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Results for “synaptic plasticity”

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At least 1,027 records · Page 57Linked to original sources
PubMed2006

Regulation of behavioral and synaptic plasticity by serotonin release within local modulatory fields in the CNS of Aplysia.

In Aplysia, serotonergic neurons are widely activated during sensitization training, but the effects of exogenous serotonin (5-HT) on reflex circuits vary, inducing short- or long-term synaptic facilitation or synaptic inhibition, depending on the site of application. During learning, it is possible that specific spatial patterns of 5-HT release evoked by training may produce different phases of sensitization or behavioral inhibition. To test this hypothesis, we examined the modulation of the tail-induced siphon withdrawal reflex by repeated noxious stimuli applied to one of three sites: the (1) ipsilateral or (2) contralateral sides of the tail or (3) the head. Ipsilateral tail shock produced long-term sensitization, whereas contralateral tail shock induced only short-term sensitization, and head shock produced inhibition. In parallel cellular experiments, tail-nerve shock evoked large 5-HT release localized around the ipsilateral tail sensory neurons (SNs) and motor neurons (MNs) but only modest 5-HT release in the contralateral pleural-pedal ganglia and in the abdominal ganglion, in which the siphon MNs are located. Head-nerve shock, in contrast, produced only modest 5-HT release in the pleural, pedal, and abdominal ganglia. Thus, each training protocol evoked a specific pattern of 5-HT release within the CNS. In addition, we found that 5-HT released in the pleural ganglia was correlated with facilitation of SN-MN synapses; however, in the abdominal ganglion, it was associated with inhibition of the synapses between identified interneurons (L29s) and siphon MNs (LFSs). Because 5-HT differentially modulates synaptic efficacy at different synaptic sites, our data can explain how specific spatial patterns of 5-HT release in local modulatory fields can contribute to the induction of short- or long-term sensitization or to behavioral inhibition.

Action Potentials↗
PubMed1987

Synaptic plasticity to estrogen in the lateral septum of the adult male and female rats.

There is no sex difference in the number of axodendritic synapses in the lateral septum of adult rats. However, the treatment of adult females with estradiol (E2) for 4 weeks increases significantly the number of synapses, whereas E2 treatment fails to increase the synaptic number in males, suggesting a possible sexually dimorphic synaptic response to estrogen.

Animals↗
PubMed1988

A plausible neural circuit for classical conditioning without synaptic plasticity.

The cellular bases of learning are currently under active investigation by both experimental and theoretical means. In this paper, a simple neuronal wiring diagram is proposed that can reproduce both simple and higher-order behavioral paradigms seen in invertebrate classical conditioning experiments. Learning in this model does not take place by modification of synaptic strength values. Instead, the model uses a layer of interneurons with modifiable thresholds for spike initiation, as suggested by the plasticity mechanisms thought to operate in Hermissenda [Alkon, D. L. (1983) Sci. Am. 249, 70-84]. The model therefore has an advantage in plausibility compared with more standard models using Hebb synapses or their functional equivalents, which have not yet been demonstrated in any invertebrate organism.

Animals↗
PubMed2004

Endocytosis and synaptic plasticity: might the tail wag the dog?

In nerve terminals, endocytosis in compensation for transmitter exocytosis was once thought 'housekeeping'. Now, several lines of research utilizing optical endocytic probes have coalesced into a new functional model. The model comprises two distinct endocytosis and vesicle-processing paradigms that are differentially regulated in response to demand for transmitter. Under some circumstances, such as recovery from short-term depression, it appears that endocytosis, and not exocytosis, is rate-limiting for transmitter release and is therefore a principal determinant of synaptic strength.

Animals↗
PubMed1993

Nitric oxide and hippocampal synaptic plasticity.

