates when low-voltage fast activity is present in the cortical EEG as opposed to states characterized by large slow waves in both unanaesthetized and anaesthetized animals. However, a smaller number of cells with increased discharge rate during slow waves was also observed in most of these studies. While it is likely that these two types of neurons have opposite roles in the regulation of cortical activation, it is not known how they respond to inputs from the brainstem or the periphery. In the present study, extracellular recordings were made in the basal forebrain of urethane-anaesthetized rats. A total of 52 neurons were studied in which the firing rate was significantly higher during fast cortical EEG waves (F-cells), and 14 neurons in which activity was significantly greater during slow waves (S-cells). The two cell types responded differently to stimulation of the pedunculopontine tegmental nucleus (PPT) and dorsal raphe nucleus (DRN) with short (0.5-1 s) trains of pulses and to noxious sensory stimuli (tail pinch). These stimulations excited most F-cells (80-96%) and inhibited the majority of S-cells (55-67%). In the few F-cells that were inhibited by stimulation, the response varied with the background firing rate of the cell: the higher the firing rate at the time of stimulation, the higher the probability of observing an inhibitory response. In contrast, single electrical pulses delivered to the PPT and DRN excited the majority (72%) of both F- and S-cells. Previous in vitro studies have shown that the application of acetylcholine or serotonin has predominantly inhibitory effects on basal forebrain cholinergic neurons. The predominantly excitatory effect of noxious, PPT and DRN stimulation on F-cells therefore suggests that glutamatergic or other excitatory afferents play a more dominant role in regulating basal forebrain neurons. We have previously shown that F-cells are more prevalent than S-cells. In combination, these findings suggest that basal forebrain neurons, and F-cells in particular, are important in mediating the ascending excitatory drive from the brainstem to the cerebral cortex.

Anesthesia, General↗

PubMed1978

A study of the factors responsible for rate-dependent shortening of the action potential in mammalian ventricular muscle.

1. An intracellular micro-electrode was used to record action potentials from superficial cells of a cat papillary muscle during isometric contractions. The muscle was stimulated regularly and test stimuli were interpolated at various times between regular (control) responses. 2. The duration of test action potentials (measured at 80% repolarization) increases exponentially with time as the interval between the test stimulus and the preceeding stimulus is increased and a curve drawn through the data reaches a plateau at test intervals of 1.0-1.5 s. This curve is considered to reflect the time course with which membrane conductances return to their pre-stimulus values after a control response, and it is known as the 'electrical restitution curve'. 3. At much longer test intervals the action potential duration duration increases again and it approaches the rested state value of about 0.5 s when the interval between stimuli is 200-300 s. 4. Interventions that raise the peak tension developed in isometric contractions, such as an increase in the rate of stimulation or in the bathing calcium concentration, displace the electrical restitution curve downwards (to shorter action potential durations) and to the left (to shorter stimulus intervals). This shift in the curve is accompanied by a reduction in its magnitude (i.e. the difference in duration between the earliest possible action potential and the plateau value), but the interventions differ in their effects on the time course of electrical restitution: an increase in stimulus frequency causes a marked slowing, whereas an increase in bathing calcium concentration produces a slight speeding up of its time course. 5. The reduction in action potential duration produced by an increase in stimulus frequency (rate-dependent shortening) can be separated into two components, one resulting from the downward displacement of the electrical restitution curve and the other depending on the time available between consecutive responses for membrane recovery. The second component becomes increasingly important at stimulus frequencies above 100 min-1. 6. Changes in action potential duration observed during the tension staircases produced by regular stimulation of a rested preparation and by paired pulse stimulation can also be accounted for by interaction of downward displacement of the electrical restitution curve and variations in the degree of recovery of the membrane between consecutive responses. 7. Downward displacement of the electrical restitution curve is thought to result from intracellular accumulation of calcium and/or extracellular accumulation of potassium, and the available evidence is considered to favour the former mechanism.

Action Potentials↗

PubMed1982

Long-term potentiation of excitatory synaptic transmission in the rat hippocampus: the role of inhibitory processes.

