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PubMedDate not supplied

Perioperative antibiotic usage by facial plastic surgeons: national survey results and comparison with evidence-based guidelines.

OBJECTIVES: To determine current practice for use of perioperative antibiotics among facial plastic surgeons, to determine the extent of use of literature support for preferences of facial plastic surgeons, and to compare patterns of use with nationally supported evidence-based guidelines. METHODS: A link to a Web site containing a questionnaire on perioperative antibiotic use was e-mailed to more than 1000 facial plastic surgeons in the United States. Responses were archived in a dedicated database and analyzed to determine patterns of use and methods of documenting that use. Current literature was used to develop evidence-based recommendations for perioperative antibiotic use, emphasizing current nationally supported guidelines. RESULTS: Preferences varied significantly for medication used, dosage and regimen, time of first dose relative to incision time, setting in which medication was administered, and procedures for which perioperative antibiotic was deemed necessary. CONCLUSIONS: Surgical site infection in facial plastic surgery can be reduced by better conformance to currently available evidence-based guidelines. We offer specific recommendations that are supported by the current literature.

Antibiotic Prophylaxis↗
PubMed1996

Plasticity of retinal ribbon synapses.

Ribbon synapses differ from conventional chemical synapses in that they contain, within the cloud of synaptic vesicles (SV's), a specialized synaptic body, most often termed synaptic ribbon (SR). This body assumes various forms. Reconstructions reveal that what appear as rod- or ribbon-like profiles in sections are in fact rectangular or horseshoe-shaped plates. Moreover, spherical, T-shaped, table-shaped, and highly pleomorphic bodies may be present. In mammals, ribbon synapses are present in afferent synapses of photoreceptors, bipolar nerve cells, and hair cells of both the organ of Corti and the vestibular organ. Synaptic ribbons (SR's) are also found in the intrinsic cells of the third eye, the pineal gland, and in the lateral line system. The precise function of SR's is enigmatic. The prevailing concept is that SR's function as conveyor belts to channel SV's to the presynaptic membrane for neurotransmitter release by means of exocytosis. The present article reviews the evidence that speaks for a plasticity of these organelles in the retina and the third eye, as reflected in changes in number, size, shape, location, and grouping pattern. SR plasticity is especially pronounced in the mammalian and submammalian pineal gland and in cones and bipolar cells of teleost fishes. Here, SR number and size wax and wane according to the environmental lighting conditions. In the pineal SR numbers increase at night and decrease during the day. In teleost cones, SR's are in their prime during daytime and decrease or disappear at night, when transmitter release is enhanced. In addition to numerical changes, SR's may also exhibit changes in size, shape, grouping pattern, and location. In the mammalian retina of adults, in contrast to the developing retina, the reported signs of SR plasticity are subtle and not always consistent. They may reflect changes in function or may represent signs of degradation. To distinguish between the-two, more detailed studies under selected experimental conditions are required. Probably the strongest evidence for SR plasticity in the mammalian retina is that in hibernating squirrels SR's leave the synaptic site and accumulate in areas as far as 5 microns from the synapse. Changes in shape include the occurrence of club-shaped SR's and round SR's or synaptic spheres (SS's). SS's may represent a special type of synaptic body, yet belonging to the family of SR's, or may be related to the catabolism of SR's. SR number is regulated by Ca2+ in teleost cones, whereas in the mammalian pineal gland cGMP is involved. An interesting biochemical feature of ribbon synapses is that they lack synapsins. The presently reviewed results suggest to us that SR's do not primarily function as conveyor belts, but are devices to immobilize SV's in inactive ribbon synapses.

Animals↗
PubMed1998

Mineralocorticoid receptor-mediated enhancement of neuronal excitability and synaptic plasticity in the dentate gyrus in vivo is dependent on the beta-adrenergic activity.