The dependence of NMDA receptor-dependent LTP on postsynaptic depolarization and increases in postsynaptic calcium, coupled with evidence supporting presynaptically mediated increases in transmitter release accompanying LTP, suggest that a retrograde transsynaptic messenger participates in the synaptic enhancement. Although many questions remain unanswered, the available evidence suggests a role for NO as such a messenger in certain LTP paradigms. It is unclear, however, whether NO contributes to LTP under differing experimental conditions and whether other messengers, acting in concert with or independent of NO, contribute to a retrograde signalling system. Furthermore, the conditions under which NMDA receptor activation, postsynaptic calcium increases and NO contribute to synaptic enhancement, synaptic depression and excitotoxic neuronal injury need to be clarified. Furthermore, efforts aimed at clarifying the molecular targets of NO must remain a priority of this line of research.

Amino Acid Oxidoreductases↗
PubMed1997

Neural recognition molecules and synaptic plasticity.

Recent studies of neural recognition molecules have revealed similarities between their functions during ontogenetic development and in neural plasticity in the adult. Observations both at the cellular level in vitro and at the behavioural level in vivo suggest that altered recognition molecule expression can lead to changes in synaptic efficacy, and alterations in synaptic function in turn evoke changes in recognition molecule expression. These changes can manifest themselves as morphological alterations and modulations of the synapse's signal transduction machinery.

Amyloid beta-Protein Precursor↗
PubMed1999

Molecular mechanisms of synaptic plasticity and memory.

To unravel the molecular and cellular bases of learning and memory is one of the most ambitious goals of modern science. The progress of recent years has not only brought us closer to understanding the molecular mechanisms underlying stable, long-lasting changes in synaptic strength, but it has also provided further evidence that these mechanisms are required for memory formation.

Amygdala↗
PubMed1999

Modulation of long-term synaptic plasticity at excitatory striatal synapses.

Modulation of long-term plasticity by both the intrinsic activation of metabotropic glutamate receptors and dopamine released from the nigrostriatal pathway was investigated at excitatory striatal synapses. Intracellular recordings demonstrated that tetanic stimulation at an intensity equal to that used for synaptic sampling produced, on average, a slight long-term depression of excitatory postsynaptic potentials. The long-term response pattern was variable, however, with some cells showing potentiation and others no plasticity. Block of metabotropic glutamate receptors with 3-aminophosphonovaleric acid changed the pattern of responses, increasing the percentage of cells showing long-term potentiation. Similarly, 6-hydroxydopamine lesions to the substantia nigra changed the pattern of response to tetanic stimulation, increasing the expression of long-term potentiation. These data indicate that metabotropic glutamate receptor and dopamine receptor activation may function to regulate the expression of activity-dependent plasticity at corticostriatial synapses. Paired-pulse stimulation revealed that post-tetanic plasticity was negatively correlated with changes in paired-pulse plasticity in the control and 6-hydroxydopamine-lesioned groups, suggesting that the expression of long-term plasticity has a presynaptic component at corticostriatal synapses.

2-Amino-5-phosphonovalerate↗
PubMed1988

Physiological aspects of synaptic plasticity: the Ia/motoneuron connection as a model.

Damage to peripheral nerves results in substantial changes in the function of spinal synapses that mediate the monosynaptic reflex. These alterations consist independently of those caused by axotomy of the postsynaptic neuron and those produced by axotomy of the presynaptic neuron. Synaptic transmission is depressed following interruption of either limb of the segmental reflex loop. These reductions in EPSP amplitude are largely reversed following reinnervation of the peripheral tissue by the cut fibers, whether or not the regenerating fiber finds the correct muscle. Alterations in synaptic transmission following damage to the spinal cord itself are more variable than those noted after peripheral nerve damage. Although segmental EPSPs are generally enhanced following spinal injury (if in fact changes do occur), these increases are superimposed on motoneuron hyperpolarization, making the net changes in reflex transmission unpredictable. Furthermore, the extent of motoneuron depolarization is also influenced by the amount of temporal summation of EPSPs during the high-frequency activation of group Ia fibers known to occur, for example, during normal walking. Because EPSP amplitude is not constant during such activation and is modulated differently at connections on different motoneurons, changes in effective levels of synaptic transmission after such lesions are very difficult to predict. Thus it is not surprising that it is not possible to make close correlations between changes in amplitude of EPSPs and reflex behavior following injury (but see chapter by M.E. Goldberger and M. Murray, this volume). These alterations in synaptic transmission can occur at a considerable physical distance from the site of injury, peripheral or central. They illustrate the interdependence in elements of the nervous system, which can also be seen as changes in properties of motoneurons themselves (e.g., input resistance, after-hyperpolarization, rheobase) following many of these injuries. Altered cell properties complicate the functional interpretation of synaptic changes obtained after injury but must be considered in evaluating the sequelae of lesions in the peripheral and central nervous system.

