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PubMed2005

Congenital iodine deficiency and hypothyroidism impair LTP and decrease C-fos and C-jun expression in rat hippocampus.

Iodine is essential for the synthesis of triiodothyronine (T(3)) and thyroxine (T(4)). Iodine deficiency leads to inadequate thyroid hormone. Thyroid hormones deficiency during brain development affects cognitive functions, such as attention, learning, and memory. However, the mechanism underlying these deficits is unclear. To investigate the role of iodine deficiency and hypothyroidism in synaptic plasticity, this study examined the induction of long-term synaptic plasticity (LTP) and expression of immediate early (IEA) gene proteins in rat hippocampus following congenital iodine deficiency or hypothyroidism. Through gestation and lactation, iodine-deficient or hypothyroid dam rats were administered with either iodine-deficient diet or methimazole-added drinking water. Exposure was terminated on postnatal day (PN) 30. In hippocampus of pup rats, the induction of LTP in area CA1 was determined on PN60 and the expression of c-fos and c-jun proteins was examined on PN20, PN30 and PN60. Compared to control pups, both treated groups have shown: (1) significantly lower concentrations of serum FT(3) and FT(4), (2) much smaller population spike (PS) amplitude (p<0.01) and field-excitatory postsynaptic potential (f-EPSP) slope induced by high-frequency stimulation (HFS) (P<0.01), and (3) significantly lower integrated optical density (IOD) total of c-fos and c-jun expression (P<0.05 or P<0.01). In summary, iodine deficiency and hypothyroidism during critical periods of brain development impair LTP induction and decrease the expression of c-fos and c-jun proteins in hippocampus.

Aging↗

PubMed2001

Initial recovery of vision after early monocular deprivation in kittens is faster when both eyes are open.

A comparison was made of the speed of visual recovery in the deprived eye of kittens after a 6-day period of monocular deprivation imposed at 5-9 weeks of age in two postdeprivation conditions. In one condition, binocular recovery (BR), both eyes were open, whereas in the other condition, reverse lid-suture (RLS), the formerly nondeprived eye was closed to force the animal to use the originally deprived eye. In littermate pairs, BR kittens began to recover form vision 12 to 30 h before those subjected to RLS. The vision of the deprived eye of the BR animals remained superior to that of their RLS littermates for 4-8 days. Although this finding is difficult to reconcile with competitive mechanisms of synaptic plasticity, it supports a prediction of an alternative model of synaptic plasticity [Bienenstock, E. L., Cooper, L. N. & Munro, P. W. (1982) J. Neurosci. 2, 32-48] for slower initial recovery with RLS because of the time required to reset the modification threshold.

Aging↗

PubMed1992

Inhibition of nitric oxide synthesis impairs two different forms of learning.

Nitric oxide (NO), an intercellular messenger in the central nervous system of vertebrates, plays an important role in the establishment of synaptic plasticity. In order to investigate the role of NO and synaptic plasticity in learning, we injected rats and rabbits with the NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME) prior to training on two tests of learning. Rats treated with L-NAME were impaired in learning a spatial learning task, while rabbits given the NO synthase inhibitor demonstrated learning deficits in the conditioned eyeblink response. The results support the hypothesis that NO plays a critical role in acquisition of two different forms of learning.

Animals↗

PubMed1999

Long-term depression in hippocampal interneurons: joint requirement for pre- and postsynaptic events.

Long-term depression (LTD) is a well-known form of synaptic plasticity of principal neurons in the mammalian brain. Whether such changes occur in interneurons is still controversial. CA3 hippocampal interneurons expressing Ca2+-permeable AMPA receptors exhibited LTD after tetanic stimulation of CA3 excitatory inputs. LTD was independent of NMDA receptors and required both Ca2+ influx through postsynaptic AMPA receptors and activation of presynaptic mGluR7-like receptors. These results point to the capability of interneurons to undergo plastic changes of synaptic strength through joint activation of pre- and postsynaptic glutamate receptors.

Animals↗

PubMed1992

An analytical short- and long-term memory model of presynaptic plasticity.

