Plasticity of neuronal functions in the visual system.
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Animals↗
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Results for “Neuronal Plasticity”
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Differential GABAA receptor clustering determines GABA synapse plasticity in rat oxytocin neurons around parturition and the onset of lactation.
Expression, functional properties, and clustering of alpha 1-, alpha 2-, and alpha 3-subunit containing GABA(A) receptors (GABA(A)Rs) were studied in dorsomedial SON neurons of the adult female rat supraoptic nucleus (SON) around parturition. We show that, although the decay time constant (tau(decay)) of GABAergic postsynaptic currents between and within individual recordings was very diverse, ranging from fast (i.e., alpha 1-like) to significantly slower (i.e., non-alpha 1-like), there was an overall shift towards slower decaying synaptic currents during the onset of lactation. This shift is not due to changes in mRNA expression levels, because real-time quantitative PCR assays indicated that the relative contribution of alpha 1, alpha 2, and alpha 3 remained the same before and after parturition. Also, changes in phosphorylation levels are not likely to affect the tau(decay) of postsynaptic currents. In alpha-latrotoxin (alpha-LTX)-induced bursts of synaptic currents from individual synapses, the tau(decay) of consecutive synaptic events within bursts was very similar, but between bursts there were large differences in tau(decay). This suggested that different synapses within individual SON neurons contain distinct GABA(A)R subtypes. Using multilabeling confocal microscopy, we examined the distribution of postsynaptic alpha 1-, alpha 2-, and alpha 3-GABA(A)Rs, based on colocalization with gephyrin. We show that the three GABA(A)R subtypes occurred either in segregated clusters of one subtype as well as in mixed clusters of two or possibly even three receptor subtypes. After parturition, the density and proportion of clusters containing alpha 2- (or alpha 3-), but not alpha1-GABA(A)Rs, was significantly increased. Thus, the functional synaptic diversity at the postsynaptic level in dorsomedial SON neurons is correlated with a differential clustering of distinct GABA(A)R subtypes at individual synapses.
Animals↗
Peptide plasticity in primary sensory neurons and spinal cord during adjuvant-induced arthritis in the rat: an immunocytochemical and in situ hybridization study.
Chronic polyarthritis due to complete Freund's adjuvant injection is characterized by severe inflammation and pain. In the present immunocytochemical and in situ hybridization study on the rat, we quantitatively investigated peptide and peptide messenger RNA expression in the sensory circuit at the spinal level, i.e. sensory neurons in the dorsal root ganglia and in nerve endings and local neurons in the dorsal horn of the spinal cord. The immunocytochemical experiments were carried out five, 13 and 21 days after complete Freund's adjuvant injection, whereas in situ hybridization study was performed after 21 days from complete Freund's adjuvant injection. The main results in the present study are the following: (i) a decrease in substance P-, calcitonin gene-related peptide- and galanin-like immunoreactivities in dorsal root ganglia is observed five days after complete Freund's adjuvant injection, with recovery (calcitonin gene-related peptide and galanin) or even an increase (substance P) after 21 days; (ii) calcitonin gene-related peptide, substance P and galanin peptide levels are increased in dorsal root ganglia after 21 days; (iii) opioid peptide (enkephalin and dynorphin), substance P and galanin messenger RNAs are strongly up-regulated in dorsal horn neurons after 21 days; (iv) neuropeptide Y content increases in dorsal root fibres and neuropeptide Y messenger RNA levels decrease in spinal neurons after 21 days; and (v) a dramatic decrease in calcitonin gene-related peptide and cholecystokinin messenger RNA levels is found in motoneurons in the ventral horn after 21 days. These data indicate that peptide expression in dorsal root ganglia and the spinal cord is markedly influenced by severe inflammation with distinct and individual temporal patterns, which are also related to the severe rearrangement of joint structure during polyarthritis. The increase in galanin levels in dorsal root ganglia 21 days after complete Freund's adjuvant injection can be related to the structural damage of nerve fibres. Thus, there may be a transition from inflammatory to neuropathic pain, which could have consequences for treatment of patients with rheumatoid arthritis.
Animals↗
Early presynaptic changes during plasticity in cultured hippocampal neurons.
Long-lasting increase in synaptic strength is thought to underlie learning. An explosion of data has characterized changes in postsynaptic (pstS) AMPA receptor cycling during potentiation. However, changes occurring within the presynaptic (prS) terminal remain largely unknown. We show that appearance of new release sites during potentiation between cultured hippocampal neurons is due to (a) conversion of nonrecycling sites to recycling sites, (b) formation of new releasing sites from areas containing diffuse staining for the prS marker Vesicle-Associated Membrane Protein-2 and (c) budding of new recycling sites from previously existing recycling sites. In addition, potentiation is accompanied by a release probability increase in pre-existing boutons depending upon their individual probability. These prS changes precede and regulate fluorescence increase for pstS GFP-tagged-AMPA-receptor subunit GluR1. These results suggest that potentiation involves early changes in the prS terminal including remodeling and release probability increase of pre-existing synapses.
