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[0] Schicknick H, Schott BH, Budinger E, Smalla KH, Riedel A, Seidenbecher CI, Scheich H, Gundelfinger ED, Tischmeyer W, Dopaminergic modulation of auditory cortex-dependent memory consolidation through mTOR.Cereb Cortex 18:11, 2646-58 (2008 Nov)

[0] Pawlak V, Kerr JN, Dopamine receptor activation is required for corticostriatal spike-timing-dependent plasticity.J Neurosci 28:10, 2435-46 (2008 Mar 5)

[0] Buonomano DV, Merzenich MM, Cortical plasticity: from synapses to maps.Annu Rev Neurosci 21no Issue 149-86 (1998)

[0] Recanzone GH, Schreiner CE, Merzenich MM, Plasticity in the frequency representation of primary auditory cortex following discrimination training in adult owl monkeys.J Neurosci 13:1, 87-103 (1993 Jan)

[0] Li CS, Padoa-Schioppa C, Bizzi E, Neuronal correlates of motor performance and motor learning in the primary motor cortex of monkeys adapting to an external force field.Neuron 30:2, 593-607 (2001 May)[1] Caminiti R, Johnson PB, Urbano A, Making arm movements within different parts of space: dynamic aspects in the primate motor cortex.J Neurosci 10:7, 2039-58 (1990 Jul)

[0] Kilgard MP, Merzenich MM, Cortical map reorganization enabled by nucleus basalis activity.Science 279:5357, 1714-8 (1998 Mar 13)

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ref: -0 tags: synaptic plasticity 2-photon imaging inhibition excitation spines dendrites synapses 2p date: 05-31-2019 23:02 gmt revision:2 [1] [0] [head]

PMID-22542188 Clustered dynamics of inhibitory synapses and dendritic spines in the adult neocortex.

  • Cre-recombinase-dependent labeling of postsynapitc scaffolding via Gephryn-Teal fluorophore fusion.
  • Also added Cre-eYFP to lavel the neurons
  • Electroporated in utero e16 mice.
    • Low concentration of Cre, high concentrations of Gephryn-Teal and Cre-eYFP constructs to attain sparse labeling.
  • Located the same dendrite imaged in-vivo in fixed tissue - !! - using serial-section electron microscopy.
  • 2230 dendritic spines and 1211 inhibitory synapses from 83 dendritic segments in 14 cells of 6 animals.
  • Some spines had inhibitory synapses on them -- 0.7 / 10um, vs 4.4 / 10um dendrite for excitatory spines. ~ 1.7 inhibitory
  • Suggest that the data support the idea that inhibitory inputs maybe gating excitation.
  • Furthermore, co-inervated spines are stable, both during mormal experience and during monocular deprivation.
  • Monocular deprivation induces a pronounced loss of inhibitory synapses in binocular cortex.

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ref: -0 tags: DBS dopamine synaptic plasticity striatum date: 02-27-2012 21:57 gmt revision:7 [6] [5] [4] [3] [2] [1] [head]

PMID-11285003 Dopaminergic control of synaptic plasticity in the dorsal striatum.

  • Repetitive stimulation of corticostriatal fibers causes a massive release of glutamate and DA in the striatum, and depending on the glutamate receptor subtype preferentially activated, produces either long-term depression (LTD) or long-term potentiation (LTP) of excitatory synaptic transmission.
  • D1 and D2 (like) receptors interact synergistically to allow LTD formation, and in opposition while inducing LTP.
  • Stimulation of DA receptors has been shown to modulate voltage-dependent conductances in striatal spiny neurons, but it does not cause depolarization or hyperpolarization (Calabresi et al 2000a PMID-11052221; Nicola et al 2000)
  • Striatal spiny neurons present a high degree of colocalization of subtypes of DA and glutamate receptors. PMID-9215599
  • Striatal cells have up and down states. Wilson and Kawaguchi 1996 PMID-8601819
  • Both LTD and LTP are induced in the striatum by the repetitive stimulation of corticostriatal fibers.
    • Repetition is associated with the dramatic increase of both glutamate and DA in the striatum. (presynaptic?)
  • LTP is enhanced by blocking or removing D2 receptors.
  • More complexity here - in terms of receptors and blocking. (sure magnesium blocks NMDA receptors, but there are many other drugs used...)

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ref: Prescott-2009.02 tags: PD levodopa synaptic plasticity SNr STN DBS date: 02-22-2012 18:28 gmt revision:2 [1] [0] [head]

PMID-19050033[0] Levodopa enhances synaptic plasticity in the substantia nigra pars reticulata of Parkinson's disease patients

  • In the SNpc -> SNr.
  • High frequency stimulation (HFS--four trains of 2 s at 100 Hz) in the SNr failed to induce a lasting change in test fEPs (1 Hz) amplitudes in patients OFF medication (decayed to baseline by 160 s). Following oral L-dopa administration, HFS induced a potentiation of the fEP amplitudes (+29.3% of baseline at 160 s following a plateau).
  • Aberrant synaptic plasticity may play a role in the pathophysiology of Parkinson's disease.