A mathematical model, called the Learning Gate Model (LGM), that describes phenomena responsible for biological synaptic plasticity, is presented. The functionality of the model are mainly based on the work of Kandel and colleagues on the most elementary forms of learning observed in the Aplysia Californica marine mollusc. In particular, emphasis is placed on the double temporal dynamics of synaptic plasticity and the temporal specificity of classical conditioning. By properly modeling the effect of the binding of Ca++ ions to the serotonin-sensitive adenylate cyclase enzyme, it is shown how a positively accelerated learning curve can be obtained for sensitization and classical conditioning. Phenomena of spontaneous recovery and second-order conditioning are reproduced through simulations. Mathematical analyses of the temporal trace of conditioned stimulus and of the Short-Term Memory steady state are also given.

Animals↗

PubMed1997

Synapse-specific, long-term facilitation of aplysia sensory to motor synapses: a function for local protein synthesis in memory storage.

The requirement for transcription during long-lasting synaptic plasticity has raised the question of whether the cellular unit of synaptic plasticity is the soma and its nucleus or the synapse. To address this question, we cultured a single bifurcated Aplysia sensory neuron making synapses with two spatially separated motor neurons. By perfusing serotonin onto the synapses made onto one motor neuron, we found that a single axonal branch can undergo long-term branch-specific facilitation. This branch-specific facilitation depends on CREB-mediated transcription and involves the growth of new synaptic connections exclusively at the treated branch. Branch-specific long-term facilitation requires local protein synthesis in the presynaptic but not the postsynaptic cell. In fact, presynaptic sensory neuron axons deprived of their cell bodies are capable of protein synthesis, and this protein synthesis is stimulated 3-fold by exposure to serotonin.

Animals↗

PubMed2003

Synapse number and synaptic efficacy are regulated by presynaptic cAMP and protein kinase A.

The mechanisms by which neurons regulate the number and strength of synapses during development and synaptic plasticity have not yet been defined fully. This lack of fundamental knowledge in the fields of neurodevelopment and synaptic plasticity can be attributed, in part, to compensatory mechanisms by which neurons accommodate for the loss of function in their synaptic partners. This is generally achieved either by scaling up neuronal transmitter release capabilities or by enhancing the postsynaptic responsiveness. Here, we demonstrate that regulation of synaptic strength and number between identified Lymnaea neurons visceral dorsal 4 (VD4, the presynaptic cell) and left pedal dorsal 1 (LPeD1, the postsynaptic cell) requires presynaptic activation of a cAMP-PKA-dependent signal. Experimental activation of the cAMP-PKA pathway resulted in reduced synaptic efficacy, whereas inhibition of the cAMP-PKA cascade permitted hyperinnervation and an overall enhancement of synaptic strength. Because synaptic transmission between VD4 and LPeD1 does not require a cAMP-PKA pathway, our data show that these messengers may play a novel role in regulating the synaptic efficacy during early synaptogenesis and plasticity.

Animals↗

PubMed2004

Nicotine-mediated plasticity in robust nucleus of the archistriatum of the adult zebra finch.

Activation of neuronal nicotinic acetylcholine receptors (nAChRs) modulates the induction of long-term potentiation (LTP), a possible cellular mechanism for learning. This study was undertaken to determine the effects of activation of nAChRs by nicotine on long-term plasticity in the songbird zebra finch, which is a valuable model to study synaptic plasticity and its implications to behavioral learning. Electrophysiological recordings in the robust nucleus of the archistriatum (RA) in adult zebra finch brain slices reveal that tetanic stimulation alone does not produce LTP. However, LTP is induced by such stimulation in the presence of nicotine. The nicotine-mediated LTP is blocked by dihydro-beta-erythroidine (DHbetaE, 1 microM), an antagonist having a greater effect against nAChRs containing the alpha 4 subunit. In the presence of methyllcaconitine (MLA, 10 nM), an antagonist of nAChRs containing the alpha 7 subunit, a long-term depression (LTD) is unmasked, implicating a bi-directional type of plasticity in the zebra finch RA, which is modulated by differential activation of nAChR subtypes. Intracellular recordings from single neurons show a depression of the afterhyperpolarization (AHP) and an increase in frequency of evoked and spontaneous action potentials in the presence of nicotine. These results suggest that nicotinic cholinergic mechanisms may play a critical role in synaptic plasticity in the zebra finch song system and thereby influence song learning and plasticity.

