Presynaptic mechanisms involved in the expression of STP and LTP at CA1 synapses in the hippocampus

Lauri, Sari E.; Palmer, Mary J.; Segerstråle, Mikael; Vesikansa, Aino; Taira, Tomi; Collingridge, Graham L.

doi:10.1016/j.neuropharm.2006.06.017

Cited by 74 publications

(67 citation statements)

References 49 publications

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“…However, in slices exposed to leptin (22-56) post-tetanic potentiation (PTP) and some STP was observed after HFS, suggesting that this fragment may influence the transient enhancement of synaptic strength induced by HFS. As PTP and STP are thought to involve presynaptic expression mechanisms (Zucker and Regehr 2002;Lauri et al 2007), it is feasible that leptin (22-56) can act presynaptically to influence glutamate release mechanisms.…”

Section: Discussionmentioning

confidence: 99%

A Leptin Fragment Mirrors the Cognitive Enhancing and Neuroprotective Actions of Leptin

et al. 2016

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A key pathology of Alzheimer's disease (AD) is amyloid β (Aβ) accumulation that triggers synaptic impairments and neuronal death. Metabolic disruption is common in AD and recent evidence implicates impaired leptin function in AD. Thus the leptin system may be a novel therapeutic target in AD. Indeed, leptin has cognitive enhancing properties and it prevents the aberrant effects of Aβ on hippocampal synaptic function and neuronal viability. However, as leptin is a large peptide, development of smaller leptin-mimetics may be the best therapeutic approach. Thus, we have examined the cognitive enhancing and neuroprotective properties of known bioactive leptin fragments. Here we show that the leptin (116-130) fragment, but not leptin (22-56), mirrored the ability of leptin to promote AMPA receptor trafficking to synapses and facilitate activity-dependent hippocampal synaptic plasticity. Administration of leptin (116-130) also mirrored the cognitive enhancing effects of leptin as it enhanced performance in episodic-like memory tests. Moreover, leptin (116-130) prevented hippocampal synaptic disruption and neuronal cell death in models of amyloid toxicity. These findings establish further the importance of the leptin system as a therapeutic target in AD.

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Section: Discussionmentioning

confidence: 99%

A Leptin Fragment Mirrors the Cognitive Enhancing and Neuroprotective Actions of Leptin

et al. 2016

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“…This type of plasticity is thought to play an important role in short-term adaptations to sensory inputs, transient changes in behavioral states, and short-lasting forms of memory (Citri and Malenka, 2008). Additional support for this proposal is that, as illustrated in Figure 3, there are some indications that (e.g., because of the differential effects evoked by the paired pulses for appetitive and consummatory behaviors) presynaptic changes could be taking place in the observed changes in synaptic strength (Zucker and Regehr, 2002;Volianskis and Jensen, 2003;Lauri et al, 2007;Madroñal et al, 2009).…”

Section: General Findings and Commentsmentioning

confidence: 91%

Differential Contribution of Hippocampal Circuits to Appetitive and Consummatory Behaviors during Operant Conditioning of Behaving Mice

et al. 2013

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Operant conditioning is a type of associative learning involving different and complex sensorimotor and cognitive processes. Because the hippocampus has been related to some motor and cognitive functions involved in this type of learning (such as object recognition, spatial orientation, and associative learning tasks), we decided to study in behaving mice the putative changes in strength taking place at the hippocampal CA3-CA1 synapses during the acquisition and performance of an operant conditioning task. Mice were chronically implanted with stimulating electrodes in the Schaffer collaterals and with recording electrodes in the hippocampal CA1 area and trained to an operant task using a fixed-ratio (1:1) schedule. We recorded the field EPSPs (fEPSPs) evoked at the CA3-CA1 synapse during the performance of appetitive (going to the lever, lever press) and consummatory (going to the feeder, eating) behaviors. In addition, we recorded the local field potential activity of the CA1 area during similar behavioral displays. fEPSPs evoked at the CA3-CA1 synapse presented larger amplitudes for appetitive than for consummatory behaviors. This differential change in synaptic strength took place in relation to the learning process, depending mainly on the moment in which mice reached the selected criterion. Thus, selective changes in CA3-CA1 synaptic strength were dependent on both the behavior display and the learning stage. In addition, significant changes in theta band power peaks and their corresponding discrete frequencies were noticed during these behaviors across the sequence of events characterizing this type of associative learning but not during the acquisition process.

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“…Lauri and co-workers (371,372) suggested that kainate receptors that are highly expressed throughout the neonatal brain shift function during maturation and modulate the occurrence of GDPs. The activation of these receptors by ambient glutamate tonically reduces glutamate release.…”

Section: A Gdps In the Hippocampus: A Prototype Of Early Network Patmentioning

confidence: 99%

GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations

Ben-Ari

Gaı̈arsa

Tyzio

et al. 2007

Physiological Reviews

1,118

1,123

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Developing networks follow common rules to shift from silent cells to coactive networks that operate via thousands of synapses. This review deals with some of these rules and in particular those concerning the crucial role of the neurotransmitter γ-aminobuytric acid (GABA), which operates primarily via chloride-permeable GABAAreceptor channels. In all developing animal species and brain structures investigated, neurons have a higher intracellular chloride concentration at an early stage leading to an efflux of chloride and excitatory actions of GABA in immature neurons. This triggers sodium spikes, activates voltage-gated calcium channels, and acts in synergy with NMDA channels by removing the voltage-dependent magnesium block. GABA signaling is also established before glutamatergic transmission, suggesting that GABA is the principal excitatory transmitter during early development. In fact, even before synapse formation, GABA signaling can modulate the cell cycle and migration. The consequence of these rules is that developing networks generate primitive patterns of network activity, notably the giant depolarizing potentials (GDPs), largely through the excitatory actions of GABA and its synergistic interactions with glutamate signaling. These early types of network activity are likely required for neurons to fire together and thus to “wire together” so that functional units within cortical networks are formed. In addition, depolarizing GABA has a strong impact on synaptic plasticity and pathological insults, notably seizures of the immature brain. In conclusion, it is suggested that an evolutionary preserved role for excitatory GABA in immature cells provides an important mechanism in the formation of synapses and activity in neuronal networks.

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Presynaptic mechanisms involved in the expression of STP and LTP at CA1 synapses in the hippocampus

Cited by 74 publications

References 49 publications

A Leptin Fragment Mirrors the Cognitive Enhancing and Neuroprotective Actions of Leptin

A Leptin Fragment Mirrors the Cognitive Enhancing and Neuroprotective Actions of Leptin

Differential Contribution of Hippocampal Circuits to Appetitive and Consummatory Behaviors during Operant Conditioning of Behaving Mice

GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations

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