____References____

[0] Prescott IA, Dostrovsky JO, Moro E, Hodaie M, Lozano AM, Hutchison WD, Levodopa enhances synaptic plasticity in the substantia nigra pars reticulata of Parkinson's disease patients.Brain 132:Pt 2, 309-18 (2009 Feb)

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ref: Bures-1968 tags: inferior colliculus stimulation classical conditioning plasticity hebb Bures date: 01-03-2012 07:08 gmt revision:5 [4] [3] [2] [1] [0] [head]

bibtex:Bures-1968 Plastic changes of unit activity based on reinforcing properties of extracellular stimulation of single neurons

  • images/972_1.pdf
  • Trained neurons to respond to auditory stimuli throughout the brain (though mostly the IC) to a auditory tone.
    • Hebb's rule, verified.
  • Yoshii & Ogura (22): Reticular units, originally not responding to sciatic nerve US, started to respond to the CS after a few tens of trials, however the conditioned reactions disappeared with continued training.
    • This must be regarded as response to arousal at the initial stages of classical aversive (sciatic nerve pain?) conditioning.
  • Used capilary electrodes 1um in diameter, filled with KCl or sodium glutamate
  • Stimulation current 10-50nA DC, 0.3-1 sec.
  • Were able to record and stimulate at the same time using these glass microelectrodes.
  • The majority of units (cortex, reticular formation, thalamus) showed no response, though some did. These responses tended to fade with overtraining.
  • Quote: "The rather low incidence of positive results int he above experiment might be due to the fact that many examined neurons lack even an indirect acoustic input and cannot, therefore, be activated by acoustic stimuli."
  • Neurons in the IC show the strongest plastic change.
  • Their study is more specific than Loucks (15), Olds and Milner (17) Delgaso (6) Doty(7) which used less specific ICMS.
  • That said, there is no behavior .. so we don't know if the stimuli is being reacted to or attended to (might explain the low # of responses in areas).
  • They also think that the response can be credited to nonspecific phenomena like dominant focus, reflex sensitization, or heterosynaptic facilitation.
    • That said, the IC did show strong responses.

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ref: Tononi-2006.02 tags: sleep synaptic homeostasis plasticity date: 03-20-2009 15:45 gmt revision:1 [0] [head]

PMID-16376591[0] Sleep function and synaptic homeostasis.

  • Sleep keeps the neural network stable & the synaptic weights in check.
    • if you don't sleep do you get epilepsy?? don't have access to the article, would have to read it.

____References____

[0] Tononi G, Cirelli C, Sleep function and synaptic homeostasis.Sleep Med Rev 10:1, 49-62 (2006 Feb)

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ref: Schicknick-2008.11 tags: dopamine plasticity auditory cortex date: 12-15-2008 04:13 gmt revision:1 [0] [head]

PMID-18321872[0] Dopaminergic Modulation of Auditory Cortex-Dependent Memory Consolidation through mTOR.

  • I will annotate this paper later, after winter break.

____References____

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ref: -0 tags: blind seeing tongue plasticity learning date: 10-08-2008 17:49 gmt revision:1 [0] [head]

“Seeing” through the tongue: cross-modal plasticity in the congenitally blind

  • tested their tongue display unit on sighted and blind volunteers; the blind volunteers showed increased PET signal in their occipital lobe, while the sighted (blindfolded) volunteers did not, though both achieved the same levels of performance on a orientation discrimination task after one week of intensive training.
  • TDU unit has 144 contacts.
  • spatial learning with this is apparently robust and rapid with people!

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ref: Pawlak-2008.03 tags: dopamine striatum cortex STDP plasticity NMDAR date: 10-08-2008 17:24 gmt revision:1 [0] [head]

PMID-18322089[0] Dopamine Receptor Activation Is Required for Corticostriatal Spike-Timing-Dependent Plasticity

  • Single action potentials (APs) backpropagate into the higher-order dendrites of striatal spiny projection neurons during cortically driven "up" states (Kerr and Plenz, 2004)
    • note: many 'up' states in the striatum do not contain an AP.
  • Blocking dopamine D1/D5 receptors prevented both LTD and LTP induction.
  • first paragraph has a ton of references! They note that burst spiking in cortical and striatal projection neurons is infrequent - mostly, there are single spikes - and so STDP investigations are more applicable than high frequency stimulation LTP induction.
  • tested in vitro -- para-horizontal sections into the dorsolateral striatum of young rat brain, whole-cell current clamp, GABA_A currents blocked.
  • striatal projection neurons (SPNs) have a strange mode of AP generation - their membrane potential rises for 120ms after current injection, followed by a spike. They used this and infrared differential microscopy of morphology to locate the projection neurons.
  • stimulated using extracellular current to layer 5 of the cortex or nearby white matter. kept microstim current to a minimum.
  • paired this with AP generation in the SPNs at varying time delays, both at low frequency (0.1Hz)
  • there are a few cholinergic neurons in the striatum, apparently.
  • demonstrated STDP: "synaptic strength is maximally enhanced when cortically evoked EPSPs lead a spike by 10 ms, whereas synaptic strength is maximally depressed when EPSPs follow a spike by 30 ms"
  • also tried eliciting bursts in the SPN, but: "the timing of EPSPs with single APs is as efficient in inducing synaptic plasticity as the timing of EPSPs with AP bursts"
  • the STDP / LTP / LTD was NMDA-R dependent.
  • blocked D1/D5 with SCH-23390, and found that they could not induce LTP / LTD.
  • block of D2 receptor advanced the onset of LTP and delayed the onset of LTD, to a less dramatic degree than the D1/D5 block. Long-term LTP/LTD magnitude was not effected.
  • why did these guys get in J. Neuroscience where as this is in Science? because the Science article studied medium spiny neurons, with GFP labeling the D1/D2 receptors?