Acetylcholine↗

PubMed2004

New synaptic bouton formation is disrupted by misregulation of microtubule stability in aPKC mutants.

The Baz/Par-3-Par-6-aPKC complex is an evolutionarily conserved cassette critical for the development of polarity in epithelial cells, neuroblasts, and oocytes. aPKC is also implicated in long-term synaptic plasticity in mammals and the persistence of memory in flies, suggesting a synaptic function for this cassette. Here we show that at Drosophila glutamatergic synapses, aPKC controls the formation and structure of synapses by regulating microtubule (MT) dynamics. At the presynapse, aPKC regulates the stability of MTs by promoting the association of the MAP1Brelated protein Futsch to MTs. At the postsynapse, aPKC regulates the synaptic cytoskeleton by controlling the extent of Actin-rich and MT-rich areas. In addition, we show that Baz and Par-6 are also expressed at synapses and that their synaptic localization depends on aPKC activity. Our findings establish a novel role for this complex during synapse development and provide a cellular context for understanding the role of aPKC in synaptic plasticity and memory.

Actin Cytoskeleton↗

PubMed1996

Experience-dependent plasticity of binocular responses in the primary visual cortex of the mouse.

An activity-dependent form of synaptic plasticity underlies the fine tuning of connections in the developing primary visual cortex of mammals such as the cat and monkey. Studies of the effects of manipulations of visual experience during a critical period have demonstrated that a correlation-based competitive process governs this plasticity. The cellular mechanisms underlying this competition, however, are poorly understood. Transgenic and gene-targeting technologies have led to the development of a new category of reagents that have the potential to help answer questions of cellular mechanism, provided that the questions can be studied in a mouse model. The current study attempts to characterize a developmental plasticity in the mouse primary visual cortex and to demonstrate its relevance to that found in higher mammals. We found that 4 d of monocular lid suture at postnatal day 28 (P28) induced a maximal loss of responsiveness of cortical neurons to the deprived eye. These ocular dominance shifts occurred during a well-defined critical period, between P19 and P32. Furthermore, binocular deprivation during this critical period did not decrease visual cortical responses, and alternating monocular deprivation resulted in a decrease in the number of binocularly responsive neurons. Finally, a laminar analysis demonstrated plasticity of both geniculocortical and intracortical connections. These results demonstrate that an activity-dependent, competitive form of synaptic plasticity that obeys correlation-based rules operates in the developing primary visual cortex of the mouse.

Animals↗

PubMed1997

Distinct forms of short-term plasticity at excitatory synapses of hippocampus and neocortex.

The expression of short- and long-term synaptic plasticity varies strongly across pathways in the central nervous system. Differences in the properties of transmitter release may underlie some of this variability. Here we compared the short-term plasticity displayed by a neocortical and a hippocampal pathway in vitro, and observed dramatic differences. Conditions known to increase transmitter release probability were more effective in hippocampus, while conditions known to decrease release probability were similarly effective in both pathways. The effects of the irreversible open-channel blocker of N-methyl-D-aspartate receptors, MK-801, implied that synapses in the neocortical pathway have a relatively high probability of transmitter release as compared with synapses in the hippocampal pathway. Differences in release probability may explain the pathway-specific variance in short- and long-term synaptic plasticity.

Animals↗

PubMed2006

Distribution of NMDA receptor subunit NR1 in arctic ground squirrel central nervous system.

