scholarly journals Protracted Withdrawal from Alcohol and Drugs of Abuse Impairs Long-Term Potentiation of Intrinsic Excitability in the Juxtacapsular Bed Nucleus of the Stria Terminalis

2009 ◽  
Vol 29 (17) ◽  
pp. 5389-5401 ◽  
Author(s):  
W. Francesconi ◽  
F. Berton ◽  
V. Repunte-Canonigo ◽  
K. Hagihara ◽  
D. Thurbon ◽  
...  
Keyword(s):  
Drugs Of Abuse ◽  
Long Term Potentiation ◽  
Intrinsic Excitability ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Alcohol And Drugs ◽  
Term Potentiation

Long-term potentiation of intrinsic excitability in trigeminal motoneurons

2010 ◽  
Vol 1312 ◽  
pp. 32-40 ◽  
Author(s):  
Reiko Okamoto ◽  
Akifumi Enomoto ◽  
Hidehiko Koizumi ◽  
Susumu Tanaka ◽  
Kohji Ishihama ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Intrinsic Excitability ◽  
Term Potentiation ◽  
Trigeminal Motoneurons

scholarly journals Fast and flexible sequence induction in spiking neural networks via rapid excitability changes

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Rich Pang ◽  
Adrienne L Fairhall
Keyword(s):  
Neural Networks ◽  
Cognitive Flexibility ◽  
Long Term Potentiation ◽  
Spiking Neural Networks ◽  
Intrinsic Excitability ◽  
Stimulus Response ◽  
Term Potentiation ◽  
Spiking Network ◽  
Sequence Induction

Cognitive flexibility likely depends on modulation of the dynamics underlying how biological neural networks process information. While dynamics can be reshaped by gradually modifying connectivity, less is known about mechanisms operating on faster timescales. A compelling entrypoint to this problem is the observation that exploratory behaviors can rapidly cause selective hippocampal sequences to ‘replay’ during rest. Using a spiking network model, we asked whether simplified replay could arise from three biological components: fixed recurrent connectivity; stochastic ‘gating’ inputs; and rapid gating input scaling via long-term potentiation of intrinsic excitability (LTP-IE). Indeed, these enabled both forward and reverse replay of recent sensorimotor-evoked sequences, despite unchanged recurrent weights. LTP-IE ‘tags’ specific neurons with increased spiking probability under gating input, and ordering is reconstructed from recurrent connectivity. We further show how LTP-IE can implement temporary stimulus-response mappings. This elucidates a novel combination of mechanisms that might play a role in rapid cognitive flexibility.

Dopamine D1/5 Receptor-Mediated Long-Term Potentiation of Intrinsic Excitability in Rat Prefrontal Cortical Neurons: Ca2+-Dependent Intracellular Signaling

2007 ◽  
Vol 97 (3) ◽  
pp. 2448-2464 ◽  
Author(s):  
Long Chen ◽  
Joseph D. Bohanick ◽  
Makoto Nishihara ◽  
Jeremy K. Seamans ◽  
Charles R. Yang
Keyword(s):  
Protein Kinase ◽  
Cortical Neurons ◽  
Intracellular Signaling ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Intrinsic Excitability ◽  
Term Potentiation ◽  
Voltage Dependent ◽  
Spike Firing

Prefrontal cortex (PFC) dopamine D1/5 receptors modulate long- and short-term neuronal plasticity that may contribute to cognitive functions. Synergistic to synaptic strength modulation, direct postsynaptic D1/5 receptor activation also modulates voltage-dependent ionic currents that regulate spike firing, thus altering the neuronal input–output relationships in a process called long-term potentiation of intrinsic excitability (LTP-IE). Here, the intracellular signals that mediate this D1/5 receptor-dependent LTP-IE were determined using whole cell current-clamp recordings in layer V/VI rat pyramidal neurons from PFC slices. After blockade of all major amino acid receptors ( Vhold = −65 mV) brief tetanic stimulation (20 Hz) of local afferents or application of the D1 agonist SKF81297 (0.2–50 μM) induced LTP-IE, as shown by a prolonged (>40 min) increase in depolarizing pulse-evoked spike firing. Pretreatment with the D1/5 antagonist SCH23390 (1 μM) blocked both the tetani- and D1/5 agonist-induced LTP-IE, suggesting a D1/5 receptor-mediated mechanism. The SKF81297 -induced LTP-IE was significantly attenuated by Cd2+, [Ca2+]i chelation, by inhibition of phospholipase C, protein kinase-C, and Ca2+/calmodulin kinase-II, but not by inhibition of adenylate cyclase, protein kinase-A, MAP kinase, or L-type Ca2+ channels. Thus this form of D1/5 receptor-mediated LTP-IE relied on Ca2+ influx via non-L-type Ca2+ channels, activation of PLC, intracellular Ca2+ elevation, activation of Ca2+-dependent CaMKII, and PKC to mediate modulation of voltage-dependent ion channel(s). This D1/5 receptor-mediated modulation by PKC coexists with the previously described PKA-dependent modulation of K+ and Ca2+ currents to dynamically regulate overall excitability of PFC neurons.

scholarly journals Hippocampal Neuropeptide Y2 receptor blockade improves spatial memory retrieval and modulates limbic brain metabolism

2021 ◽  
Author(s):  
Marta Mendez-Couz ◽  
Hector Gonzalez-Pardo ◽  
Jorge L Arias ◽  
Nelida M Conejo
Keyword(s):  
Spatial Memory ◽  
Brain Metabolism ◽  
Drugs Of Abuse ◽  
Dorsal Hippocampus ◽  
Long Term Potentiation ◽  
Brain Regions ◽  
Memory Recall ◽  
Y2 Receptor ◽  
Term Potentiation

Introduction: The neuropeptide Y (NPY) is broadly distributed in the central nervous system (CNS), and it has been related to neuroprotective functions. NPY seems to be an important component to counteract brain damage and cognitive impairment mediated by drugs of abuse and neurodegenerative diseases, and both NPY and its Y2 receptor (Y2R) are highly expressed in the hippocampus, critical for learning and memory. We have recently demonstrated its influence on cognitive functions; however, the specific mechanism and involved brain regions where NPY modulates spatial memory by acting on Y2R remain unclear. Methods: Here, we examined the involvement of the hippocampal NPY Y2R in spatial memory and associated changes in brain metabolism by bilateral administration of the selective antagonist BIIE0246 into the rat dorsal hippocampus. To further evaluate the relationship between memory functions and neuronal activity, we analysed the regional expression of the mitochondrial enzyme cytochrome c oxidase (CCO) as an index of oxidative metabolic capacity in limbic and non-limbic brain regions. Results: The acute blockade of NPY Y2R significantly improved spatial memory recall in rats trained in the Morris water maze that matched metabolic activity changes in spatial memory processing regions. Specifically, CCO activity changes were found in the dentate gyrus of the dorsal hippocampus and CA1 subfield of the ventral hippocampus, the infralimbic region of the PFC and the mammillary bodies. Conclusions: These findings suggest that the NPY hippocampal system, through its Y2R receptor, influences spatial memory recall (retrieval) and exerts control over patterns of brain activation that are relevant for associative learning, probably mediated by Y2R modulation of long-term potentiation and long-term depression.

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