Animals↗
Transient plasticity of hippocampal CA1 neuron glutamate receptors contributes to benzodiazepine withdrawal-anxiety.
Withdrawal from 1-week oral administration of the benzodiazepine (BZ), flurazepam (FZP) is associated with enhanced AMPA receptor (AMPAR)-mediated and reduced NMDA receptor (NMDAR)-mediated excitation in CA1 pyramidal neurons 2-days after cessation of FZP administration. The present study examined temporal regulation of glutamate receptor-mediated whole-cell currents in CA1 neurons from hippocampal slices prepared from 0-, 1-, 2-, and 4-day FZP-withdrawn rats in relation to expression of anxiety-like behavior during BZ withdrawal. AMPAR-mediated miniature excitatory postsynaptic current (mEPSC) amplitude was significantly increased in CA1 neurons from 1- and 2-day FZP-withdrawn rats, while evoked NMDAR EPSC amplitude was reduced only in neurons from 2-day FZP-withdrawn rats. Withdrawal-anxiety, measured in the elevated plus-maze, was observed 1 day, but not 0, 2, or 4 days, after FZP treatment with 1-day withdrawn rats spending significantly reduced time in open arms compared to controls. CA1 neuron hyperexcitability was evident from the significant increase in the frequency of extracellular, 4-AP-induced spike discharges in slices from 1-day FZP-withdrawn rats. Systemic injection of the NMDAR antagonist MK-801 (0.25 mg/kg) on day 1 of withdrawal prevented reduced NMDAR-mediated currents in CA1 neurons from 2-day FZP-withdrawn rats, whereas AMPAR-mediated currents remained upregulated. Furthermore, MK-801 'unmasked' withdrawal-anxiety in the same 2-day FZP-withdrawn rats. Systemic injection of the AMPAR antagonist GYKI-52466 (0.5 mg/kg) at the onset of withdrawal blocked increased AMPAR-mediated currents and withdrawal-anxiety in 1-day FZP-withdrawn rats. These findings suggest that increased CA1 neuron AMPAR-mediated excitation may contribute to hippocampal hyperexcitability and expression of withdrawal-anxiety after prolonged BZ exposure via NMDAR-mediated neural circuits.
Animals↗
Reactive oxygen species and nitric oxide mediate plasticity of neuronal calcium signaling.
Reactive oxygen species (ROS) and nitric oxide (NO) are important participants in signal transduction that could provide the cellular basis for activity-dependent regulation of neuronal excitability. In young rat cortical brain slices and undifferentiated PC12 cells, paired application of depolarization/agonist stimulation and oxidation induces long-lasting potentiation of subsequent Ca(2+) signaling that is reversed by hypoxia. This potentiation critically depends on NO production and involves cellular ROS utilization. The ability to develop the Ca(2+) signal potentiation is regulated by the developmental stage of nerve tissue, decreasing markedly in adult rat cortical neurons and differentiated PC12 cells.
Animals↗
Dopaminergic modulation of long-term synaptic plasticity in rat prefrontal neurons.
In rat prefrontal cortex (the prelimbic area of medial frontal cortex), the induction of long-term depression (LTD) and long-term potentiation (LTP) of glutamatergic synapses is powerfully modulated by dopamine. The presence of dopamine in the bathing medium facilitates LTD in slice preparations, whereas in the anesthetized intact brain, dopamine released from dopaminergic axon terminals in the prefrontal cortex facilitates LTP. Dopaminergic facilitation of LTD is at least partly achieved by postsynaptic biochemical mechanisms in which enzymatic processes triggered by dopamine receptor activation cooperate with those triggered by glutamate metabotropic receptor activation. Evidence suggests that dopamine facilitates LTP also in the slice condition. In this case, dopamine receptors must be pre-stimulated ('primed') before the application of high-frequency stimuli in the presence of dopamine. This procedure may mimic baseline stimulation of dopamine receptors that occurs under physiological conditions.
Animals↗
Use of a recombinant pseudorabies virus to analyze motor cortical reorganization after unilateral facial denervation.