1. The possibility that changes in inhibitory processes are responsible for long-term potentiation (l.t.p.) was examined using the rat hippocampal slice preparation.2. Inhibitory pathways were characterized using both extra- and intracellular recordings from the CA1 pyramidal cell layer. Stimulating electrodes were placed in either stratum radiatum or the alveus to allow orthodromic or antidromic activation of the pyramidal cells.3. Using extracellular recordings, inhibition was studied by applying paired pulses at interstimulus intervals of 20-500 msec through either the same or different stimulating electrodes, and quantifying the reduction in the population spike. An antidromic conditioning pulse was least effective in influencing the test response, while paired stimuli delivered through separate stimulators in stratum radiatum revealed the longest duration effects. Inhibition was either reduced or enhanced, depending upon the stimulation paradigm, with increasing stimulus intensity.4. With l.t.p., alterations in paired-pulse inhibition were observed corresponding to the changes in conditioning pulse amplitude. Reducing stimulus intensity to restore the initial conditioning pulse amplitude eliminated these effects.5. Using intracellular recordings, the effects of l.t.p. on inhibition were studied by examining changes in e.p.s.p.-i.p.s.p. sequences, i.p.s.p.s evoked by antidromic stimulation, and spontaneous depolarizing i.p.s.p.s observed with KCl-filled electrodes.6. Following l.t.p. enhanced e.p.s.p.s and slightly reduced, but prolonged, i.p.s.p.s were observed in response to orthodromic stimulation. Antidromically evoked, as well as spontaneous, i.p.s.p.s were unaffected.7 It is concluded that alterations in inhibitory processes are not responsible for l.t.p. in hippocampal subfield CA1. However, changes in the strength of inhibitory synapses as a consequence of long-term potentiation may modify the functional character of the hippocampal connexions.

Action Potentials↗

PubMed2006

Glycogen synthase kinase 3- and extracellular signal-regulated kinase-dependent phosphorylation of paxillin regulates cytoskeletal rearrangement.

Paxillin is a 68-kDa focal adhesion-associated protein that plays an important role in controlling cell spreading and migration. Phosphorylation of paxillin regulates its biological activity and thus has warranted investigation. Serine 126 and serine 130 were previously identified as two major extracellular signal-regulated kinase (ERK)-dependent phosphorylation sites in Raf-transformed fibroblasts. Here serine 126 is identified as a phosphorylation site induced by lipopolysaccharide (LPS) stimulation of RAW264.7 cells. A number of other stimuli, including adhesion and colony-stimulating factor, induce serine 126 phosphorylation in RAW264.7 cells, and nerve growth factor (NGF) treatment induces serine 126 phosphorylation in PC12 cells. The kinase responsible for phosphorylation of this site is identified as glycogen synthase kinase 3 (GSK-3). Interestingly, this GSK-3-dependent phosphorylation is regulated via an ERK-dependent priming mechanism, i.e., phosphorylation of serine 130. Phosphorylation of S126/S130 was required to promote spreading in paxillin null cells, and LPS-induced spreading of RAW264.7 cells was inhibited by expression of the paxillin S126A/S130A mutant. Furthermore, this mutant also retarded NGF-induced PC12 cell neurite outgrowth. Hence, phosphorylation of paxillin on serines 126 and 130, which is mediated by an ERK/GSK-3 dual-kinase mechanism, plays an important role in cytoskeletal rearrangement.

Animals↗

PubMed1998

CD40 ligand/CD40 stimulation regulates the production of IFN-gamma from human peripheral blood mononuclear cells in an IL-12- and/or CD28-dependent manner.

CD40 ligand (CD40L)/CD40 costimulation is an important regulator of Th1 responses. Two mechanisms by which CD40L/CD40 stimulation may enhance IFN-gamma are via direct induction of IL-12 and augmentation of the expression of costimulatory molecules such as B7 from APCs. We examined the ability of CD40L/CD40 stimulation to regulate the production of IFN-gamma through IL-12 and/or CD28 costimulation from human PBMCs stimulated with T cell-specific stimuli. The roles of exogenous and endogenous CD40L/CD40 stimulation were evaluated using a trimeric soluble CD40L agonist (CD40T) and an anti-CD40L Ab, respectively. The presence of CD40T in cultures increased the production of IL-12 and IFN-gamma from PBMCs stimulated with varying amounts of PHA. The mechanism, however, by which CD40T enhanced IFN-gamma varied according to the level of T cell activation. Under maximal stimulatory conditions (PHA, 1/100), an IL-12-dependent pathway was dominant. At relatively low levels of T cell stimulation (PHA, 1/500 and 1/1000), however, an additional IL-12-independent CD28-dependent pathway was elucidated. We further studied the role of exogenous CD28 stimulation in regulating the production of IFN-gamma. The enhancement of IFN-gamma production induced by direct CD28 stimulation was primarily dependent on endogenous IL-12 or CD40L/CD40 stimulation. Together, these data suggest that the production of IFN-gamma involves a complex interaction between two interdependent, yet distinct, costimulatory pathways and provide evidence that CD40T may be an effective adjuvant for the enhancement of responses.

