Synaptic plasticity in the subiculum

Behr, Jüergen; Wozny, Christian; Fidzinski, Pawel; Schmitz, Dietmar

doi:10.1016/j.pneurobio.2009.09.002

Cited by 43 publications

(52 citation statements)

References 94 publications

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“…In regular-firing neurons of the subiculum, LTP is induced by postsynaptic activation of NMDARs, whereas in burst-firing neurons LTP is induced by presynaptic activation of PKA (Wozny et al, 2008; Behr et al, 2009). We asked whether LTP may also be differentially affected by the presynaptic β-neurexin KO in regular- and burst-firing neurons similar to endocannabinoid signaling.…”

Section: Resultsmentioning

confidence: 99%

β-Neurexins Control Neural Circuits by Regulating Synaptic Endocannabinoid Signaling

Anderson

Aoto

Tabuchi

et al. 2015

Cell

132

161

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α- and β-neurexins are presynaptic cell-adhesion molecules implicated in autism and schizophrenia. We find that although β-neurexins are expressed at much lower levels than α-neurexins, conditional knockout of β-neurexins with continued expression of α-neurexins dramatically decreased neurotransmitter release at excitatory synapses in cultured cortical neurons. The β-neurexin knockout phenotype was attenuated by CB1-receptor inhibition which blocks presynaptic endocannabinoid signaling or by 2-arachidonoylglycerol synthesis inhibition which impairs postsynaptic endocannabinoid release. In synapses formed by CA1-region pyramidal neurons onto burst-firing subiculum neurons, presynaptic in vivo knockout of β-neurexins aggravated endocannabinoid-mediated inhibition of synaptic transmission and blocked LTP; presynaptic CB1-receptor antagonists or postsynaptic 2-arachidonoylglycerol synthesis inhibition again reversed this block. Moreover, conditional knockout of β-neurexins in CA1-region neurons impaired contextual fear memories. Thus, our data suggest that presynaptic β-neurexins control synaptic strength in excitatory synapses by regulating postsynaptic 2-arachidonoylglycerol synthesis, revealing an unexpected role for β-neurexins in the endocannabinoid-dependent regulation of neural circuits.

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Section: Resultsmentioning

confidence: 99%

β-Neurexins Control Neural Circuits by Regulating Synaptic Endocannabinoid Signaling

Anderson

Aoto

Tabuchi

et al. 2015

Cell

132

161

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“…Other presynaptic forms of plasticity that are mechanistically similar to MF-LTP have been identified in multiple brain areas, including the cerebellum, the amygdala (see Pape and Pare 2010) and subiculum (Table 1) (see Behr et al 2009). In the cerebellum, repetitive parallel fiber (PF) stimulation triggers presynaptic LTP at PF to Purkinje cell synapses.…”

Section: Mossy Fiber To Ca3 Pyramidal Cell Synapse As a Model For Prementioning

confidence: 98%

“…MF-LTP is a prototype for mechanistically similar, presynaptically expressed, NMDAR-independent and cAMP/ PKA-dependent forms of LTP found in several brain areas including the cerebellum (Salin et al 1996a), thalamus (Castro-Alamancos and Calcagnotto 1999), subiculum (Behr et al 2009), amygdala (Lopez de Armentia and Sah 2007), and neocortex (Chen et al 2009). MF-LTP is mechanistically distinct from classical NMDAR-dependent LTP at the Schaffer collateral to CA1 pyramidal cell synapse (Sch-CA1) (Nicoll and Malenka 1995).…”

