Plasticity of cerebellar parallel fibers following developmental deficits in synaptic number

Chen, S.; Hillman, Dean E.

doi:10.1016/0006-8993(85)91595-1

Cited by 9 publications

(2 citation statements)

References 28 publications

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“…Since this increase was not seen in all groups where one might have anticipated it, we do not wish to overinterpret these results. Nonetheless, previous research has shown that age-related (Jones, 1988) and lesion-induced (Anthes et al, 1993;Chen and Hillman, 1985;Hillman and Chen, 1985) reductions in synaptic number are also accompanied by an elongation of the remaining synapses. Increasing synaptic length may reflect an attempt to maintain a constant level of synaptic transmission in a neural pathway that has fewer synaptic contacts.…”

Section: Nmda Antagonist-induced Alterations In Synaptic Lengthmentioning

confidence: 97%

Effect of chronic administration of NMDA antagonists on synaptic development

Brooks

Petit

LeBoutillier

1997

Synapse

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The current research assessed the role of the N-methyl-D-aspartate (NMDA) receptor in developmental synaptic plasticity. This was accomplished by quantitative analysis of synaptic number and morphology following pharmacological manipulation of NMDA receptor activity using either the competitive antagonist 2-amino-5-phosphonovaleric acid (APV) or the noncompetitive antagonist phencyclidine (PCP). In the first group, 15-day-old male Long-Evans rats were implanted with osmotic minipumps, which administered 50 mM APV or vehicle at a rate of 0.5 microliter per h into the subjects' occipital cortex for 14 days. At age 30 days (P30), the rats were sacrificed and their occipital neocortices were examined. A second group of rats was given subcutaneous injections of 10 mg/kg PCP or vehicle once daily beginning on P5 for a period of 15 days, and was sacrificed on P20. To determine the effects following withdrawal from long-term NMDA antagonism, a third group of animals was given the same PCP injection routine until P20, but was sacrificed on P21, P26, P36, and P56. Developmental administration of APV was associated with a decreased molecular layer depth and estimated total number of synapses. Similarly, PCP induced a reduction in brain weight, molecular layer depth, and estimated total number of synapses. Withdrawal from NMDA antagonism was initially associated with similar results, i.e., reduced brain weight, cortex depth, synaptic density, and estimated total number of synapses, along with an increase in synaptic length. By P36, however, there was a transitory rebound associated with increased molecular layer depth and estimated total number of synapses. These results support the suggestion that NMDA receptor activation is integral to naturally occurring developmental synaptogenesis, and underscore the importance of NMDA receptor involvement in the process of synaptic plasticity.

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Section: Nmda Antagonist-induced Alterations In Synaptic Lengthmentioning

confidence: 97%

Effect of chronic administration of NMDA antagonists on synaptic development

Brooks

Petit

LeBoutillier

1997

Synapse

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“…These data clearly show that there are regional, age, and sex-related differences in the numerical density of these contacts. The synaptic density values can be strongly influenced also by environmental and/or experimental conditions (Uzunova and HBmori, 1974;Hillman andChen, 1981b, 1984;Chen and Hillman, 1985).…”

Section: Numerical Density Of Purkinje Dendritic Spinesmentioning

confidence: 99%

Developmental dynamics of Purkinje cells and dendritic spines in rat cerebellar cortex

