Dark Exposure Extends the Integration Window for Spike-Timing-Dependent Plasticity.

Dark exposure extends the integration window for spike-timing-dependent plasticity.

Filed under: Depression Treatment

J Neurosci. 2012 Oct 24; 32(43): 15027-35
Guo Y, Huang S, de Pasquale R, McGehrin K, Lee HK, Zhao K, Kirkwood A

Metaplasticity, the adaptive changes of long-term potentiation (LTP) and long-term depression (LTD) in response to fluctuations in neural activity is well documented in visual cortex, where dark rearing shifts the frequency threshold for the induction of LTP and LTD. Here we studied metaplasticity affecting spike-timing-dependent plasticity, in which the polarity of plasticity is determined not by the stimulation frequency, but by the temporal relationship between near-coincidental presynaptic and postsynaptic firing. We found that in mouse visual cortex the same regime of deprivation that restricts the frequency range for inducing rate-dependent LTD extends the integration window for inducing timing-dependent LTD, enabling LTD induction with random presynaptic and postsynaptic firing. Notably, the underlying mechanism for the changes in both rate-dependent and time-dependent LTD appears to be an increase of NR2b-containing NMDAR at the synapse. Thus, the rules of metaplasticity might manifest in opposite directions, depending on the plasticity-induction paradigms.
HubMed – depression

Developmental switch in spike timing-dependent plasticity at layers 4-2/3 in the rodent barrel cortex.

Filed under: Depression Treatment

J Neurosci. 2012 Oct 24; 32(43): 15000-11
Itami C, Kimura F

Sensory deprivation during the critical period induces long-lasting changes in cortical maps. In the rodent somatosensory cortex (S1), its precise initiation mechanism is not known, yet spike timing-dependent plasticity (STDP) at layer 4 (L4)-L2/3 synapses are thought to be crucial. Whisker stimulation causes “L4 followed by L2/3” cell firings, while acute single whisker deprivation suddenly reverses the sequential order in L4 and L2/3 neurons in the deprived column (Celikel et al., 2004). Reversed spike sequence then leads to long-term depression through an STDP mechanism (timing-dependent long-term depression), known as deprivation-induced suppression at L4-L2/3 synapses (Bender et al., 2006a), an important first step in the map reorganization. Here we show that STDP properties change dramatically on postnatal day 13-15 (P13-P15) in mice S1. Before P13, timing-dependent long-term potentiation (t-LTP) was predominantly induced regardless of spiking order. The induction of t-LTP required postsynaptic influx of Ca(2+), an activation of protein kinase A, but not calcium/calmodulin-dependent protein kinase II. Consistent with the strong bias toward t-LTP, whisker deprivation (all whiskers in Row “D”) from P7-P12 failed to induce synaptic depression at L4-L2/3 synapses in the deprived column, but clear depression was seen if deprivation occurred after P14. Random activation of L4, L2/3 cells, as may occur in response to whisker stimulation before P13 during network formation, led to potentiation under the immature STDP rule, as predicted from the bias toward t-LTP regardless of spiking order. These findings describe a developmental switch in the STDP rule that may underlie the transition from synapse formation to circuit reorganization at L4-L2/3 synapses, both in distinct activity-dependent manners.
HubMed – depression

Advances with MRI in Parkinson disease: From freezing to festination.

Filed under: Depression Treatment

Neurology. 2012 Oct 24;
Filippi M, Kulisevsky J

Degeneration of dopamine neurons in the substantia nigra and intracellular deposition of Lewy body inclusions are the pathologic hallmarks of Parkinson disease (PD). Depletion of dopamine and other neurotransmitters results in motor (rest tremor, bradykinesia, and rigidity) and nonmotor (cognitive impairment, sleep disorders, fatigue, and depression) symptoms.
HubMed – depression

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