Section: Mossy Fiber To Ca3 Pyramidal Cell Synapse As a Model For Prementioning

confidence: 99%

Presynaptic LTP and LTD of Excitatory and Inhibitory Synapses

Castillo

2011

Cold Spring Harbor Perspectives in Biology

132

127

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Ubiquitous forms of long-term potentiation (LTP) and depression (LTD) are caused by enduring increases or decreases in neurotransmitter release. Such forms or presynaptic plasticity are equally observed at excitatory and inhibitory synapses and the list of locations expressing presynaptic LTP and LTD continues to grow. In addition to the mechanistically distinct forms of postsynaptic plasticity, presynaptic plasticity offers a powerful means to modify neural circuits. A wide range of induction mechanisms has been identified, some of which occur entirely in the presynaptic terminal, whereas others require retrograde signaling from the postsynaptic to presynaptic terminals. In spite of this diversity of induction mechanisms, some common induction rules can be identified across synapses. Although the precise molecular mechanism underlying long-term changes in transmitter release in most cases remains unclear, increasing evidence indicates that presynaptic LTP and LTD can occur in vivo and likely mediate some forms of learning.A t several excitatory and inhibitory synapses, neuronal activity can trigger enduring increases or decreases in neurotransmitter release, thereby producing long-term potentiation (LTP) or long-term depression (LTD) of synaptic strength, respectively. In the last decade, many studies have revealed that these forms of plasticity are ubiquitously expressed in the mammalian brain, and accumulating evidence indicates that they may underlie behavioral adaptations occurring in vivo. These studies have also uncovered a wide range of induction mechanisms, which converge on the presynaptic terminal where an enduring modification in the neurotransmitter release process takes place. Interestingly, presynaptic forms of LTP/ LTD can coexist with classical forms of postsynaptic plasticity. Such diversity expands the dynamic range and repertoire by which neurons modify their synaptic connections. This review discusses mechanistic aspects of presynaptic LTP and LTD at both excitatory and inhibitory synapses in the mammalian brain, with an emphasis on recent findings. INDUCTION MECHANISMSAs illustrated in Figure 1, presynaptic LTP/LTD at both excitatory and inhibitory synapses can be induced in a homosynaptic or heterosynaptic manner, with induction occurring either entirely at the presynaptic terminal or requiring a retrograde messenger arising from the postsynaptic neuron. Each of these four induction

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“…With regard to the correlation of hippocampal activity and the behavioral reward effect, it is noteworthy that rodent studies have described the subiculum as an integrator of the raw sensory information and its past emotional connotation (Behr, Wozny, Fidzinski, & Schmitz, 2009;Naber, Witter, & Lopes da Silva, 2000). According to those studies, the subiculum is a recipient of both raw sensory information (from perirhinal and postrhinal cortices) and already processed or modulated version of the same information.…”

Section: Neural Correlates Of Perceptual Learning and Reward Reinforcmentioning

confidence: 99%

“…According to those studies, the subiculum is a recipient of both raw sensory information (from perirhinal and postrhinal cortices) and already processed or modulated version of the same information. Septal areas could modulate sensory input to the subiculum to signal the "emotional connotation in relation to the context of the situation where the organism was stimulated" (Behr et al, 2009). Thus, the correlation of hippocampal activity and the strength of the reward effect could reflect the learned reward association with respect to the currently perceived stimulus.…”

Section: Neural Correlates Of Perceptual Learning and Reward Reinforcmentioning

confidence: 99%

A Hippocampal Signature of Perceptual Learning in Object Recognition

Guggenmos

Rothkirch

Obermayer

et al. 2015

Journal of Cognitive Neuroscience

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Perceptual learning is the improvement in perceptual performance through training or exposure. Here, we used fMRI before and after extensive behavioral training to investigate the effects of perceptual learning on the recognition of objects under challenging viewing conditions. Objects belonged either to trained or untrained categories. Trained categories were further subdivided into trained and untrained exemplars and were coupled with high or low monetary rewards during training. After a 3-day training, object recognition was markedly improved. Although there was a considerable transfer of learning to untrained exemplars within categories, an enhancing effect of reward reinforcement was specific to trained exemplars. fMRI showed that hippocampus responses to both trained and untrained exemplars of trained categories were enhanced by perceptual learning and correlated with the effect of reward reinforcement. Our results suggest a key role of hippocampus in object recognition after perceptual learning.

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Synaptic plasticity in the subiculum

Cited by 43 publications

References 94 publications

β-Neurexins Control Neural Circuits by Regulating Synaptic Endocannabinoid Signaling

β-Neurexins Control Neural Circuits by Regulating Synaptic Endocannabinoid Signaling

Presynaptic LTP and LTD of Excitatory and Inhibitory Synapses

A Hippocampal Signature of Perceptual Learning in Object Recognition

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