Increased density of excitatory amino acid transport sites in the hippocampal formation following an entorhinal lesion

Anderson, Kevin J.; Bridges, Richard J.; Cotman, Carl W.

doi:10.1016/0006-8993(91)90633-7

Cited by 58 publications

(10 citation statements)

References 29 publications

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“…Studies of D-aspartate binding to transporter sites in frozen postmortem tisssue revealed reductions in many cortical areas (Palmer et al, 1986;Cowburn et al, 1988), however, the relevance of this measure to glutamate uptake is doubtful (Danbolt and StormMathisen, 1986;Anderson et al, 1991). Functional measurement of Na þ -dependent D-aspartate uptake in fresh postmortem tissue also revealed significant reductions (Figure 3).…”

Section: Glutamatergic Changes In Admentioning

confidence: 90%

Glutamatergic systems in Alzheimer's disease

Francis

2003

Int. J. Geriat. Psychiatry

209

130

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Glutamate is the major transmitter of the brain and is involved in all aspects of cognitive function since it is the transmitter of cortical and hippocampal pyramidal neurones. Furthermore, glutamate and glutamate receptors are involved in long-term potentiation, a process believed to underlie learning and memory. Histological studies indicate loss of pyramidal neurones and their synapses in Alzheimer's disease (AD), this together with biochemical evidence suggests presynaptic (and postsynaptic) glutamatergic hypoactivity. This represents a 'double blow' as the activity of glutamatergic neurones is heavily influenced by the cholinergic system, which is also dysfunctional in AD. The clinical relevance of these changes is emphasised because glutamatergic and cholinergic dysfunction are strong correlates of cognitive decline in AD. The mechanism by which glutamatergic (and cholinergic) cells die is likely to be a combination of necrosis and apoptosis caused by a range of factors which include tangle formation and the effects of too much and too little glutamatergic neurotransmission.

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Section: Glutamatergic Changes In Admentioning

confidence: 90%

Glutamatergic systems in Alzheimer's disease

Francis

2003

Int. J. Geriat. Psychiatry

209

130

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“…It seems reasonable to hypothesize that, after hearing deficits, modifications of synaptic organization may occur at any level of the central auditory system and may underlie functional changes, such as the observed cortical plasticity. It can be hypothesized further that these modifications may result from synaptic loss (Goldberger and Murray, 1982;Guillery, 1972), synaptic loss followed by synaptogenesis (Erb and Povlishock, 1991;Goldberger and Murray, 1974;Steward, 1989, review), regulatory changes in transmission mediated by existing synapses (Anderson et al, 1991;Darlington et al, 1991;Smith et al, 1991;Snyder et al, 1990;Ułas et al, 1990;Waddington and Cross, 1978), or a combination of these events. It is unclear, however, which of these mechanisms operate in the adult auditory system and underlie various functional changes after hearing loss.…”

Section: Introductionmentioning

confidence: 97%

Synaptophysin immunoreactivity in the cochlear nucleus after unilateral cochlear or ossicular removal

Benson

Gross

Suneja

et al. 1997

Synapse

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This study determined if unilateral cochlear removal in adult guinea pigs led to synaptic loss followed by synaptogenesis in the cochlear nucleus (CN) and if unilateral middle ear ossicle removal led to synaptic loss in the CN. Synaptic endings were identified immunohistochemically, using a monoclonal antibody to synaptophysin. Immunolabeling was quantified densitometrically in the CN 4-161 days after cochlear removal and 161 days after ossicle removal. Fiber degeneration was visualized with the Nauta-Rasmussen silver method. Tissue shrinkage was measured from drawings of CN sections. Compared to the contralateral side, immunolabeling density ipsilaterally was reduced by 4 days in the anterior division of the anteroventral CN (a-AVCN) and by 7 days in the anterior part of the posteroventral CN (a-PVCN). At 7 days, preterminal fiber degeneration was abundant in both areas. These findings were consistent with the loss of cochlear nerve endings and fibers. At later times, immunolabeling density recovered. In the a-AVCN, tissue shrinkage explained approximately half the recovery of staining density; the rest was attributed to synaptogenesis. In the a-PVCN, the entire recovery was attributed to tissue shrinkage. In the polymorphic layer of the dorsal CN, immunostaining density increased transiently at 4 days, while at 7 days preterminal fiber degeneration was abundant. A net loss of synaptic endings was not detected immunohistochemically. The increased immunostaining density may reflect a transient growth of immature processes or presynaptic endings. Ossicle removal produced a deficit in immunolabeling density only in the ipsilateral a-PVCN, without fiber degeneration, suggesting a loss of presynaptic endings or of synaptophysin expression.

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“…Previously, Taxt and Strom-Mathisen (1984) demonstrated a decline in sodium-dependent t)-[3H]aspartate uptake sites in the hippocampus after an entohinal lesion and suggested that the finding was consistent with the loss of uptake sites into degenerating presynaptic terminals. In non-neuronal sites, on the other hand, Anderson et al (1991) suggested that the increase in the density of excitatory amino acid transport sites paralleled an increased number of reactive astrocytes in the denervated region. Thus, sodium-dependent excitatory amino acid transport sites are located on both presynaptic terminals and astrocytes.…”

Section: (Bc)mentioning

confidence: 97%

“…Sodium-dependent D@H]aspartate binding Autoradiographic distribution of sodium-dependent D-[3H]aspartate binding was carried out using the method of Anderson et al (1991Anderson et al ( , 1993 with minor modifications. Brain sections were preincubated for 10rain at 30~ in 50mM Tris-HC1 buffer (pH 7.4).…”

Section: Receptor Autoradiographymentioning

confidence: 99%

Age-related changes of sodium-dependentd-[3H]aspartate and [3H]FK506 binding in rat brain

Araki

Kato

Shuto

et al. 1997

J. Neural Transmission

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We investigated age-related changes in excitatory amino acid transport sites and FK506 binding protein (FKBP) in 3-week-, and 6-, 12-, 18- and 24-month-old Fischer 344 rat brains using receptor autoradiography. Sodium-dependent D-[3H]aspartate and [3H]FK506 were used to label excitatory amino acid transport sites and immunophilin (FKBP), respectively. In immature rats (3-week-old), sodium-dependent D-[3H]aspartate binding was lower in the frontal cortex, parietal cortex, striatum, nucleus accumbens, whole hippocampus, thalamus and cerebellum as compared to adult animals (6-month-old), whereas [3H]FK506 binding was significantly lower in only the hippocampus, thalamus and cerebellum. 3[H]FK506 binding exhibited no significant change in the brain regions examined during aging. However, sodium-dependent D-[3H]aspartate binding showed a conspicuous reduction in the substantia nigra in 18-month-old rats. Thereafter, a significant reduction in sodium-dependent D-[3H]aspartate binding was found in the thalamus, substantia nigra and cerebellum in 24-month-old rats. Other regions also showed about 10-25% reduction in sodium-dependent D-[3H]aspartate binding. The results indicate that excitatory amino acid transport sites are more susceptible to aging process than immunophilin. Further, our findings demonstrate the conspicuous differences in the developmental pattern between excitatory amino acid transport sites and immunophilin in immature rat brain.

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Increased density of excitatory amino acid transport sites in the hippocampal formation following an entorhinal lesion

Cited by 58 publications

References 29 publications

Glutamatergic systems in Alzheimer's disease

Glutamatergic systems in Alzheimer's disease

Synaptophysin immunoreactivity in the cochlear nucleus after unilateral cochlear or ossicular removal

Age-related changes of sodium-dependentd-[3H]aspartate and [3H]FK506 binding in rat brain

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