The dentate gyrus neurons in the hippocampus contain a high density of both mineralocorticoid and adrenergic receptors. By in vivo extracellular recording from adrenalectomized rats we investigated the possible relationships between the two systems with regard to neuronal excitability and activity-dependent synaptic plasticity. Pretreatment with aldosterone significantly enhanced both basal neuronal excitability and tetanically evoked synaptic plasticity in adrenalectomized, but not sham-operated rats. The enhancement was blocked by spironolactone, indicating a mineralocorticoid receptor-dependent effect. The adrenomedullary hormone epinephrine also significantly enhanced synaptic plasticity via activation of beta-adrenergic receptors. Beta-adrenergic antagonist propranolol, infused directly into the dentate gyrus granule cell layer, significantly reduced the effect of aldosterone on neuronal excitability and partly canceled the aldosterone-enhanced synaptic plasticity. No effect of propranolol was found after its amygdaloid infusion. The mineralocorticoid receptor antagonist spironolactone did not affect the epinephrine-induced effects. These results indicate that the pretreated adrenal steroids interact with the catecholaminergic system in the dentate gyrus of adrenalectomized rats and that the functional beta-adrenergic pathway is involved in the mechanism of mineralocorticoid-induced cellular effects in vivo.

Adrenalectomy↗
PubMed1998

Seasonal plasticity of the song control system in wild Nuttall's white-crowned sparrows.

Seasonal plasticity in the morphology of telencephalic nuclei that control song behavior has been reported for diverse species of songbirds. The only published report of a lack of seasonal changes in the song nuclei of a seasonally breeding bird is that of Baker et al. in the Nuttall's subspecies of white-crowned sparrow (Zonotrichia leucophrys nuttalli). In this study, they brought wild birds into the laboratory and exposed them to either "summer" or "winter" photoperiods. Previous studies have shown that exposing wild-caught white-crowned sparrows to long-day photoperiods in the laboratory may not induce circulating concentrations of testosterone (T) as high as those seen in wild breeding birds. Changes in circulating T are primarily responsible for the seasonal morphological changes in the song nuclei. To determine whether there is seasonal plasticity of the song system in this subspecies, we measured circulating T, morphological attributes of the song nuclei, and song behavior in wild Nuttall's white-crowned sparrows during the spring and fall. Testis size and circulating T concentrations were greater in spring than fall birds. The absolute volumes of the song nuclei HVc, RA, and Area X, and their volumes relative to those of either the total telencephalon or three thalamic nonsong nuclei, were significantly greater in the spring than fall sparrows. Song behavior also changed seasonally; fall birds sang shorter songs than did spring birds. These results show that there is seasonal plasticity of the song system in wild Nuttall's white-crowned sparrows. Seasonal plasticity can now be regarded as a common feature of the seasonally breeding songbirds studied thus far.

Animals↗
PubMed1998

Parallel nature of hippocampal synaptic plasticity.

This study demonstrates that the mechanisms involved in the production of long-term potentiation (LTP) in the hippocampus appear to be independent of those which generate shorter-lasting plasticity, but that both processes are activated concurrently following an LTP-inducing stimulus. Adult male Sprague-Dawley rats were anesthetized using either pentobarbital or secobarbital to record extracellular field potentials from the hippocampal CA1 pyramidal cell layer in response to stimulation of commissural afferents. Plasticity was generated by the delivery of a five-pulse patterned stimulus train, consisting of one priming pulse followed 170 milliseconds later by a burst of four pulses at 200 Hz. While similar LTP was observed in both groups, short-term plasticity was absent in the secobarbital-anesthetized animals. This result suggests that different plasticity mechanisms in the hippocampus are activated in parallel by the triggering stimulus.

Animals↗
PubMed2000

Synaptic plasticity in the hippocampal area CA1-subiculum projection: implications for theories of memory.

This paper reviews investigations of synaptic plasticity in the major, and underexplored, pathway from hippocampal area CA1 to the subiculum. This brain area is the major synaptic relay for the majority of hippocampal area CA1 neurons, making the subiculum the last relay of the hippocampal formation prior to the cortex. The subiculum thus has a very major role in mediating hippocampal-cortical interactions. We demonstrate that the projection from hippocampal area CA1 to the subiculum sustains plasticity on a number of levels. We show that this pathway is capable of undergoing both long-term potentiation (LTP) and paired-pulse facilitation (PPF, a short-term plastic effect). Although we failed to induce long-term depression (LTD) of this pathway with low-frequency stimulation (LFS) and two-pulse stimulation (TPS), both protocols can induce a "late-developing" potentiation of synaptic transmission. We further demonstrate that baseline synaptic transmission can be dissociated from paired-pulse stimulation of the same pathway; we also show that it is possible, using appropriate protocols, to change PPF to paired-pulse depression, thus revealing subtle and previously undescribed mechanisms which regulate short-term synaptic plasticity. Finally, we successfully recorded from individual subicular units in the freely-moving animal, and provide a description of the characteristics of such neurons in a pellet-chasing task. We discuss the implications of these findings in relation to theories of the biological consolidation of memory.