Animals↗
PubMed1983

Synaptic plasticity in the cerebral cortex of mice: effects of radiation and anesthesia.

In the neuropil of layers II and III of the frontal cortex of adult mice, as seen in the electron microscope, sodium pentobarbital anesthesia alone results in a significant decrease in synaptic profile length at 1 day after anesthetization, followed by a return to normal or above normal levels after 2-28 days, while the number of synaptic profiles per unit cross section (profile incidence) is not altered; irradiation with 5-500 rad plateau argon particles significantly inhibits the profile shortening effect of anesthesia at 1 day after exposure, but this inhibition is not dose related; an inverse dose relationship in profile incidence appears at 2 days following irradiation with argon particles; at 1 to 2 hours after 150 or 220 rad x-irradiation, profile incidence is significantly reduced while the length is increased, effects that appear to be dose related and unaffected by adrenalectomy.

Animals↗
PubMed2002

Different metabotropic glutamate receptors play opposite roles in synaptic plasticity of the rat medial vestibular nuclei.

In the medial vestibular nuclei (MVN) of rat brainstem slices, the role of group II and III metabotropic glutamate receptors (mGluRs) and of the subtypes of group I mGluRs: mGluR1, mGluR5, was investigated in basal synaptic transmission and in the induction and maintenance of long-term potentiation (LTP). We used selective antagonists and agonists for mGluRs and we analysed the field potentials evoked by vestibular afferent stimulation before and after high-frequency stimulation (HFS) to induce LTP. The group II and III mGluR antagonist, (R,S)-alpha-2-methyl-4sulphonophenylglycine (MSPG), induced LTP per se and caused a reduction of the paired-pulse facilitation (PPF) ratio indicating an enhancement of glutamate release. This suggests that group II and III mGluRs are activated under basal conditions to limit glutamate release. Both the group II and III mGluR selective antagonists, 2S-2-amino-2-(1S,2S-2-carboxycycloprop-1-yl)-3-(xanth-9-yl)propanoate (LY341495) and (R,S)-alpha-methylserine-O-phosphate (MSOP), induced LTP, and the selective agonists, (2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate (APDC) and L(+)-2-amino-4-phosphonobutyric acid (L-AP4) depressed the field potentials and prevented HFS-LTP, with a prevailing contribution of group II mGluRs over that of group III mGluRs. The mGluR1 antagonist, 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester (CPCCOEt) prevented the full development and maintenance of HFS-LTP. By contrast, the mGluR5 antagonist, 2-methyl-6-phenylethynylpyridine (MPEP) induced LTP per se, which was impeded by CPCCOEt, and it had no effect on LTP once induced by HFS. The PPF analysis showed an enhancement of glutamate release during MPEP potentiation. The group I mGluR agonist, (R,S)-3,5-dihydroxyphenylglycine (DHPG) induced LTP per se, which was blocked by CPCCOEt. By contrast the mGluR5 agonist, (R,S)-2-chloro-5-hydroxypheylglycine (CHPG) prevented LTP elicited by HFS and DHPG as well. In conclusion vestibular LTP is inhibited by group II and III mGluRs during the early induction phase while it is facilitated by mGluR1 for achieving its full expression and consolidation. An additional inhibitory control is exerted by mGluR5 at the level of this facilitatory phase.

Amino Acids↗
PubMed1992

Synaptic plasticity in the rat striatum following chronic haloperidol treatment.

