Sensitivity to theta-burst timing permits LTP in dorsal striatal adult brain slice

Hawes, Sarah; Gillani, Fawad; Evans, Rebekah C.; Benkert, Elizabeth A.; Blackwell, Kim T.

doi:10.1152/jn.00115.2013

Cited by 48 publications

(60 citation statements)

References 90 publications

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“…Consistent with the facilitating role of the amygdala in associative memory3435 and cortico-striatal plasticity28, frequencies in the theta range, alone or when combined with higher-frequencies, have been shown to promote long-term potentiation of cortico-striatal3637, including prefronto-striatal30, synaptic efficacy. Such plasticity may rely in the temporal relationship of striatal spikes to the ongoing theta rhythm as found in hippocampal place cells38.…”

Section: Discussionmentioning

confidence: 77%

Updating temporal expectancy of an aversive event engages striatal plasticity under amygdala control

et al. 2017

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Pavlovian aversive conditioning requires learning of the association between a conditioned stimulus (CS) and an unconditioned, aversive stimulus (US) but also involves encoding the time interval between the two stimuli. The neurobiological bases of this time interval learning are unknown. Here, we show that in rats, the dorsal striatum and basal amygdala belong to a common functional network underlying temporal expectancy and learning of a CS–US interval. Importantly, changes in coherence between striatum and amygdala local field potentials (LFPs) were found to couple these structures during interval estimation within the lower range of the theta rhythm (3–6 Hz). Strikingly, we also show that a change to the CS–US time interval results in long-term changes in cortico-striatal synaptic efficacy under the control of the amygdala. Collectively, this study reveals physiological correlates of plasticity mechanisms of interval timing that take place in the striatum and are regulated by the amygdala.

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Section: Discussionmentioning

confidence: 77%

Updating temporal expectancy of an aversive event engages striatal plasticity under amygdala control

et al. 2017

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“…Stimulation of cortical afferents with the TBS reliably induces NMDAR-dependent LTP at these synapses in normal Mg 2+ solution (Hawes et al, 2013). Consistently, we also found that LTP could be induced from most (7/8) of recorded MSNs by TBS with the same total number of stimuli as that of HFS used above (Figure 1E; see Experimental Procedures).…”

Section: Resultsmentioning

confidence: 99%

“…Pairing presynaptic stimulation with postsynaptic depolarization (Pawlak and Kerr, 2008; Shen et al, 2008) was also effective in NMDAR- and D1/D5R–dependent LTP at corticostriatal synapses, but the same pairing stimulation could also result in LTD induction (Shindou et al, 2011). On the other hand, TBS could reliably induce LTP that requires the activation of both NMDARs and BDNF signaling at both corticostriatal synapses (Figure 1G and 3B; Hawes et al, 2013) and hippocampal synapses (McGuinness et al, 2010; Zakharenko et al, 2003; Zakharenko et al, 2001). …”

Section: Discussionmentioning

confidence: 99%

Essential Role of Presynaptic NMDA Receptors in Activity-Dependent BDNF Secretion and Corticostriatal LTP

Park

Popescu

Poo

2014

Neuron

125

138

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SUMMARY Activation of N-methyl-D-aspartate subtype of glutamate receptors (NMDARs) in postsynaptic dendrites is required for long-term potentiation (LTP) of many excitatory synapses, but the role of presynaptic axonal NMDARs in synaptic plasticity remains to be clarified. Here we report that axonal NMDARs play an essential role in LTP induction at mouse corticostriatal synapses by triggering activity-induced presynaptic secretion of brain-derived neurotrophic factor (BDNF). Genetic depletion of either BDNF or the NMDAR subunit GluN1 specifically in cortical axons abolished corticostriatal LTP in response to theta burst stimulation (TBS). Furthermore, functional axonal NMDARs were required for TBS-triggered prolonged axonal Ca2+ elevation and BDNF secretion, supporting the notion that activation of axonal NMDARs induces BDNF secretion via enhancing Ca2+ signals in the presynaptic nerve terminals. These results demonstrate that presynaptic NMDARs are equally important as postsynaptic NMDARs in LTP induction of corticostriatal synapses due to their role in mediating activity-induced presynaptic BDNF secretion.

