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Results for “synaptic plasticity”

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At least 1,189 records · Page 66Linked to original sources
PubMed1989

Synaptic plasticity in the hypoglossal nucleus of female canaries: structural correlates of season, hemisphere, and testosterone treatment.

The caudal portion of the hypoglossal nucleus (nXIIts) contains the motor neurons that control the syrinx in songbirds. In canaries, song occurs seasonally, is principally produced by males, and appears to be produced predominantly by muscles on the left side of the syrinx. The present study measures the effect of seasonal change and manipulation of testosterone levels on synapse number and morphology in nXIIts in adult female canaries. We find that synapse density is lower in testosterone-treated birds than in control birds and lower in fall than in spring. The number of vesicles per presynaptic profile increases in the spring as a result of a general increase in this measure in all synapses. The number of vesicles per presynaptic profile also increases with testosterone treatment, primarily due to an increase in the proportion of synapses associated with unusually high vesicle counts. Together, these changes suggest that large reserves of neurotransmitter may be necessary to sustain singing. Several ultrastructural differences between hemispheres are found. Postsynaptic thickenings are longer, and postsynaptic processes are larger on the left side than on the right side. In the spring, there are more vesicles per synapse on the left than on the right, but this lateralization is reversed in the fall. Thus, lateralization of song production is associated with lateral asymmetries in synapse morphology. These hemispheric differences are relatively small, like those seen at the light microscope level, encouraging further consideration of peripheral as well as CNS sources of functional lateralization. The seasonal and testosterone-induced changes in synapse number and morphology may be components of the periodic reorganization of canary vocalization.

Animals↗
PubMed1997

Postnatal development of synaptic plasticity in the CA3 hippocampal region of control and lead-exposed Wistar rats.

The object of this study was to compare the postnatal development of mossy fiber potentiation (MFP) and paired-pulse facilitation in the CA3 region of control and led-exposed rats. The postnatal development of MFP was not influenced by the chronic pre- and postnatal lead exposure nor did we find a statistically significant impairment of MFP in region CA3 following lead exposure in the four age groups studied. In contrast to the adult animals, in the three immature groups of the control as well as the lead-exposed animals MFP was preceded by a posttetanic depression after which MFP developed slowly. The results of the paired-pulse procedure depended both on the age and on the interstimulus interval (ISI) in control and lead-exposed animals. The differences between control and lead-exposed rats were statistically significant only in the adult animals at an ISI of 10 ms. In this case paired-pulse stimulation resulted in an increase of the second evoked response relative to the first response in the lead-exposed animals while the same procedure decreased the second evoked response in the control animals. It is concluded that although low lead exposure had no effect on the expression of MFP in hippocampal CA3 region, inhibitory mechanisms as revealed by paired-pulse stimulation are impaired by lead in adult rats.

Age Factors↗
PubMed1999

Synaptic plasticity of feedback connections in rat visual cortex.

The issue we want to address in the present paper is to establish whether electrical stimulation of latero medial (LM) area, a secondary visual area in the rat, is able to induce Long Term Potentiation (LTP) and Long Term Depression (LTD) in primary visual cortex (V1). To this aim rat slices containing area V1 and LM were prepared at P23 and P40 and field potentials in layers 2/3 of area V1 were recorded stimulating LM. We showed that it was never possible to induce LTP in area V1, unless bicuculline, a gamma-aminobutyric acid (GABA) receptors blocker, was applied to the slice. In contrast, LTD was normally inducible. Thus, cortical gabaergic circuitry in area V1 controls LTP but not LTD elicited by stimulation of feedback connections from LM.

Aging↗
PubMed2003

How necessary is the activation of the immediate early gene zif268 in synaptic plasticity and learning?

The immediate early genes (IEGs) are activated rapidly and transiently in response to a multitude of stimuli. The zif268 belongs to a category of regulatory IEGs that activate downstream target genes and is considered to be a triggering mechanism to activate the genomic response in neurons. Several studies have shown that zif268 mRNA is upregulated during different forms of associative learning, and following tetanic stimulation that induces long-lasting LTP. To date, there is a general consensus that zif268 activation may constitute a critical mechanism for the encoding of long-lasting memories, however this is based on relatively few studies. Given the fact that zif268 can be activated by a number of different types of stimuli, it becomes important to determine exactly how it may be implicated in memory. Examination of the current literature suggests that zif268 is necessary in the processing of several types of memory, however, it is not entirely clear what aspects of memory zif268 may be implicated in. Here, we review the existing literature and emphasise that understanding the signalling pathways that lead to activation of the IEGs and the downstream targets of these genes will advance our understanding of how functional activation of zif268 may be implicated in processing long-term memories.

Animals↗
PubMed2001

The cortico-basal ganglia-thalamocortical circuit with synaptic plasticity. II. Mechanism of synergistic modulation of thalamic activity via the direct and indirect pathways through the basal ganglia.