A unilateral facial nerve injury (n7x) was found to influence the transcallosal spread of the attenuated strain of pseudorabies virus (PRV Bartha) from the affected (left) primary motor cortex (MI) to the contralateral MI of rats. We used Ba-DupLac, a recombinant PRV strain, for the tracing experiments since this virus was demonstrated to exhibit much more restricted transportation kinetics than that of PRV Bartha, and is therefore more suitable for studies of neuronal plasticity. Ba-Duplac injection primarily infected several neurons around the penetration channel, but hardly any transcallosally infected neurons were observed in the contraleral MI. In contrast, after right facial nerve injury, Ba-DupLac was transported from the primarily infected neurons in the left MI to the contralateral side, and resulted in the labeling of several neurons due to a transneuronal infection. These results reveal that a peripheral nerve injury induces changes in the Ba-DupLac infection pattern in the related cortical areas. These findings and the literature data suggest that this phenomenon may be related to the changes in the expression or to the redistribution of cell-adhesion molecules, which are known to facilitate the entrance and/or transmission of PRV into neurons.
Animals↗
Testosterone-dependent plasticity of avian forebrain neurons is not restricted to the song control system.
Testosterone is acting on brain areas involved in the control of sexual behaviour, for example the preoptic area and the song system. We now demonstrate that it also affects other avian brain areas, as exemplified here by measurement of spine densities. Depletion of testosterone by castration or application of cyproterone acetate leads to a decrease in spine density in secondary sensory areas like lateral neo- and hyperstriatum and hyperstriatum accessorium and dorsale, or in associative areas such as the caudal archi- and neostriatum. We conclude that testosterone is acting directly on the spines, and suggest that the mechanism of spine density control by hormones may have arisen because of energy demands.
Animals↗
Distinct patterns of plasticity in prefrontal cortex neurons that encode slow and fast responses to stress.
The prefrontal cortex (PFC) has been implicated in cognitive and affective responses to acute and chronic stress; however, direct evidence for the reactivity or adaptability of PFC neurons to stress is lacking. We followed the unit activity of medial PFC (mPFC) neurons in awake rats during two consecutive exposures to restraint stress or to a non-aversive novel object. The majority (75%) of mPFC neurons had significant responses to the initial restraint that was differentiated into one of three temporal patterns: (i) phasic increase in firing rate during the restraint period, (ii) slow onset increase in firing rate that was sustained for > 2 h after restraint, and (iii) brief bi-phasic responses to initiation and termination of restraint. Exposure to a novel object elicited an exposure-locked phasic response in 40% of the neurons. None of the neurons displayed the sustained activation that was prominent after restraint. A second exposure to the object no longer elicited this phasic response while neurons in the three restraint-responsive groups modified their firing rate during the second restraint in a manner that was specific to their pattern of response to the first restraint. These findings demonstrate that whereas some mPFC neurons respond phasically to novel stimuli irrespective of their aversive nature, a separate population of PFC neurons responds to a stressful stimulus with a sustained increase in firing rate that persists in the absence of that stimulus. These neurons may be a substrate for adaptive responses that are necessary for behavioral modification.
Action Potentials↗
Serotonin receptor antagonists discriminate between PKA- and PKC-mediated plasticity in aplysia sensory neurons.
Highly selective serotonin (5-hydroxytryptamine, 5-HT) receptor antagonists developed for mammals are ineffective in Aplysia due to the evolutionary divergence of neurotransmitter receptors and because the higher ionic strength of physiological saline for marine invertebrates reduces antagonist affinity. It has therefore been difficult to identify antagonists that specifically block individual signaling cascades initiated by 5-HT. We studied two broad-spectrum 5-HT receptor antagonists that have been characterized biochemically in Aplysia CNS: methiothepin and spiperone. Methiothepin is highly effective in inhibiting adenylyl cyclase (AC)-coupled 5-HT receptors in Aplysia. Spiperone, which blocks phospholipase C (PLC)-coupled 5-HT receptors in mammals, does not block AC-coupled 5-HT receptors in Aplysia. In electrophysiological studies, we explored whether methiothepin and spiperone can be used in parallel to distinguish between the AC-cAMP and PLC-protein kinase C (PKC) modulatory cascades that are initiated by 5-HT. 5-HT-induced broadening of the sensory neuron action potential in the presence of tetraethylammonium/nifedipine, which is mediated by modulation of the S-K+ currents, was used an assay for the AC-cAMP cascade. Spike broadening initiated by 5 microM 5-HT was unaffected by 100 microM spiperone, whereas it was effectively blocked by 100 microM methiothepin. Facilitation of highly depressed sensory neuron-to-motor neuron synapses by 5-HT was used as an assay for the PLC-PKC cascade. Spiperone completely blocked facilitation of highly depressed synapses by 5 microM 5-HT. In contrast, methiothepin produced a modest, nonsignificant, reduction in the facilitation of depressed synapses. Interestingly, these experiments revealed that the PLC-PKC cascade undergoes desensitization during exposure to 5-HT.
Action Potentials↗
Effects of acetylcholine and atropine on plasticity of central auditory neurons caused by conditioning in bats.