Animals↗
PubMed2000

Genetic analysis of learning behavior-induced structural plasticity.

It is well-documented that enriched environment and behavioral training can lead to improved learning and memory, as well as structural and morphological changes in the brain. It has been hypothesized that such experience-dependent behavioral improvement results from structural modifications that may represent some forms of possible memory substrates for these behavioral experiences. It was generally assumed until now that, like the activity-dependent structural plasticity observed in the developing brain, behavioral experience-induced structural plasticity would require the activation of the NMDA receptor, a molecular switch for learning and memory. Recent genetic and anatomical analyses reveal that behavioral experience-induced increases in spine and synapse density in the hippocampal CA1 region occur despite the deletion of the NMDA receptor in conditional knockout mice. Recent studies indicate that the molecular mechanism of behavioral experience-induced structural plasticity in the adult brain differs from that of the developing brain, and can be disassociated from the NMDA-mediated long-term potentiation (LTP) phenomenon. Deepening the understanding of the molecular mechanism of experience-induced structural plasticity should facilitate the study of the relationship between structural changes and memory formation. Using an integrated approach with genomic, genetic, and modern histological techniques should move us closer in this direction.

Animals↗
PubMed2002

Modulation of use-dependent plasticity by d-amphetamine.

Use-dependent plasticity, thought to contribute to functional recovery after brain injury, is elicited by motor training. The purpose of this study was to determine if administration of d-amphetamine facilitates the effects of motor training on use-dependent plasticity. Healthy human volunteers underwent a training period of voluntary thumb movements under the effects of placebo or d-amphetamine in different sessions in a randomized double-blind, counterbalanced design. Previous work in a drug-naive condition showed that such training causes changes in the direction of thumb movements evoked by transcranial magnetic stimulation and in transcranial magnetic stimulation-evoked electromyographic responses. The endpoint measure of the study was the magnitude of training-induced changes in transcranial magnetic stimulation-evoked kinematic and electromyographic responses in the d-amphetamine and in the placebo conditions. Motor training resulted in increased magnitude, faster development and longer lasting duration of use-dependent plasticity under d-amphetamine compared to the placebo session. These results document a facilitatory effect of d-amphetamine on use-dependent plasticity, a possible mechanism mediating the beneficial effect of this drug on functional recovery after cortical lesions.

Adult↗
PubMed2005

Development of human visual cortex: a balance between excitatory and inhibitory plasticity mechanisms.

Formation of neural circuitry in the developing visual cortex is shaped by experience during the critical period. A number of mechanisms, including N-methyl-D-aspartate (NMDA) receptor activation and gamma-aminobutyric acid (GABA)-mediated inhibition, are crucial in determining onset and closure of the critical period for visual plasticity. Animal models have shown that a threshold level of tonic inhibition must be reached for critical period plasticity to occur and that NMDA receptors contribute to Hebbian synaptic plasticity in the developing visual cortex. There are a number of developmental changes in these glutamatergic and GABAergic mechanisms that have been linked to plasticity; however, those changes have been shown only in animal models, and their development in the human visual cortex is not known. We have addressed this question by studying the expression of the major glutamatergic receptors, GABA(A) receptors, and glutamic acid decarboxylase (GAD) isoforms during the first 6 years of postnatal development of human visual cortex. There are significant changes in the expression of these proteins during postnatal development of human visual cortex. The time course of the changes is quite prolonged and suggests that it may set the pace for the prolonged critical period in human visual development. The changes also affect the nature of spatial and temporal integration in visual cortical neurons and thereby contribute to the maturation of visual functions.

Blotting, Western↗
PubMed2003

Prenatal administration of morphine decreases CREBSerine-133 phosphorylation and synaptic plasticity range mediated by glutamatergic transmission in the hippocampal CA1 area of cognitive-deficient rat offspring.

