Plasticity in the human central nervous system

Cooke, Sam F

doi:10.1093/brain/awl082

Cited by 977 publications

(707 citation statements)

References 137 publications

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“…DA prolongs long-term potentiation (LTP; Frey et al, 1990Frey et al, , 1993Huang and Kandel, 1995), a cellular mechanism necessary for successful memory formation and consolidation (for review, see Cooke and Bliss, 2006). In humans, molecular imaging studies have related higher D2 receptor binding in hippocampus to better recall of verbal (Takahashi et al, 2007) and pictorial (Takahashi et al, 2008) memory.…”

Section: Dopaminergic Modulation Of Episodic Memorymentioning

confidence: 99%

Dopamine and glutamate receptor genes interactively influence episodic memory in old age

Papenberg¹,

Li²,

Nagel³

et al. 2014

Neurobiology of Aging

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a b s t r a c tBoth the dopaminergic and glutamatergic systems modulate episodic memory consolidation. Evidence from animal studies suggests that these two neurotransmitters may interact in influencing memory performance. Given that individual differences in episodic memory are heritable, we investigated whether variations of the dopamine D2 receptor gene (rs6277, C957T) and the N-methyl-D-aspartate 3A (NR3A) gene, coding for the N-methyl-D-aspartate 3A subunit of the glutamate N-methyl-D-aspartate receptor (rs10989591, Val362Met), interactively modulate episodic memory in large samples of younger (20e31 years; n ¼ 670) and older (59e71 years; n ¼ 832) adults. We found a reliable gene-gene interaction, which was observed in older adults only: older individuals carrying genotypes associated with greater D2 and N-methyl-D-aspartate receptor efficacy showed better episodic performance. These results are in line with findings showing magnification of genetic effects on memory in old age, presumably as a consequence of reduced brain resources. Our findings underscore the need for investigating interactive effects of multiple genes to understand individual difference in episodic memory.

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Section: Dopaminergic Modulation Of Episodic Memorymentioning

confidence: 99%

Dopamine and glutamate receptor genes interactively influence episodic memory in old age

Papenberg¹,

Li²,

Nagel³

et al. 2014

Neurobiology of Aging

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“…Such event is known as short-term potentiation. [31][32][33][34][35] If the stimuli repeat themselves many times, they give rise to synthesis of proteins to be stored in the CNS as memory and the effect will last. This process is known as long-term potentiation.…”

Section: Potentiation and Functional Recoverymentioning

confidence: 99%

“…This process is known as long-term potentiation. [31][32][33][34][35] This is probably the most important end result rehabilitation professionals would like to see and exploit,such as intensive and extensive physical training leading to functional recovery.…”

Section: Potentiation and Functional Recoverymentioning

confidence: 99%

Neural plasticity and functional recovery of human central nervous system with special reference to spinal cord injury

Wang

Sun

2010

Spinal Cord

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Study design: Literature review. Objective: To study the progress that has been made in neural plasticity for the past few decades. Setting: United Kingdom/China. Methods: An electronic search of relevant publications through PubMed was conducted using two key words: 'axonal regeneration' and 'neural plasticity'. The search included publications of the past three decades of all languages and of both animal and human studies. After confirmation of immense increase of publications on neural plasticity, reviewing of neural plasticity alone was conducted. The review covered only the most important and clinically relevant publications. For convenience of reading by busy clinicians, discussions focused on cellular and functional levels, and only the most investigated molecules were mentioned. The size of references is also planned to be concise rather than comprehensive into three digits. Results: Neural plasticity is about memory and learning. The entire process of neural plasticity is presented in the sequence of (1) lesion-induced plasticity, (2) clearance of debris, (3) collateral sprouting (4) potentiation. The recent discovery and understanding of the important role of Chondroitinase in clearance of debris is discussed in detail. Conclusion: Neural plasticity has enormous potentials in facilitating functional recovery. It is a realistic target than structural axonal regeneration at current level of neuroscience.

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“…Since the first experimental demonstrations of long-term potentiation (LTP) and depression (LTD), a wealth of empirical data regarding the induction, expression and maintenance of synaptic plasticity in different cortical regions has been obtained [4][5][6][7][8]. In spite of the heterogeneity of plasticity mechanisms observed throughout the brain, changes in the strength of excitatory synapses afferent on CA1 pyramidal neurons in the hippocampus represent the best studied form in the mammalian cortex [9][10][11][12]. At these synapses, Calcium influx into dendritic spines represents the critical signal for synaptic plasticity induction [13][14][15][16][17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Calcium control of triphasic hippocampal STDP

Bush¹,

Jin

2012

J Comput Neurosci

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Synaptic plasticity is believed to represent the neural correlate of mammalian learning and memory function. It has been demonstrated that changes in synaptic conductance can be induced by approximately synchronous pairings of pre-and post-synaptic action potentials delivered at low frequencies. It has also been established that NMDAr-dependent Calcium influx into dendritic spines represents the critical signal for plasticity induction, and can account for this spike-timing dependent plasticity (STDP) as well as experimental data obtained using other stimulation protocols. However, subsequent empirical studies have delineated a more complex relationship between spike-timing, firing rate, stimulus duration and post-synaptic bursting in dictating changes in the conductance of hippocampal excitatory synapses. It has yet to be established whether the Calcium control hypothesis can account for this more recent data. Here, we present a detailed biophysical model of single dendritic spines on a CA1 pyramidal neuron, describe the NMDAr-dependent Calcium influx generated by different stimulation protocols, and present a parsimonious model of Calcium driven kinase and phosphotase dynamics that dictate transitions between binary synaptic weight states. We demonstrate the manner in which this model can account for various experimental observations of synaptic plasticity and be used to make predictions regarding the dynamics of depolarisation and NMDAr activation generated by STDP protocols as well as the synaptic weight change induced under other experimental conditions. We then discuss how this parsimonious, unified computational model of synaptic plasticity might be utilised to appraise the activity-dependent refinement of neural circuitry induced by more realistic firing patterns. IntroductionSynaptic plasticity -the process of activity dependent change in synaptic conductance -is widely believed to represent the neural correlate of mammalian learning and memory function [1][2][3]. Since the first experimental demonstrations of long-term potentiation (LTP) and depression (LTD), a wealth of empirical data regarding the induction, expression and maintenance of synaptic plasticity in different cortical regions has been obtained [4][5][6][7][8]. In spite of the heterogeneity of plasticity mechanisms observed throughout the brain, changes in the strength of excitatory synapses afferent on CA1 pyramidal neurons in the hippocampus represent the best studied form in the mammalian cortex [9][10][11][12]. At these synapses, Calcium influx into dendritic spines represents the critical signal for synaptic plasticity induction [13][14][15][16][17][18][19][20]. Large, transient elevations in intracellular [Ca 2+ ] generate LTP via the preferential activation of kinase pathways while modest, sustained elevations in intracellular [Ca 2+ ] generate LTD via the preferential activation of phosphotase pathways [21][22][23][24][25]. Initially, empirical observations of synaptic plasticity were mediated by tetanic stimulation protoc...

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Plasticity in the human central nervous system

Cited by 977 publications

References 137 publications

Dopamine and glutamate receptor genes interactively influence episodic memory in old age

Dopamine and glutamate receptor genes interactively influence episodic memory in old age

Neural plasticity and functional recovery of human central nervous system with special reference to spinal cord injury

Calcium control of triphasic hippocampal STDP

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