In the big brown bat (Eptesicus fuscus), conditioning with acoustic stimuli followed by electric leg-stimulation causes shifts in frequency-tuning curves and best frequencies (hereafter BF shifts) of collicular and cortical neurons, i.e., reorganization of the cochleotopic (frequency) maps in the inferior colliculus (IC) and auditory cortex (AC). The collicular BF shift recovers 180 min after the conditioning, but the cortical BF shift lasts longer than 26 h. The collicular BF shift is not caused by conditioning, as the AC is inactivated during conditioning. Therefore it has been concluded that the collicular BF shift is caused by the corticofugal auditory system. The collicular and cortical BF shifts both are not caused by conditioning as the somatosensory cortex is inactivated during conditioning. Therefore it has been hypothesized that the cortical BF shift is mostly caused by both the subcortical (e.g., collicular) BF shift and the activity of nonauditory systems such as the somatosensory cortex excited by an unconditioned leg-stimulation and the cholinergic basal forebrain. The main aims of our present studies are to examine whether acetylcholine (ACh) applied to the AC augments the collicular and cortical BF shifts caused by the conditioning and whether atropine applied to the AC abolishes the cortical BF shift but not the collicular BF shift, as expected from the preceding hypothesis. In the awake bat, we made the following findings. ACh applied to the AC augments not only the cortical BF shift but also the collicular BF shift through the corticofugal system. Atropine applied to the AC reduces the collicular BF shift and abolishes the cortical BF shift which otherwise would be caused. ACh applied to the IC significantly augments the collicular BF shift but affects the cortical BF shift only slightly. ACh makes the cortical BF shift long-lasting beyond 4 h, but it cannot make the collicular BF shift long-lasting beyond 3 h. Atropine applied to the IC abolishes the collicular BF shift. It reduces the cortical BF shift but does not abolish it. Our findings favor the hypothesis that the BF shifts evoked by the corticofugal system, and an increased ACh level in the AC evoked by the basal forebrain are both necessary to evoke a long-lasting cortical BF shift.
Acetylcholine↗
Acute pain following musculoskeletal injuries and orthopaedic surgery: mechanisms and management.
The undertreatment of acute pain associated with musculoskeletal conditions and surgical procedures is a focus of growing concern to orthopaedic surgeons. Fortunately, the armamentarium now includes recent advances in the understanding of how undertreated acute pain can lead to chronic pain, the development of new therapeutic agents, and new approaches to pain management. The concept of neuronal plasticity (the ability of neurons to profoundly alter their structure, function, or biochemical profile in response to repeated afferent sensory input) is now central to the understanding of the development of chronic pain from acute pain. Local inflammation in injured tissue increases the sensitization of specialized peripheral sensory neurons (nociceptors), leading to repeated afferent input into the central nervous system. Resolving inflammation before these events occur may prevent modifications in the central nervous system that lead to chronic pain. Therefore, it is important to reduce pain and inflammation at both the central and peripheral level. In addition to traditional agents (aspirin, nonspecific nonsteroidal anti-inflammatory drugs, opioids, local anesthetics, and regional blocks), more recently developed agents, such as cyclooxygenase-2 specific inhibitors, are now available. Combinations of these agents, as well as combinations of pharmacologic and nonpharmacologic approaches, are being used as multimodal therapy to treat the multiple sources of acute pain. Clinical practice guidelines for the management of acute pain now emphasize the incorporation of new knowledge into solid, evidence-based practice. This knowledge, combined with further understanding of the anatomic, physiologic, cellular, and molecular basis of pain, will provide the basis forfuture approaches to the management of acute pain in orthopaedic practice.
Acute Disease↗
[Changes in the plastic properties of the neuron under the action of antibodies to specific glycolipid antigens of the glia].
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Animals↗
Nerve growth factor activity and aging in CNS.
This is a discussion of aging in CNS and the influence of the nerve growth factor (NGF) protein. The paper considers neuronal plasticity and neuronotrophic substances, neuronal cell death and the nerve growth factor protein, including its effects, receptors, and model systems for the study of CNS aging.
Aging↗
Nerve growth factor-ganglioside interaction in the plasticity of central cholinergic neurons.
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Animals↗
Study of plasticity of neurone populations in model situations.
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Acoustic Stimulation↗
[Impulse synchronization in the mechanisms of adaptive plasticity of neuronal populations of the posterior hypothalamus].
An increase in the firing rate induced minimization of the reward (a weak electrical skin stimulation) and altered the neuronal activity patterns in the posterior hypothalamus. The estimation of the expected random coincidence functions between the two neuronal activity trains belonging to adjacent cells showed the synchronization both in high- and low-frequency ranges. In the process of adaptive alterations of the neuronal activity, fluctuations of the expected randon coincidence coefficients occurred.
Adaptation, Physiological↗