Adjuvants, Immunologic↗

PubMed2002

Dentine hypersensitivity in subjects recruited for clinical trials: clinical evaluation, prevalence and intra-oral distribution.

Relatively few studies have reported on the frequency, distribution and severity of dentine hypersensitivity (DH) in subjects recruited for clinical trials of desensitizing agents. Potential subjects (n= 48 M, 81 F, mean age 35.1 years) for inclusion into such a study were screened to determine the extent of the problem. 117 subjects (41 M, 76 F) mean age 24.9 years were clinically examined. Evaluation by questionnaire indicated that the prevalence of DH was proportionately higher in the 20-29.9 years (34.9%), and 30-39.9 years groups (33.3%), respectively. Sensitivity to cold was the main presenting symptom. Tactile (probe) and cold air (dental air syringe) stimuli were used to clinically evaluate DH. Of the teeth eligible for evaluation 1561/3136 (49.8%) responded to either one or both of the test stimuli; 274/3136 (8.7%) responded to tactile only stimulation, 779/3136 (24.8%) to thermal only stimulation and 508/3136 (16.2%) to both tactile and thermal stimulation. Of those teeth responding to the stimuli, 477 (30.6%) were premolars, 437 (28%) incisors, 415 (26.8%) molars and 232 (14.9%) canines. The results agree with those of previously reported studies in that DH is most frequently observed on premolars and that proportionately more teeth are sensitive to evaporative than to tactile stimulation. Furthermore it would appear from the results of the study that tactile is less effective than thermal/evaporative stimulation in the evaluation of DH.

Adult↗

PubMed2002

Sound motion evoked magnetic fields.

OBJECTIVE: The aim of present study was to determine which brain regions are involved in the conscious perception of sound motion in humans. METHODS: Six kinds of sound stimuli were studied. Two static sound stimuli with durations of 100 or 1000 ms remained at a fixed position during the stimulation period. Four moving sound stimuli with duration of 100 or 1000 ms were moving from left to right, or right to left, during the stimulation period. Evoked magnetic fields were recorded using a 151-channel whole cortex magnetoencephalographic system. RESULTS: The response identified in all sound stimuli was M100. Responses identified only in moving sound stimuli were M180, M280 and M680. Contour maps and dipoles overlapped on magnetic resonance imaging indicated that both the M100 and M680 responses were generated in the superior temporal cortex (left and right), while M180 and M280 were generated in the parietal cortex (right). CONCLUSIONS: The results of this MEG study indicated that the right parietal cortex was involved in sound motion processing. We hypothesize that the right parietal cortex, in association with the left and right superior temporal cortex, forms a network to process sound motion information.

Acoustic Stimulation↗

PubMed1983

Influences of the limbic system on hypothalamo-neurohypophysial system.

(1) Effects of stimulations of various limbic structures (the olfactory bulb, olfactory tubercle, prepyriform cortex, endopyriform nucleus and various parts of amygdaloid nuclei) on the neurosecretory neurons in the supraoptic (SON) and paraventricular nuclei (PVN) of the hypothalamus were studied. All regions stimulated received strong inputs from the olfactory bulb. (2) Out of 195 "identified' neurosecretory neurons tested one-half or more (49-74%, depending on the structures stimulated) were inhibited by stimuli consisting of 1-3 short pulses. The inhibition occurred immediately after the stimulus in approximately one-fifty of all inhibited neurons, in the remaining four-fifths inhibition occurred after more than 20 ms latency. Inhibition of neurosecretory neuron activity lasted for several hundred milliseconds, often followed by clear post-inhibitory excitation or rebound. (3) In 23 neurons, a distinct "evoked' response of brief duration occurred with a 30 ms latency following stimulation of the lateral and medical amygdala, olfactory tubercle and prepyriform cortex. In another 17 neurons, a general increase in background activity with a longer latency (50-100 ms) occurred following stimulation of nearly all amygdaloid nuclei, olfactory tubercle and the pyriform cortex: lateral amygdala stimulation caused an excitation of the largest proportion of neurosecretory cells (30%) while none was excited by stimulation of the olfactory bulb and endopyriform cortex, except those occurring as post-inhibitory excitation. (4) There was a convergence of afferent impulses on single neurosecretory cells. A large proportion (42%) of the neurons received inputs from 2 to 4 limbic regions. (5) Neurosecretory cells which were influenced by limbic stimuli were also inhibited by baroreceptor activation and excited by osmotic stimulation. "Unidentified' neurons within SON and PVN and "atypical neurosecretory cells' (those responding to pituitary stalk stimulation with varying latencies) were also affected by the forebrain stimulation; some of these were also affected by an osmotic stimulus. A part of this group may send their axons to the median eminence.