Hibernation is a natural model of neuroprotection and adult synaptic plasticity. NMDA receptors (NMDAR), which play key roles in excitotoxicity and synaptic plasticity, have not been characterized in a hibernating species. Tolerance to excitotoxicity and cognitive enhancement in Arctic ground squirrels (AGS, Spermophilus parryii) suggests that NMDAR expression may decrease in hibernation and increase upon arousal. NMDAR consist of at least one NMDAR1 (NR1) subunit, which is required for receptor function. Localization of NR1 reflects localization of the majority, if not all, NMDAR complexes. The purpose of this study, therefore, was to characterize the distribution of NR1 subunits in AGS central nervous system using immunohistochemistry. In addition, we compare NR1 expression in hippocampus of hibernating AGS (hAGS) and inter-bout euthermic AGS (ibeAGS) and assess changes in cell somata size using NR1 stained sections in three hippocampal sub-regions (CA1, CA3, and dentate gyrus). For the first time, we report that immunoreactivity of anti-NR1 is widely distributed throughout the central nervous system in AGS and is similar to other species. No differences exist in the expression and distribution of NR1 in hAGS and ibeAGS. However, we report a significant decrease in size of hippocampal CA1 and dentate gyrus NR1-expressing neuronal somata during hibernation torpor.

Animals↗

PubMedDate not supplied

The balance between postsynaptic Ca(2+)-dependent protein kinase and phosphatase activities controlling synaptic strength.

The activities of protein kinases and phosphatases are believed to regulate neuronal activity and synaptic plasticity in brain. Numerous in vivo and in vitro studies have shown that synaptic strength appears stable under basal conditions and during long-term potentiation (LTP) expression. This may reflect a balance between protein kinase and phosphatase activities. To provide experimental evidence for this hypothesis, and based on our knowledge that Ca2+/CaM activates protein kinases and phosphatases and that postsynaptic Ca2+/CaM signal pathways play important roles in synaptic plasticity, we examined the contribution of postsynaptic Ca(2+)-dependent protein kinases and calcineurin (CaN) in regulating synaptic strength. We show that inhibiting postsynaptic Ca2+/CaM-dependent protein kinase II (CaM-KII) and Ca2+/phospholipitidyserine-dependent protein kinase (PKC) in hippocampal CA1 neurons attenuates significantly the expression of LTP, but not basal synaptic transmission. On the other hand, the inhibition of postsynaptic CaN enhances synaptic transmission at potentiated and naive synapses, and increases significantly the magnitude of synaptic potentiation during the induction phase of LTP. These results indicate that postsynaptic CaM-KII and PKC activities are essential for maintaining LTP expression, but CaN activity limits synaptic strength at stable levels during both basal and potentiated synaptic transmission; that is, the dynamic balance between protein phosphorylation and dephosphorylation that sets physiological synaptic strength is dominated by CaN activity.

Animals↗

PubMed1991

Subdural application of hemoglobin to the cerebellum blocks vestibuloocular reflex adaptation.

Vestibuloocular reflex (VOR) was induced by horizontal sinusoidal whole-body rotation in darkness in rabbits and a monkey. One eye was observed through an infrared TV camera. The gain of VOR was adaptively changed when the animal was continuously rotated for 3 h with the observed eye exposed to the screen moving in phase or out of phase with the head. Injection of 0.1 ml saline solution containing 10 microM hemoglobin into the subdural space over the cerebellar flocculus ipsilateral to the observed eye abolished the VOR adaptation. Since hemoglobin absorbs nitric oxide, which mediates synaptic plasticity in the cerebellar cortex, these results support the view that synaptic plasticity of the flocculus plays a key role in the VOR adaptation.

Adaptation, Physiological↗

PubMed2006

Difference in organization of corticostriatal and thalamostriatal synapses between patch and matrix compartments of rat neostriatum.

The neostriatum, which possesses a mosaic organization consisting of patch and matrix compartments, receives glutamatergic excitatory afferents from the cerebral cortex and thalamus. Differences in the synaptic organization of these striatopetal afferents between the patch and matrix compartments were examined in the rat using confocal laser scanning and electron microscopes. Thalamostriatal terminals immunopositive for vesicular glutamate transporter (VGluT) 2 were less dense in the patch than in the matrix compartment, although the density of VGluT1-immunopositive corticostriatal terminals was almost evenly distributed in both the compartments. Quantitative analysis of ultrastructural images revealed that 84% of VGluT2-positive synapses in the patch compartment were formed with dendritic spines, whereas 70% in the matrix compartment were made with dendritic shafts. By contrast, VGluT1-positive terminals display a similar preference for specific synaptic targets in both compartments: about 80% made synapses with dendritic spines. In addition, VGluT2-positive axospinous synapses in the patch compartment were larger than the VGluT1-positive axospinous synapses in both compartments. As axospinous synapses are generally found in neuronal connections showing high synaptic plasticity, the present findings suggest that the thalamostriatal connection requires higher synaptic plasticity in the patch compartment than in the matrix compartment.