Takács

Hámori

1994

J of Neuroscience Research

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Quantitative morphological changes of the developing Purkinje cells were studied from 6 to 90 postnatal (PN) days in the IVth lobule of vermis in the cerebellum of rats. The soma size (mean diameter) of Purkinje cells increased rapidly between 6 PN (on average 10 microns) and 18 PN (about 17 microns) days; it did not change between 18 and 25 PN days, but increased moderately again between 25 and 48 PN days (22-23 microns) and stabilized on the same value. In contrast, the number of Purkinje cells/100 microns (the "linear density") decreased rapidly from 6 to 18 PN days. The molecular layer area belonging to 1 Purkinje cell increased rapidly from 6 to 25 PN days (from about 370 to 6,200 microns 2) and less rapidly between PN days 30 to 48 (up to 9,300 microns 2), followed by a moderate decrease at PN day 90 (about 6,600 microns 2). The volume belonging to 1 Purkinje cell dendritic arbor was about 5,500 microns 3 at PN day 6, 93,000 microns 3 at PN day 25, and 100,000 microns 3 at PN day 90. The numerical density of dendritic spines in the molecular layer showed a biphasic curve: a rapid increase from PN days 6 to 21 followed by a significant but short decrease at PN day 25, moderate rise from PN days 25 to 48, and a subsequent decline between PN days 48 and 90. The number of spines belonging to 1 Purkinje cell showed two developmental "peaks": the first peak at 21 PN days was moderate (5.6 x 10(4) spines/Purkinje cell) while the second maximum at 48 PN days was more significant (1.2 x 10(5) spines/Purkinje cell), which then declined to 6.3 x 10(4) spines/Purkinje cell at PN day 90. It is suggested that the temporary overproduction and the following decline in the number of Purkinje dendritic spines during the development of the cerebellar cortex may be the morphological indicator of the dynamics of synaptogenetic and of synaptic stabilization processes.

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Compensation in the number of presynaptic dense projections and synaptic vesicles in remaining parallel fibres following cerebellar lesions

Hillman

Chen

1985

J Neurocytol

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Our previous investigations demonstrated an increase in the size of remaining synaptic sites as an intermediate or possible alternative to sprouting plasticity. The total amount of postsynaptic contact area remained relatively constant for each target neuron even though there was a marked decrease in the number of sites on these neurons. In addition, enlarged boutons containing numerous synaptic vesicles were positioned adjacent to enlarged postsynaptic sites. The question posed by this study was to determine whether dense projections, parts of the presynaptic grids of the remaining parallel fibres, spread to cover the enlarged postsynaptic sites, or if the number of these densities increased on each site to maintain the structural organization of the presynaptic grid. In addition, the number of synaptic vesicles per bouton was quantitated to determine whether they compensated by increasing their number in relationship to the increased area of the presynaptic grid. The number of parallel fibre synapses on Purkinje cells was reduced by transection of a narrow bundle of parallel fibres accompanied by a small lesion undercutting the molecular layer to destroy granule cells contributing to this bundle. The number of presynaptic dense projections was quantitated in control and lesioned preparations (using ethanolic acid staining) in order to determine their correlation to the area of each site. In addition, the average number of synaptic vesicles in boutons was compared to the average size of boutons and the average contact area of the synaptic sites. At 3 to 7 days following partial deafferentation of Purkinje cells in adult rats, the density of dense projections of parallel fibre synapses on Purkinje cell spines remained uniform. This occurred throughout a range of reduction in the number of synapses in conjunction with a reciprocal increase in the size of sites. The finding of a uniform density of these projections and an increase in the size implies that each granule cell axon must gain dense projections. In addition, the remaining presynaptic boutons had a uniform density of synaptic vesicles even though the volume of the boutons and the area of the synaptic contact doubled. Thus, the number of synaptic vesicles gained in proportion to the total enlargement of the contact site and the bouton size. These results strongly suggest that deficits or losses in synaptic connections of parallel fibre on Purkinje cell spines produces a compensation in the total number of synaptic vesicles and presynaptic dense projections of the remaining boutons.(ABSTRACT TRUNCATED AT 400 WORDS)

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Plasticity of cerebellar parallel fibers following developmental deficits in synaptic number

Cited by 9 publications

References 28 publications

Effect of chronic administration of NMDA antagonists on synaptic development

Effect of chronic administration of NMDA antagonists on synaptic development

Developmental dynamics of Purkinje cells and dendritic spines in rat cerebellar cortex

Compensation in the number of presynaptic dense projections and synaptic vesicles in remaining parallel fibres following cerebellar lesions

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