The central nervous system (CNS) exhibits remarkable plasticity in early life and can be altered significantly by various prenatal influences. We previously showed that prenatal exposure to morphine altered kinetic properties of N-methyl-D-aspartate (NMDA) receptor-mediated synaptic currents in the hippocampus of young rat offspring at the age of 14 days (P14). The present study further investigates whether NMDA receptor-mediated synaptic plasticity and/or cyclic adenosine monophosphate-responsive element-binding protein (CREBSerine-133), an important transcription factor underlying learning and memory, can be altered by prenatal morphine exposure in these offspring. Subsequently, the Morris water maze task was performed at the older ages (P28-P31). The magnitude of long-term depression (LTD) generated by a low-frequency stimulation (LFS, 1 Hz for 15 min) in hippocampal slices from the vehicle-control offspring (P14) was significantly larger than that in slices from the morphine-treated offspring, although there was no such difference in the magnitude of long-term potentiation (LTP) elicited by a high-frequency stimulation (100 Hz for 1 s) between the two groups. Comparison of the expression range of glutamatergic synaptic plasticity in slices from the vehicle-control and morphine-treated offspring, calculated as the difference in the maximal magnitude between LTP and LTD, demonstrated a remarkably smaller range in the slices from the morphine-treated offspring. In addition, the decreased phosphorylation of CREBSerine-133 and the impaired ability of spatial learning were also seen in the morphine-treated offspring, as compared with the vehicle-control offspring. Collectively, the study suggests that maternal exposure to morphine reduces the range of synaptic plasticity by decreasing the expression of LTD, but not of LTP, in CA1 pyramidal neurons of the hippocampus from rat offspring. More importantly, decreased phosphorylation of CREBSerine-133 may play a role for the impaired spatial learning and memory in rat offspring exposure to prenatal morphine. Thus, the findings here may provide important insights into cellular/molecular mechanisms underlying pathophysiological changes in the CNS of young offspring from morphine-addicted mothers and serve as a basis for possible therapeutic intervention.

Animals↗
PubMed1993

Hippocampal plasticity induced by primed burst, but not long-term potentiation, stimulation is impaired in area CA1 of aged Fischer 344 rats.

The effect of two types of electrical stimulation designed to induce long-lasting plasticity of the Schaffer/commissural inputs to CA1 pyramidal neurons was investigated using in vitro hippocampal slices made from young (3-6 month) and old (24-27 month) Fischer 344 rats. The first stimulation paradigm, primed burst (PB) stimulation, consisted of a total of five physiologically patterned stimuli: a single priming pulse followed 170 ms later by a burst of four pulses at 200 Hz. The second stimulation paradigm, long-term potentiation (LTP) stimulation, consisted of a 200 Hz/1 second train (a total of 200 stimuli). Primed burst and LTP stimulation were equally effective at inducing a lasting increase in the population spike recorded from slices made from young rats. However, the enhancement of population spike amplitude produced by PB, but not LTP, stimulation was significantly less in slices made from old rats. These results suggest that the capacity of the hippocampus to demonstrate long-lasting synaptic plasticity is not altered with age, but that engaging plasticity-inducing mechanisms becomes more difficult. Furthermore, these data suggest that physiologically patterned paradigms for inducing long-lasting synaptic plasticity may more accurately assess the functional status of hippocampal memory encoding mechanisms than does conventional LTP stimulation.

Action Potentials↗
PubMed1986

Kinetics of sorption of ionizable solutes by plastic infusion bags.

Aqueous solutions of several ionizable substances were stored in plastic infusion bags and the sorption of the substances monitored with time. The substances used were p-nitrophenol, p-toluidine, warfarin sodium [3-(alpha-acetonylbenzyl)-4-hydroxycoumarin sodium salt] and trifluoperazine hydrochloride (10-[3-(4-methyl-1-piperazinyl)propyl]-2-(trifluoromethyl)phenothiazine dihydrochloride). The rate and extent of sorption for each substance varied with pH and was consistent with a preferential uptake of the un-ionized species. The uptake of p-nitrophenol and p-toluidine was adequately described by a diffusion model derived assuming that sorption is rate-controlled by the diffusivity of the solute in the plastic matrix, and that only the un-ionized species was sorbed by the plastic matrix. However, the uptake of warfarin sodium and trifluoperazine hydrochloride was described more accurately by a diffusion model in which the diffusional resistance of the plastic matrix and of an interfacial resistance barrier both contributed to the diffusional resistance encountered in the sorption process. It appeared that the rate of uptake of the un-ionized form of these solutes was diminished due to the influence of interfacial or aqueous diffusional barriers. Solute lipophilicity and degree of ionization appeared to be important factors determining the relative contribution of the respective barriers to the overall diffusional resistance.

Absorption↗
PubMed1995

Plastic hollow waveguides: properties and possibilities as a flexible radiation delivery system for CO2-laser radiation.

