scholarly journals REM sleep–active MCH neurons are involved in forgetting hippocampus-dependent memories

Science ◽  
2019 ◽  
Vol 365 (6459) ◽  
pp. 1308-1313 ◽  
Author(s):  
Shuntaro Izawa ◽  
Srikanta Chowdhury ◽  
Toh Miyazaki ◽  
Yasutaka Mukai ◽  
Daisuke Ono ◽  
...  
Keyword(s):  
Rem Sleep ◽  
Pyramidal Neurons ◽  
Dorsal Hippocampus ◽  
Sleep State ◽  
Hippocampal Pyramidal Neurons ◽  
State Dependent ◽  
Dependent Inhibition ◽  
Melanin Concentrating Hormone ◽  
Hippocampus Dependent Memory

The neural mechanisms underlying memory regulation during sleep are not yet fully understood. We found that melanin concentrating hormone–producing neurons (MCH neurons) in the hypothalamus actively contribute to forgetting in rapid eye movement (REM) sleep. Hypothalamic MCH neurons densely innervated the dorsal hippocampus. Activation or inhibition of MCH neurons impaired or improved hippocampus-dependent memory, respectively. Activation of MCH nerve terminals in vitro reduced firing of hippocampal pyramidal neurons by increasing inhibitory inputs. Wake- and REM sleep–active MCH neurons were distinct populations that were randomly distributed in the hypothalamus. REM sleep state–dependent inhibition of MCH neurons impaired hippocampus-dependent memory without affecting sleep architecture or quality. REM sleep–active MCH neurons in the hypothalamus are thus involved in active forgetting in the hippocampus.

scholarly journals Increasing SK2 channel activity impairs associative learning

2012 ◽  
Vol 108 (3) ◽  
pp. 863-870 ◽  
Author(s):  
Bridget M. McKay ◽  
M. Matthew Oh ◽  
Roberto Galvez ◽  
Jeffrey Burgdorf ◽  
Roger A. Kroes ◽  
...  
Keyword(s):  
Associative Learning ◽  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
Dorsal Hippocampus ◽  
Eyeblink Conditioning ◽  
Excitatory Postsynaptic Potential ◽  
Sk Channels ◽  
Hippocampal Pyramidal Neurons ◽  
Trace Eyeblink Conditioning

Enhanced intrinsic neuronal excitability of hippocampal pyramidal neurons via reductions in the postburst afterhyperpolarization (AHP) has been hypothesized to be a biomarker of successful learning. This is supported by considerable evidence that pharmacologic enhancement of neuronal excitability facilitates learning. However, it has yet to be demonstrated that pharmacologic reduction of neuronal excitability restricted to the hippocampus can retard acquisition of a hippocampus-dependent task. Thus, the present study was designed to address this latter point using a small conductance potassium (SK) channel activator NS309 focally applied to the dorsal hippocampus. SK channels are important contributors to intrinsic excitability, as measured by the medium postburst AHP. NS309 increased the medium AHP and reduced excitatory postsynaptic potential width of CA1 neurons in vitro. In vivo, NS309 reduced the spontaneous firing rate of CA1 pyramidal neurons and impaired trace eyeblink conditioning in rats. Conversely, trace eyeblink conditioning reduced levels of SK2 channel mRNA and protein in the hippocampus. Therefore, the present findings indicate that modulation of SK channels is an important cellular mechanism for associative learning and further support postburst AHP reductions in hippocampal pyramidal neurons as a biomarker of successful learning.

Sleep, not REM sleep, is the royal road to dreams

2000 ◽  
Vol 23 (6) ◽  
pp. 911-912 ◽  
Author(s):  
Alexander A. Borbély ◽  
Lutz Wittmann
Keyword(s):  
Functional Imaging ◽  
Rem Sleep ◽  
Sleep State ◽  
Common Features ◽  
State Dependent ◽  
Royal Road ◽  
The Common ◽  
Pet Scans ◽  
Nonrem Sleep

The advent of functional imaging has reinforced the attempts to define dreaming as a sleep state-dependent phenomenon. PET scans revealed major differences between nonREM sleep and REM sleep. However, because dreaming occurs throughout sleep, the common features of the two sleep states, rather than the differences, could help define the prerequisite for the occurrence of dreams.[Hobson et al.; Nielsen; Solms; Revonsuo; Vertes & Eastman]

Metrifonate Decreases sI AHP in CA1 Pyramidal Neurons In Vitro

2001 ◽  
Vol 85 (1) ◽  
pp. 319-322 ◽  
Author(s):  
John M. Power ◽  
M. Mathew Oh ◽  
John F. Disterhoft
Keyword(s):  
Pyramidal Neurons ◽  
Slow Component ◽  
Cell Voltage ◽  
Current Clamp ◽  
Hippocampal Pyramidal Neurons ◽  
Tail Current ◽  
Electrode Current ◽  
Ca1 Pyramidal Neurons ◽  
Age Related