Action Potentials↗

PubMed1988

Are serine proteases involved in immune complex activation of neutrophils?

Soybean polypeptides and diisopropylfluorophosphate (DFP) have been reported to inhibit neutrophil functions such as the oxidative burst, chemotaxis, and/or phagocytosis in response to soluble stimuli; these observations would be compatible with the involvement of an active serine protease in neutrophil stimulation. We have investigated the possibility of such involvement when particulate stimuli such as immune complexes are utilized. The depolarization of the neutrophils' membrane potential, one of the earliest indicators of stimulation, and superoxide production, which is detectable 30-45 sec later, were our indicators of neutrophil response to immune complexes. The neutrophils were equilibrated with, and after 5 min washed free of, up to 60 mM DFP, a potent covalent serine protease inhibitor. At DFP concentrations below 24 mM, such treatment did not perturb neutrophil activation as measured by either of the above parameters, nor did F- alone under comparable conditions. Additionally, the immune complex induced responses of neutrophils preincubated for 3 min with N-alpha-p-tosyl-L-lysine chloromethylketone (TLCK), L-1-tosylamido-2-phenyl-ethyl-chloromethylketone (TPCK), or phenyl-methyl-sulfonyl-fluoride (PMSF), covalent serine protease inhibitors which have, however, been shown to function in other capacities, e.g., as superoxide dismutases; 1 mM PMSF or 0.5 mM TLCK consistently reduced the observed membrane depolarization, one of the earliest consequences of neutrophil activation, by 20-30%, while 0.1 mM TLCK and 0.01 mM TPCK had little or no effect. The inhibition of superoxide production, a slightly later stimulus response, by PMSF, TLCK, and TPCK was more profound (50-75%); these compounds have, however, been shown to have activities other than serine protease inhibitors--for example, as superoxide dismutases. Since DFP is purely a serine protease inhibitor, and since the three other compounds do not affect depolarization (the earlier and superoxide independent event), our results indicate that active serine proteases do not appear to be necessary for immune-complex-initiated neutrophil stimulation. Other stimuli, which are known to activate neutrophils by different pathways, were not investigated.

Antigen-Antibody Complex↗

PubMed1994

Activation of macrophages for cytolysis of virally infected cells by monoclonal antibody to the 73-kDa lipopolysaccharide receptor.

The abilities of lipopolysaccharide (LPS) and mAb5D3 (a monoclonal antibody specific for the 73 kDa LPS receptor) to activate bone marrow culture derived macrophages (BMCM) for cytolysis of vesicular stomatitis virus infected BALB/c3T3 (VSV-3T3) and the tumor target, P815, were compared. Activation for cytolysis of VSV-3T3 cells occurred at a lower level of either LPS or mAb5D3 than activation for cytolysis of P815. With both targets and under several stimulation conditions there was a constant differential between the two activating stimuli. These data indicate that stimulation of the 73 kDa LPS receptor at low levels of either mAb5D3 or LPS can activate BMCM for cytolysis of VSV-3T3 but not P815. Further, the constant relative efficiency of mAb5D3 to LPS in both target systems suggests that there is a common receptor for both LPS mediated effects.

3T3 Cells↗

PubMed2004

Current knowledge about physiotherapeutic strategies in osteoporosis prevention and treatment.