BACKGROUND AND OBJECTIVES: One significant inconvenience of the CO2 laser is the lack of flexible fibers essential for endoscopic applications. The goal of this study is to test the feasibility of hollow waveguides in view of a practical use in medicine. STUDY DESIGN/MATERIALS AND METHODS: Various types of plastic hollow waveguides for flexible delivery of CO2 laser radiation were examined. The transmission losses, divergence angle, damage threshold, and input and output beam profiles were determined. The interaction process between radiation transmitted through these guides with soft as well as hard tissues was studied. RESULTS: Plastic hollow waveguides can transmit high power (up to 50 W) with low losses (straight guide 1 dB/m) even through bendings. The divergence angle is < 13 degrees. Cutting quality and extent of thermal damage are comparable to incisions performed with a free laser beam. CONCLUSION: The results of this study show good cutting quality and durability of these flexible plastic hollow waveguides, which render possible to deliver CO2 radiation in the power range needed for most surgical applications with affordable transmission losses. Plastic hollow waveguides are, therefore, a real alternative to replace the mirror arms.

Animals↗
PubMed2005

Striatal synaptic plasticity: implications for motor learning and Parkinson's disease.

Changing the strength of synaptic connections between neurons is widely assumed to be the mechanism by which memory traces are encoded and stored in the central nervous system. Plastic changes appear to follow a regional specialization and underlie the specific type of memory mediated by the brain area in which plasticity occurs. Thus, long-term changes occurring at excitatory corticostriatal synapses should be critically involved in motor learning. Indeed, repetitive stimulation of the corticostriatal pathway can cause either a long-lasting increase or an enduring decrease in synaptic strength, respectively referred to as long-term potentiation (LTP), and long-term depression, both requiring a complex sequence of biochemical events. Once established, LTP can be reversed to control levels by a low-frequency stimulation protocol, an active phenomenon defined "synaptic depotentiation," required to erase redundant information. In the 6-hydroxydopamine rat model of Parkinson's disease (PD), striatal synaptic plasticity has been shown to be impaired, although chronic treatment with levodopa was able to restore it. Of interest, a consistent number of L-dopa-treated animals developed involuntary movements, resembling human dyskinesias. Strikingly, electrophysiological recordings from the dyskinetic group of rats demonstrated a selective impairment of synaptic depotentiation. This survey will provide an overview of plastic changes occurring at striatal synapses. The potential relevance of these findings in the control of motor function and in the pathogenesis both of PD and L-dopa-induced motor complications will be discussed.

Animals↗
PubMed2001

Mechanisms underlying human motor system plasticity.

There has been increased interest in the ability of the adult human nervous system to reorganize and adapt to environmental changes throughout life. This ability has been termed "plasticity." Plastic changes in the cerebral cortex have been studied: (a) as modifications of sensory or motor cortical representation of specific body parts (cortical maps, body representation level); and (b) as changes in the efficacy of existing synapses or generation of new synapses (neuronal or synaptic level). In this review, we describe paradigms used to study mechanisms of plasticity in the intact human motor system, the functional relevance of such plasticity, and possible ways to modulate it.

Animals↗
PubMed2006

alpha-Tocopherol affects neuronal plasticity in adult rat dentate gyrus: the possible role of PKCdelta.

Hippocampus dentate gyrus (DG) is characterized by neuronal plasticity processes in adulthood, and polysialylation of NCAM promotes neuronal plasticity. In previous investigations we found that alpha-tocopherol increased the PSA-NCAM-positive granule cell number in adult rat DG, suggesting that alpha-tocopherol may enhance neuronal plasticity. To verify this hypothesis, in the present study, structural remodeling in adult rat DG was investigated under alpha-tocopherol supplementation conditions. PSA-NCAM expression was evaluated by Western blotting, evaluation of PSA-NCAM-positive granule cell density, and morphometric analysis of PSA-NCAM-positive processes. In addition, the optical density of synaptophysin immunoreactivity and the synaptic profile density, examined by electron microscopy, were evaluated. Moreover, considering that PSA-NCAM expression has been found to be related to PKCdelta activity and alpha-tocopherol has been shown to inhibit PKC activity in vitro, Western blotting and immunohistochemistry followed by densitometry were used to analyze PKC. Our results demonstrated that an increase in PSA-NCAM expression and optical density of DG molecular layer synaptophysin immunoreactivity occurred in alpha-tocopherol-treated rats. Electron microscopy analysis showed that the increase in synaptophysin expression was related to an increase in synaptic profile density. In addition, Western blotting revealed a decrease in phospho-PKC Pan and phospho-PKCdelta, demonstrating that alpha-tocopherol is also able to inhibit PKC activity in vivo. Likewise, immunoreactivity for the active form of PKCdelta was lower in alpha-tocopherol-treated rats than in controls, while no changes were found in PKCdelta expression. These results demonstrate that alpha-tocopherol is an exogenous factor affecting neuronal plasticity in adult rat DG, possibly through PKCdelta inhibition.