____References____

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ref: Buonomano-1998.01 tags: cortical plasticity learning review LTD LTP date: 10-07-2008 03:27 gmt revision:1 [0] [head]

PMID-9530495[0] Cortical plasticity: from synapses to maps

  • focuses on synaptic plasticity as the underlying mechanism of behavior-dependent cortical maps/representations.
  • "within limits, the cortex can allocate cortical area in a use-dependent manner"
  • synaptic plasticity -> STDP via NMDA, etc.
    • demonstrated with intracellular recordings of cat M1 & simultaneous stimulation of the ventrolateral thalamus & intracellular depolarization. Facilitation was short lasting and not present in all neurons.
    • demonstrated in rat auditory cortex / recording in layer 2/3 , stimulate layer 2/3 & White matter/6.
    • review of Ca+ hypothesis of LTP/LTD balance: if the Ca+ influc is below a threshold, LTD occurs; if it is above a certain threshold, LTP.
      • not sure how long LTD has been demonstrated -- 15 min?
  • cellular conditioning = direct induction of plastic changes in the selective responses of individual neurons in vivo as a result of short-term conditioning protocols. this is what we are interested in, for now.
    • this review does not explicitly deal with BG-DA / ACh reinforcement, only timing dependent plasticity, in visual and auditory cortex.
  • cortical plasticity:
    • talk about the revealing/unmasking of hidden responses when sections of cortex are deafferented or digits were amputated.
    • talk about training-based approaches: training increases cortical representation of a sensory modality / skill/ etc. The cortex can differentially 'allocate' area in a use-dependent manner throughout life.
    • cortical map changes are not reflected by changes in thalamic somatotopy.

____References____

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ref: Recanzone-1993.01 tags: plasticity cortex learning auditory owl monkeys SUA date: 10-06-2008 22:46 gmt revision:1 [0] [head]

PMID-8423485[0] Plasticity in the frequency representation of primary auditory cortex following discrimination training in adult owl monkeys

  • Measured tonotopic organization (hence plasticity) in the owl monkey auditory cortex following training on a frequency discrimination task.
  • improvement in performance correlates with an improvement in neuronal tuning.
  • two controls:
    • monkeys that were engaged in a tactile discrimination task
    • monkeys that received the same auditory stimuli but had no reason to attend to it
  • lots of delicious behavior graphs

____References____

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ref: Li-2001.05 tags: Bizzi motor learning force field MIT M1 plasticity memory direction tuning transform date: 09-24-2008 22:49 gmt revision:5 [4] [3] [2] [1] [0] [head]

PMID-11395017[0] Neuronal correlates of motor performance and motor learning in the primary motor cortex of monkeys adapting to an external force field

  • this is concerned with memory cells, cells that 'remember' or remain permanently changed after learning the force-field.
  • In the above figure, the blue lines (or rather vertices of the blue lines) indicate the firing rate during the movement period (and 200ms before); angular position indicates the target of the movement. The force-field in this case was a curl field where force was proportional to velocity.
  • Preferred direction of the motor cortical units changed when the preferred driection of the EMGs changed
  • evidence of encoding of an internal model in the changes in tuning properties of the cells.
    • this can suppor both online performance and motor learning.
    • but what mechanisms allow the motor cortex to change in this way???
  • also see [1]

____References____

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ref: Kilgard-1998.03 tags: dopamine basal_forebrain nucleus_basalis cortical_plasticity date: 0-0-2007 0:0 revision:0 [head]

PMID-9497289[0] Cortical map reorganization enabled by nucleus basalis activity

  • idea, very cool: that stimulation in the nucleus basalis (partially acetylcholine-releasing center in the brain) of the rat, when paired with audio tone presentation, causes the auditory cortex to to reorganize so as to better represent the presented stimulus(stimuli). Note the rats were not tasked with anything, and were placed in a soundproofed box.
  • stimulation protocol: 200ms of 70-150ua current delivered to the NB through bipolar platinum stimulation electrodes. current was set at the threshold needed to desynchronize cortical EEG during slow-wave sleep.
    • how ever did they come up with this metric? EEG desynchronizaton?
____References____