Physiological and morphological plasticity induced by chronic treatment with NT‐3 or NT‐4/5 in hippocampal slice cultures

Schwyzer, Lucia; Mateos, José; Abegg, Mathias; Rietschin, Lotty; Heeb, L.; Thompson, Scott M.; Lüthi, Andreas; Gähwiler, Beat H.; McKinney, R. Anne

doi:10.1046/j.1460-9568.2002.02259.x

Cited by 30 publications

(24 citation statements)

References 46 publications

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“…Interestingly, the gene encoding neurotrophin 3 (NT-3) is among the candidate genes containing NBRE elements in their 5Ј-promoter upstream region. Neurotrophins in general, and NT-3 in particular, have been associated with sprouting, axonal growth, synaptic plasticity, and learning (Kang and Schuman 1996;Kaisho et al 1999;Schwyzer et al 2002;Xu et al 2002;Mizuno et al 2003). Hence, one possible role of Nurr1 during learning is the activation of cellular machineries necessary to promote synaptic connectivity and plasticity, which are also relevant during development.…”

Section: Suppression Of Nurr1 In Ca3 During Mid-acquisition Results Imentioning

confidence: 99%

Knockdown of Nurr1 in the rat hippocampus: Implications to spatial discrimination learning and memory

Colón-Cesario

Martínez-Montemayor²,

Félix³

et al. 2006

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Nurr1 expression is up-regulated in the brain following associative learning experiences, but its relevance to cognitive processes remains unclear. In these studies, rats initially received bilateral hippocampal infusions of control or antisense oligodeoxynucleotides (ODNs) 1 h prior to training in a holeboard spatial discrimination task. Such pre-training infusions of nurr1 antisense ODNs caused a moderate effect in learning the task and also impaired LTM tested 7 d later. In a second experiment, ODN infusions were given immediately after the animals had received two sessions of training, during which all animals showed normal learning. Although antisense treated rats were significantly impaired during the post-infusion stages of acquisition of the task, no group differences were observed during the LTM test given 7 d later. These animals were subjected 3 d later to reversal training in the same maze in the absence of any additional treatments. Remarkably, rats previously treated with antisense ODNs displayed perseveration: The animals were fixated with the previously learned pattern of baited holes, causing them to be significantly impaired in the extinction of acquired spatial preferences and future learning. We postulate that Nurr1 function in the hippocampus is important for normal cognitive processes.Learning requires the continued ability of the brain to establish new synaptic configurations and could be viewed as the continuation of the developmental process. Nurr1 (also known as HZF-3) (Peña de Ortiz and Jamieson Jr. 1996; Peña de Ge et al. 2003) is a member of the inducible nuclear receptor family of transcription factors (Law et al. 1992;Xing et al. 1997;Honkaniemi and Sharp 1999;Wang et al. 2003) that has been shown to play a key role in neural development. Specifically, expression of nurr1 is critical for the development of mesencephalic dopaminergic precursor neurons (Zetterstrom et al. 1997;Castillo et al. 1998;Saucedo-Cardenas et al. 1998 On the other hand, recent studies showed that nurr1 mutant heterozygous mice subjected to post-weaning isolation display a disruption of prepulse inhibition (a model of sensorimotor gating in the brain that is disrupted in patients with schizophrenia) (for review, see Van den Buuse et al. 2003), which is possibly related to decreased dopamine neurotransmission in the mutant heterozygous genotype (Eells et al. 2006). Disordered cognitive processes stemming from impaired hippocampal function are an important part of the positive symptoms in schizophrenia (Harvey et al. 2001;Antonova et al. 2004;Sweatt 2004;Johnson 2005). The holeboard spatial discrimination task was initially developed to study thought disorders in animal models of schizophrenia (Oades and Isaacson 1978). In this hippocampal-dependent task (Oades 1981), animals learn to discriminate between relevant versus irrelevant stimuli, a cognitive process that is impaired in schizophrenia (Gray and Snowden 2005). Our previous studies showed increased rat hippocampal nurr1 mRNA levels after the first and thi...

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Section: Suppression Of Nurr1 In Ca3 During Mid-acquisition Results Imentioning

confidence: 99%

Knockdown of Nurr1 in the rat hippocampus: Implications to spatial discrimination learning and memory

Colón-Cesario

Martínez-Montemayor²,

Félix³

et al. 2006

Learn. Mem.

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“…In cerebellar and hippocampal cultures, activity deprivation decreases the number of GABAergic synapses, an effect reversed by the application of BDNF or neurotrophin-4 (Marty et al, 2000;Seil and DrakeBaumann, 2000). Moreover, overexpression of BDNF (Aguado et al, 2003) or chronic treatment with different neurotrophins accelerates the functional maturation of GABAergic synapses (Marty et al, 1996;Vicario-Abejon et al, 1998;Schwyzer et al, 2002). BDNF and Trk receptor-coupled PTKs are also reported to play a role in the induction of LTP at glutamatergic synapses (O'Dell et al, 1991;Grant et al, 1992;Huang and Hsu, 1999).…”

Section: Discussionmentioning

confidence: 99%

Endogenous Neurotrophins Are Required for the Induction of GABAergic Long-Term Potentiation in the Neonatal Rat Hippocampus

Gubellini¹

2005

Journal of Neuroscience

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In the developing rat hippocampus, GABAergic synapses undergo a Ca 2ϩ -dependent long-term potentiation (LTP GABA-A ); this form of synaptic plasticity is induced in CA3 pyramidal neurons by delivering repetitive depolarizing pulses (DPs) to the recorded neuron, and it is expressed as a long-lasting increase in the frequency and amplitude of spontaneous GABA A receptor-mediated postsynaptic currents. In the present study, we examined the role of endogenous tropomyosin-related kinase receptor B (TrkB) receptor ligands and associated protein tyrosine kinases (PTKs) in the induction of LTP GABA-A . The application of Lavendustin A, a broad spectrum PTK inhibitor, blocked the induction of LTP GABA-A , whereas Lavendustin B, its inactive form, had no effect. Moreover, k-252a and k-252b, two alkaloids that inhibit the kinase activity of the Trk receptor family, also prevented the induction of LTP GABA-A . On hippocampal slices incubated with the soluble form of TrkB receptor IgG (TrkB-IgG), which prevents the activation of TrkB receptors by endogenous ligands, DPs failed to induce LTP GABA-A , whereas the incubation with TrkA-IgG or TrkC-IgG had no such effect. Altogether, these data indicate that endogenous TrkB ligands and associated PTK activity are necessary for the induction of GABAergic LTP in the developing rat hippocampus.

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“…In cerebellar and hippocampal cultures, activity deprivation decreases the number of GABAergic synapses, an effect reversed by the application of BDNF or neurotrophin-4 (422,553). Overexpression of BDNF (5) or chronic treatment with different neurotrophins (421,552,639) accelerates the functional maturation of GABAergic synapses. Several studies have also shown that neurotrophins can modulate the efficacy of inhibitory synaptic transmission (29,114,187,242,295,425,608).…”

Section: Long-term Plasticity: Contribution To the Establishment Omentioning

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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Physiological and morphological plasticity induced by chronic treatment with NT‐3 or NT‐4/5 in hippocampal slice cultures

Cited by 30 publications

References 46 publications

Knockdown of Nurr1 in the rat hippocampus: Implications to spatial discrimination learning and memory

Knockdown of Nurr1 in the rat hippocampus: Implications to spatial discrimination learning and memory

Endogenous Neurotrophins Are Required for the Induction of GABAergic Long-Term Potentiation in the Neonatal Rat Hippocampus

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

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