Administration of the dopamine (DA) antagonist haloperidol leads to the development of behavioral hypersensitivity as well as enhanced neuronal growth when striatal extracts from these animals are incubated with mesencephalic cultures. For determining if alterations in neuronal growth also occur in vivo, the ultrastructure of the neuropil in the dorsolateral quadrant of the striatum from rats treated (24 days) with haloperidol (1.25 mg/kg) was examined by electron microscopy. Haloperidol-treated rats developed statistically significant behavioral hypersensitivity relative to vehicle-treated controls (p < 0.01). Evaluation of the neuropil revealed that haloperidol treatment enhanced, relative to vehicle-treated controls, the overall number of synaptic boutons by 9% (p < 0.01). The number of perforated synaptic profiles as well as the number of double synapses was increased by 20 and 50%, respectively, although this increase was not statistically significant. The number of myelinated axons remained unchanged, while the number of dendritic spines was increased by 21% (p < 0.05). These data suggest that chronic haloperidol treatment enhanced the growth and possible sprouting of presynaptic neurons and also induced postsynaptic plastic changes. These ultrastructural changes may contribute in part to hypersensitivity behaviors.

Animals↗
PubMed2006

Short-term synaptic plasticity in layer II/III of the rat anterior cingulate cortex.

Recent in vivo electrophysiological studies in our laboratory demonstrated medial thalamus (MT) induced short-term facilitation in the middle layers of the anterior cingulate cortex (ACC). The aim of the present study was to investigate different forms of short-term plasticity (STP) in layer II/III of the ACC in an in vitro slice preparation. Extracellular field potentials in layer II/III consisting of an early component (fAP) and a late component (fPSP) were activated by electrical stimulation of the deep layers. The fPSP and intracellularly recorded excitatory post-synaptic potential (EPSP) could be facilitated by paired-pulse stimulation at a low frequency (0.033Hz, pulse interval 20-400ms). An initial facilitation and subsequent depression were obtained when high frequency (12.5, 25 and 50Hz) tetanus stimulations were applied to the ACC slice. A post-tetanic augmentation 30s in duration was also observed. The effects of tetanic stimulation were altered in the presence of an increased or a decreased calcium concentration. Application of omega-conotoxin GVIA (CTX) in normal calcium concentration conditions decreased overall responses during tetanic stimulation similar to reducing calcium exposure. However CTX application did not increase paired-pulse facilitation (PPF) as is seen under low calcium conditions. These results indicate that calcium is involved in the formation of certain features of STP in layer II/III of the ACC and that N-type calcium channels contribute to some, but not all, components of these plastic changes. Two-site electrical stimulation testing showed that two separate presynaptic inputs can produce short-term facilitation. Our findings implicate a post-synaptic mechanism in STP in layer II/III of the ACC.

Animals↗
PubMed1993

Spinules: a case for retinal synaptic plasticity.

In both vertebrate and invertebrate nervous systems, a population of synapses is characterized by having finger-like indentations of the postsynaptic membrane that project into the presynaptic terminal. These 'spinules' are often transitory structures, and their presence has been associated with increased synaptic activity. We have studied the functional role of spinules in the fish retina, where they are observed in horizontal cells invaginating cone pedicles, and in synaptic terminals of bipolar cells. In the cone-horizontal cell synaptic complex, spinules are present during light adaptation; their formation is triggered by external light stimuli as well as by endogenous factors. Pharmacologically, spinules are degraded following an increase, and formed in response to a decrease of the transmitter glutamate released by the cone cells. Dopamine, released by interplexiform cells and acting via a D1 receptor-mediated increase in cAMP, and a protein-kinase-C-based mechanism are also capable of inducing spinule formation. Functionally, the presence and absence, as well as the timecourse, of spinule formation during light adaptation is closely correlated with the development of biphasic chromatic responses in a class of cone horizontal cells and the manifestation of colour-opponency in ganglion cells. This suggests that in the outer retina of fish, spinules are mediating feedback activity essential for the coding of antagonistic colour information.

Animals↗