A possible mechanism underlying the modulatory role of dopamine, adenosine and acetylcholine in the modification of corticostriatal synapses, subsequent changes in signal transduction through the "direct" and "indirect" pathways in the basal ganglia and variations in thalamic and neocortical cell activity is proposed. According to this mechanism, simultaneous activation of dopamine D1/D2 receptors as well as inactivation of adenosine A1/A(2A) receptors or muscarinic M4/M1 receptors on striatonigral/striatopallidal inhibitory cells can promote the induction of long-term potentiation/depression in the efficacy of excitatory cortical inputs to these cells. Subsequently augmented inhibition of the activity of inhibitory neurons of the output nuclei of the basal ganglia through the "direct" pathway together with reduced disinhibition of these nuclei through the "indirect" pathway synergistically increase thalamic and neocortical cell firing. The proposed mechanism can underlie such well known effects as "excitatory" and "inhibitory" influence of dopamine on striatonigral and striatopallidal cells, respectively; the opposite action of dopamine and adenosine on these cells; antiparkinsonic effects of dopamine receptor agonists and adenosine or acetylcholine muscarinic receptor antagonists.

Adenosine↗
PubMed1996

Effects of different patterns of light adaptation on cellular and synaptic plasticity in teleost retina: comparison of flickering and steady lights.

The importance of the pattern of light stimulus in inducing light-adaptive morphological (cellular and sub-cellular) changes in the outer retina of the carp was assessed. Thus, the effects of steady and flickering backgrounds (of the same intensity) on cone photomechanical movements (PMMs) and horizontal cell (HC) spinules were compared by quantitative measurements. For both phenomena, flickering stimuli had a significantly greater effect than steady, although the number of photons delivered by the former was one-half. The results demonstrate clearly that the pattern of light stimulus is indeed an important parameter in determining the extent of adaptation in the outer retina. The effects are discussed in relation to possible neurochemical bases of light-adaptive neural control mechanisms.

Adaptation, Physiological↗
PubMed2003

Microtubule-associated protein 2 (MAP2) expression during synaptic plasticity in the guinea pig cochlea.

The expression of different isoforms of microtubule-associated proteins 2 (MAP2), including the low molecular weight form MAP2c present mainly in developing neurons, was investigated in the primary auditory neurons after alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) perfusion in the guinea pig cochlea. MAP2 expression appeared to be tightly regulated in the repairing neurons. Neurite regrowth seems to involve the MAP2c isoform. In cochlear neurons, mechanisms involved in the period of development might be reactivated after excitotoxic injury in the mature cochlea.

Action Potentials↗
PubMedDate not supplied

Estrogen, synaptic plasticity and hypothalamic reproductive aging.

Unlike primates who undergo ovarian failure and loss of sex steroids at the end of reproduction, aging rodents undergo constant vaginal estrus followed by constant diestrus and finally anestrus, which indicates the absence of responsive ovarian follicles. The latter state is analogous to menopause in women. The timing of the appearance of constant estrus is determined by many factors including estrogen exposure in the brain during development and the number of times that the animal gets pregnant. The chief site of this reproductive aging in rat brains is the arcuate nucleus of the hypothalamus. The transition from normal cycles to constant estrus parallels the females' gradually decreased ability to respond to administered estradiol with a cycle of inhibition followed by disinhibition of gonadotrophin-releasing hormone. Evidence has accumulated indicating this to be due to a loss of the rat's ability to respond to markedly elevated estradiol with the usual arcuate nucleus neuro-glial plasticity that supports the estrogen-induced gonadotrophin surge (EIGS). Just as male rats are not capable of an EIGS, aged females loose this ability through repeated EIGS. Experiments indicate that in male rats the hypothalamic synaptology that develops as a result of exposure to testicular androgens in the perinatal period (brain sexual differentiation) is a result of conversion of testosterone from the testes to estrogen in the brain and is therefore due to early estrogen exposure. Aging females appear to reach a synaptology similar to males and constant estrus as a result of repeated exposure to ovarian estrogens during their reproductive careers. The relative role of aging and hormonal factors remains unclear. Morphological evidence is presented that indicates the above effects of estrogen involve changes in hypothalamic arcuate nucleus neurons and glia, including changes in the organization of perikaryal membranes as well as arcuate nucleus synaptology and the load of peroxidase in the astroglia. A possible role for free radicals (reactive oxygen species) in hypothalamic reproductive aging has been proposed. Such a mechanism is supported by evidence that the anti-oxidant vitamin E delays the onset of constant estrus and the accumulation of glial peroxidase in aging female rats. However, since the synaptology and peroxidase load in constant estrus females is independent of the age at which the constant estrus occurs, it appears that the role of (repeated) estradiol exposure is more deterministic of hypothalamic failure than is aging, per se.

Aging↗