Animals↗
PubMed1997

Morphological plasticity induced in the phrenic nucleus following cervical cold block of descending respiratory drive.

Morphological plasticity occurs in the phrenic nucleus within hours following an ipsilateral C2 spinal cord hemisection. The plasticity has been associated with the unmasking of a latent respiratory pathway (the crossed phrenic pathway) which allows recovery of the hemidiaphragm paralyzed by the hemisection during a reflex known as the crossed phrenic phenomenon. This study tests if the plasticity is induced by the generalized effects of spinal cord trauma or the more specific effect of interrupting the main descending respiratory drive to phrenic motoneurons. Electron microscopic quantitative morphometric analysis of the phrenic nucleus neuropil was carried out on four Sprague-Dawley rats (200-250 g) sacrificed 4 h following unilateral reversible cold block of the descending bulbospinal respiratory drive at the second cervical segment of the spinal cord (C2). The data from four sham-operated control animals were compared with those of the experimental group. The following morphological alterations were documented in cold block animals compared to controls: (1) a significant increase in the number of multiple synapses (i.e., terminals with synaptic active zones contacting two or more postsynaptic profiles in the same plane of section), (2) a significant increase in the number of dendrodendritic appositions, and (3) a significant increase in the length of symmetric and asymmetric synaptic active zones. The above changes are similar to the changes induced in the phrenic nucleus following C2 hemisection. We conclude therefore, that injury to the spinal cord is not a requirement for this type of morphological plasticity in the phrenic nucleus, but rather the induced changes are activity-dependent and are likely caused by the interruption of the descending bulbospinal respiratory drive to the phrenic nucleus.

Animals↗
PubMed1997

Chronic hypoxia does not induce synaptic plasticity in the phrenic nucleus.

Interruption of the main descending respiratory drive to phrenic motoneurons by cold block or spinal cord hemisection results in morphological modifications of the ipsilateral phrenic nucleus in the rat. The modifications consist of an increase in the number of multiple synapses and dendrodendritic appositions and elongation of the asymmetric and symmetric synaptic active zones. Hemisection and hemispinalization by cold block cause not only "functional deafferentation" of the ipsilateral phrenic neurons (i.e., a loss of ipsilateral descending respiratory drive), but also an increase in the remaining contralateral descending respiratory drive. The contralateral respiratory pathways connect with phrenic motoneurons ipsilateral to cold block or hemisection by decussating collateral axons which cross the spinal cord midline below the hemisection/cold block site. Thus, the phrenic nucleus synaptic plasticity could possibly be induced by functional deafferentation or by an increase of the descending respiratory drive. To differentiate between these two possible inducers of the plasticity, we assessed the synaptic morphology of the phrenic nucleus of nonoperated rats exposed to 48 h of hypoxia in an atmosphere chamber. The hypoxia exposure produces an increased descending respiratory drive without functional deafferentation. The quantitative data extracted from electron micrographs of the phrenic nucleus from four experimental rats were compared with the data from four normal breathing animals. Phrenic nucleus morphometric analysis showed that there was no significant difference in the mean number of single synapses between the samples from control animals (141 +/- 12.12) and the experimental animals (156 +/- 26.73). Similarly, no significant difference was detected in the total number of synaptic active zones of control animals (178.25 +/- 11.13) and experimental animals (195.05 +/- 5.35). Furthermore, the length of synaptic active zones of asymmetrical synapses (0.21 +/- 0.024 micron) or symmetrical synapses (0.22 +/- 0.022 micron) did not change significantly compared to the synaptic active zone length in control animals (0.21 +/- 0.018 micron for asymmetrical and 0.21 +/- 0.010 micron for symmetrical). We conclude that no synaptic plasticity occurs in the phrenic nucleus without functional deafferentation in spite of an increase in descending respiratory drive. Therefore functional deafferentation may be the primary inducer of phrenic nucleus synaptic plasticity occurring after hemisection or cold block.

Animals↗