In treating patients with osteoporosis, one option in physiotherapy is to comply with given physical norms by using physical stimuli to influence biological functions and structures (bone, muscle) for adaptation, stimulation, and regeneration. Serial physical stimuli can also be used for interventions and actions to minimise pain perception by means of biopsychosocial influence. In osteoporosis, physiotherapy has to be rated on a par with pharmacotherapy with respect to prevention, cure, and rehabilitation. Generally, two different aims can be defined: (1) those which can be achieved with physical therapy alone, such as structural improvement of the existing and pharmacologically increased bone tissue, slowing down of round-back formation, and fall prophylaxis and (2) those which can be achieved with physiotherapy and pharmacotherapy, such as effective pain relief and increased bone density. Regulation and normalisation of physical capacities with an aim towards maintenance and economisation of functions and improvement in abilities call for a skillful and case-specific use of physiotherapy.

Exercise↗

PubMed1995

Evaluation of atrial vulnerability with transoesophageal stimulation in patients with atrioventricular junctional reentrant tachycardia. Comparison with patients with ventricular pre-excitation and with normal subjects.

The aim of our work was to evaluate the inducibility of atrial fibrillation in a group of patients with atrioventricular junctional reentrant tachycardia and to compare it with that of patients with a Kent-type ventricular pre-excitation (Wolff-Parkinson-White syndrome) and a control group. One hundred and twenty-five subjects were separated into groups. Group 1 comprised 49 Wolff-Parkinson-White patients, with a mean age of 26.4, range 10-66 years; group 2, 51 patients with atrioventricular junctional reentrant tachycardia inducible by transoesophageal atrial stimulation and/or clinically documented, with a mean age of 43.4, range 16-78 years; group 3, 25 control subjects with a mean age of 26.4, range 13-76 years. Each subject underwent atrial transoesophageal stimulation with the following protocol: programmed atrial stimulation with 1 and 2 stimuli during atrial pacing of 100.min-1 and 150.min-1; atrial stimulation for 10 s at a rate of 200-300-400-500-600.min-1 with intervals of 10 s between stimulations, five successive 'ramp-up' atrial stimulations for 9 s with the rate increasing from 100 to 800.min-1 with intervals of 10 s between stimulations. The end point was the completion of the protocol or induction of sustained atrial fibrillation (> 1 min). The chi-square test was used for statistical analysis. Our results showed that in group 1 atrial fibrillation was induced in 27/49 patients (55.1%); this was sustained in 13/49 (26.5%) and non-sustained in 14/49 (28.5%); in group 2, atrial fibrillation was induced in 22/51 patients (43.0%); it was sustained in 7/51 (13.7%) and non-sustained in 15/51 (29.4%); in group 3, sustained atrial fibrillation was not induced in any subject and in only one subject was a non-sustained atrial fibrillation (4 s) induced. The chi-square test showed that group 2 vs group 1 were non-significant, while group 2 vs group 3 and group 1 vs group 3 were significant (P < 0.003 and P < 0.0007, respectively). Therefore group 2 patients showed a greater atrial vulnerability in comparison to the control subjects and a similar vulnerability to group 1 patients. It is possible that the greater atrial vulnerability in the patients of group 2 was due to the double nodal pathway.

Adolescent↗

PubMed1990

Electrophysiological studies of acetylcholine and the role of the basal forebrain in the somatosensory cortex of the cat. II. Cortical neurons excited by somatic stimuli.

1. Of the sample of 322 neurons located in somatosensory cortex and tested for their responsiveness to somatic stimulation, 91 (28%) responded to stimuli applied to the skin. The majority were located in the middle cortical layers. Each of the cells subjected to tests with glutamate and acetylcholine (ACh) was rapidly adapting to cutaneous stimuli, giving a response at the onset of skin indentation and sometimes after the stimulus withdrawal. 2. Of the 30 cells tested by pairing basal forebrain (BF) stimulation with cutaneous stimulation. 18 (60%) displayed enhanced responses to the same cutaneous stimulus after the pairing. These effects lasted for greater than 5 min in 17 cases, persisting for as long as the cell was studied, sometimes greater than 1 h. 3. The enhanced responsiveness to cutaneous stimuli could not be reversed by atropine, but in each of the 11 cells where atropine was administered while the BF stimulus was paired with the skin stimulus, the pairing produced no enhancement. 4. We conclude that pairing a BF stimulus with a cutaneous stimulus leads to long-term facilitation of the responsiveness of the cortical neuron subjected to this treatment and that this effect is mediated by the release of acetylcholine from BF cholinergic neurons that act on muscarinic receptors found on neurons in the somatosensory cortex.

Acetylcholine↗