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[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)

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ref: -0 tags: NMDA spike hebbian learning states pyramidal cell dendrites date: 10-03-2018 01:15 gmt revision:0 [head]

PMID-20544831 The decade of the dendritic NMDA spike.

  • NMDA spikes occur in the finer basal, oblique, and tuft dendrites.
  • Typically 40-50 mV, up to 100's of ms in duration.
  • Look similar to cortical up-down states.
  • Permit / form the substrate for spatially and temporally local computation on the dendrites that can enhance the representational or computational repertoire of individual neurons.

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ref: -0 tags: microstim ICMS axons soma Nowak NMDA date: 01-27-2012 23:30 gmt revision:1 [0] [head]

PMID-9504843 Axons, but not cell bodies, are activated by electrical stimulation in cortical gray matter. I. Evidence from chronaxie measurements.

  • Slice experiments / in vitro.
  • The chronaxie for orthodromic activation was similar to that for axonal activation, but was 40 times smaller than the chronaxie for direct cell body activation. This suggests that, whenever a postsynaptic response is elicited after electrical stimulation of the cortical gray matter, axons (either axonal branches or axon initial segments), but not cell bodies, are the neuronal elements activated.

PMID-9504844 Axons, but not cell bodies, are activated by electrical stimulation in cortical gray matter. II. Evidence from selective inactivation of cell bodies and axon initial segments.

  • Blocked soma and proximal axons / dendrites from firing AP through iontophoresis of NMDA.
  • When the NMDA-induced depolarization block was performed at the site of electrical stimulation, an unexpected increase in the amplitude of the orthodromic (backwards, into the white matter) responses was observed.
    • Possibly due to an increase in axonal excitability (?)
    • Superexitability eventually washed out, leading to responses that was 15-20% lower than before NMDA soma / proximal axon block.
  • "Since the neocortex is organised as a network of local and long-range reciprocal connections, great attention must be paid to the interpretation of data obtained with electrical stimulation."

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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: Di-1994.06 tags: dopamine NMDA striatum globus_pallidus ion_channels neurotransmitters date: 0-0-2007 0:0 revision:0 [head]

PMID-7521083 Modulatory functions of neurotransmitters in the striatum: ACh/dopamine/NMDA interactions.

  • in striatum, 2 basic classes of neural transmission:
    • fast neural transmission:
      • glutamate response in striatum to cortical/thalamic input via AMPA on medium spiny neurons
      • GABA output of the striatum
    • modulatory neural transmission:
      • NMDA
      • DA dopamine
      • substance P
      • ACh acetylecholine (large aspiny neurons, 30um soma! 1-2% of the population)
  • input to the cholinergic large aspiny neurons
    • GABA/substance P medium-spiny neurons which project to SNr + GPi
    • DA neurons from tegmentum, a8 a9 a10 groups
    • Glu neurons in the thalamus, and, to a lesser extent, from the cortex
  • DA D2 autoreceptors inhibit/regulate the release of DA, and it can also modulate the release of ACh + glu
    • specifically D2 has been demonstrated to inhibit ACh release, but not D1 (accourse)
  • figure 2 is kinda nice for the neurotransmitters in the basal ganglia
  • not really all that clear of an article