Metrifonate, a cholinesterase inhibitor, has been shown to enhance learning in aging rabbits and rats, and to alleviate the cognitive deficits observed in Alzheimer's disease patients. We have previously determined that bath application of metrifonate reduces the spike frequency adaptation and postburst afterhyperpolarization (AHP) in rabbit CA1 pyramidal neurons in vitro using sharp electrode current-clamp recording. The postburst AHP and accommodation observed in current clamp are the result of four slow outward potassium currents (s I AHP, I AHP, I M, and I C) and the hyperpolarization activated mixed cation current, I h. We recorded from visually identified CA1 hippocampal pyramidal neurons in vitro using whole cell voltage-clamp technique to better isolate and characterize which component currents of the AHP are affected by metrifonate. We observed an age-related enhancement of the slow component of the AHP tail current (s I AHP), but not of the fast decaying component of the AHP tail current ( I AHP, I M, and I C). Bath perfusion of metrifonate reduced s I AHP at concentrations that cause a reduction of the AHP and accommodation in current-clamp recordings, with no apparent reduction of I AHP, I M, and I C. The functional consequences of metrifonate administration are apparently mediated solely through modulation of the s I AHP.

scholarly journals Transient oxytocin signaling primes the development and function of excitatory hippocampal neurons

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Silvia Ripamonti ◽  
Mateusz C Ambrozkiewicz ◽  
Francesca Guzzi ◽  
Marta Gravati ◽  
Gerardo Biella ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Hippocampal Pyramidal Neurons ◽  
Excitatory Transmission ◽  
Oxytocin Receptors ◽  
Synapse Density ◽  
Protein Components ◽  
And Function

Beyond its role in parturition and lactation, oxytocin influences higher brain processes that control social behavior of mammals, and perturbed oxytocin signaling has been linked to the pathogenesis of several psychiatric disorders. However, it is still largely unknown how oxytocin exactly regulates neuronal function. We show that early, transient oxytocin exposure in vitro inhibits the development of hippocampal glutamatergic neurons, leading to reduced dendrite complexity, synapse density, and excitatory transmission, while sparing GABAergic neurons. Conversely, genetic elimination of oxytocin receptors increases the expression of protein components of excitatory synapses and excitatory synaptic transmission in vitro. In vivo, oxytocin-receptor-deficient hippocampal pyramidal neurons develop more complex dendrites, which leads to increased spine number and reduced γ-oscillations. These results indicate that oxytocin controls the development of hippocampal excitatory neurons and contributes to the maintenance of a physiological excitation/inhibition balance, whose disruption can cause neurobehavioral disturbances.

scholarly journals Modeling unitary fields and the single-neuron contribution to local field potentials in the hippocampus

2019 ◽  
Author(s):  
Maria Teleńczuk ◽  
Bartosz Teleńczuk ◽  
Alain Destexhe
Keyword(s):  
Local Field ◽  
Computational Models ◽  
Pyramidal Neurons ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Inhibitory Synapses ◽  
Simple Method ◽  
Hippocampal Pyramidal Neurons

AbstractSynaptic currents represent a major contribution to the local field potential (LFP) in brain tissue, but the respective contribution of excitatory and inhibitory synapses is not known. Here, we provide estimates of this contribution by using computational models of hippocampal pyramidal neurons, constrained by in vitro recordings. We focus on the unitary LFP (uLFP) generated by single neurons in the CA3 region of the hippocampus. We first reproduce experimental results for hippocampal basket cells, and in particular how inhibitory uLFP are distributed within hippocampal layers. Next, we calculate the uLFP generated by pyramidal neurons, using morphologically-reconstructed CA3 pyramidal cells. The model shows that the excitatory uLFP is of small amplitude, smaller than inhibitory uLFPs. Indeed, when the two are simulated together, inhibitory uLFPs mask excitatory uLFPs, which might create the illusion that the inhibitory field is generated by pyramidal cells. These results provide an explanation for the observation that excitatory and inhibitory uLFPs are of the same polarity, in vivo and in vitro. These results also show that somatic inhibitory currents are large contributors of the LFP, which is important information to interpret this signal. Finally, the results of our model might form the basis of a simple method to compute the LFP, which could be applied to point neurons for each cell type, thus providing a simple biologically-grounded method to calculate LFPs from neural networks.

Sign in / Sign up

Export Citation Format

Share Document