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“…To ensure our studies were physiologically relevant, spike-timing dependant plasticity paradigms were used (Pawlak and Kerr, 2008) that most likely mimic in vivo stimulation patterns observed during striatal based learning (DeCoteau et al, 2007a,b; Tort et al, 2008; Hawes et al, 2013). Methods employed to generate slices preserved thalamic and cortical inputs onto striatal output neurons, and also retained output basal ganglia nuclei, thus retaining striatal inputs and outputs as well as feedback loops (Beurrier et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Selective loss of bi-directional synaptic plasticity in the direct and indirect striatal output pathways accompanies generation of parkinsonism and l-DOPA induced dyskinesia in mouse models

Thiele

Chen

et al. 2014

Neurobiology of Disease

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Parkinsonian symptoms arise due to over-activity of the indirect striatal output pathway, and under-activity of the direct striatal output pathway. l-DOPA-induced dyskinesia (LID) is caused when the opposite circuitry problems are established, with the indirect pathway becoming underactive, and the direct pathway becoming over-active. Here, we define synaptic plasticity abnormalities in these pathways associated with parkinsonism, symptomatic benefits of l-DOPA, and LID. We applied spike-timing dependent plasticity protocols to corticostriatal synapses in slices from 6-OHDA-lesioned mouse models of parkinsonism and LID, generated in BAC transgenic mice with eGFP targeting the direct or indirect output pathways, with and without l-DOPA present. In naïve mice, bidirectional synaptic plasticity, i.e. LTP and LTD, was induced, resulting in an EPSP amplitude change of approximately 50% in each direction in both striatal output pathways, as shown previously. In parkinsonism and dyskinesia, both pathways exhibited unidirectional plasticity, irrespective of stimulation paradigm. In parkinsonian animals, the indirect pathway only exhibited LTP (LTP protocol: 143.5 ± 14.6%; LTD protocol 177.7 ± 22.3% of baseline), whereas the direct pathway only showed LTD (LTP protocol: 74.3 ± 4.0% and LTD protocol: 63.3 ± 8.7%). A symptomatic dose of l-DOPA restored bidirectional plasticity on both pathways to levels comparable to naïve animals (Indirect pathway: LTP protocol: 124.4± 22.0% and LTD protocol: 52.1± 18.5% of baseline. Direct pathway: LTP protocol: 140.7 ± 7.3% and LTD protocol: 58.4 ± 6.0% of baseline). In dyskinesia, in the presence of l-DOPA, the indirect pathway exhibited only LTD (LTP protocol: 68.9 ± 21.3% and LTD protocol 52.0 ± 14.2% of baseline), whereas in the direct pathway, only LTP could be induced (LTP protocol: 156.6 ± 13.2% and LTD protocol 166.7 ± 15.8% of baseline). We conclude that normal motor control requires bidirectional plasticity of both striatal outputs, which underlies the symptomatic benefits of l-DOPA. Switching from bidirectional to unidirectional plasticity drives global changes in striatal pathway excitability, and underpins parkinsonism and dyskinesia.

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Sensitivity to theta-burst timing permits LTP in dorsal striatal adult brain slice

Cited by 48 publications

References 90 publications

Updating temporal expectancy of an aversive event engages striatal plasticity under amygdala control

Updating temporal expectancy of an aversive event engages striatal plasticity under amygdala control

Essential Role of Presynaptic NMDA Receptors in Activity-Dependent BDNF Secretion and Corticostriatal LTP

Selective loss of bi-directional synaptic plasticity in the direct and indirect striatal output pathways accompanies generation of parkinsonism and l-DOPA induced dyskinesia in mouse models

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