Animals↗

PubMed2002

Neurotrophins and cortical development.

The mammalian cerebral cortex requires the proper formation of exquisitely precise circuits to function correctly. These neuronal circuits are assembled during development by the formation of synaptic connections between hundreds of thousands of differentiating neurons. Although the development of the cerebral cortex has been well described anatomically, the cellular and molecular mechanisms that guide neuronal differentiation and formation of connections are just beginning to be understood. Moreover, despite evidence that coordinated patterns of activity underlie reorganization of brain circuits during critical periods of development, the molecular signals that translate activity into structural and functional changes in connections remain unknown. Recently, the neurotrophins have emerged as attractive candidates not only for regulating neuronal differentiation in the developing brain, but also for mediating activity-dependent synaptic plasticity. The neurotrophins meet many of the criteria required for molecular signals involved in neuronal differentiation and plasticity. They are present in the cerebral cortex during development and their expression is regulated by synaptic activity. In turn, the neurotrophins themselves strongly influence both short-term synaptic plasticity and long-term potentiation and depression. In addition to their functional effects, the neurotrophins also profoundly regulate the structural changes that underlie axonal and dendritic differentiation. Finally, the neurotrophins have been implicated in mediating synaptic competition required for activity-dependent plasticity during the critical period. This chapter presents and discusses the rapidly accumulating evidence that the neurotrophins are critical for neuronal differentiation and that they may be involved in activity-dependent synaptic refinement in the developing cerebral cortex.

Animals↗

PubMed2002

Dynamic structural changes of synaptic contacts in the visual system of insects.

The visual system of insects provides an excellent model to study processes of transduction and transmission of photic information, synaptogenesis, synaptic plasticity, and wiring between photoreceptors and their visual interneurons in the optic lobe. This review describes synaptic contacts between photoreceptors and other neurons in the visual system of insects, especially in the fly's first optic neuropile (the lamina), and summarizes changes observed in the synapses of visual cells that have been reported both in phylogeny and ontogeny, and also examples of synaptic plasticity in adult insects that have been evoked by intrinsic and extrinsic factors. Plasticity observed in synapses of the insect's visual system seems to exemplify not only synaptic contacts in insects but, given that similar examples of plasticity have been found in other animal groups, may also be a general phenomenon in the nervous system.

Animals↗

PubMed2000

Laminin degradation by plasmin regulates long-term potentiation.

Plasmin is converted from its zymogen plasminogen by tissue type or urokinase type plasminogen activator (PA) and degrades many components of the extracellular matrix (ECM). To explore the possibility that the PA-plasmin system regulates synaptic plasticity, we investigated the effect of plasmin on degradation of ECM and synaptic plasticity by using organotypic hippocampal cultures. High-frequency stimulation produced long-term potentiation (LTP) in control slices, whereas the potentiation was induced but not maintained in slices pretreated with 100 nM plasmin for 6 hr. The baseline synaptic responses were not affected by pretreatment with plasmin. The impairment of LTP maintenance was not observed in slices pretreated with 100 nM plasmin for 6 hr, washed, and then cultured for 24-48 hr in the absence of plasmin. To identify substrates of plasmin, the expression of three major components of ECM, laminin, fibronectin, and type IV collagen, was investigated by immunofluorescence imaging. The three ECM components were widely distributed in the hippocampus, and only laminin was degraded by plasmin pretreatment. The expression level of laminin returned to normal levels when the slices were cultured for 24-48 hr after washout of plasmin. Furthermore, preincubation with anti-laminin antibodies prevented both the degradation of laminin and the impairment of LTP maintenance by plasmin. These results suggest that the laminin-mediated cell-ECM interaction may be necessary for the maintenance of LTP.

Animals↗