Hippocampus: Intrinsic Organization

2017 ◽  
pp. 199-216
Author(s):  
Peter Somogyi ◽  
Thomas Klausberger
Keyword(s):  
Cerebral Cortex ◽  
Granule Cells ◽  
Pyramidal Cells ◽  
Spike Timing ◽  
Gabaergic Neurons ◽  
Brain State ◽  
Firing Rates ◽  
State Dependent ◽  
Postsynaptic Cell

The hippocampus, together with the subiculum, represent an associational area of the cerebral cortex that is intimately involved in mnemonic processes. Through its connections with other areas of the temporal lobe, the prefrontal cortex (PFC) and subcortical areas, it contributes to the encoding, association, consolidation, and recall of representations of the external and internal world in the combined firing rates and spike timing of glutamatergic pyramidal and granule cells. Pyramidal cell assemblies are formed and segregated from other assemblies by the dynamic strengthening and weakening of glutamatergic synaptic weights both on pyramidal cells and GABAergic interneurons. Interneurons, generate postsynaptic cell domain and brain state–dependent rhythmic changes in excitability, which are key for the formation, consolidation, and recall of representations. The chapter attempts to allocate explicit roles for some GABAergic neurons, based on their firing patterns in vivo as observed in identified neurons.

scholarly journals Selective attenuation of Ether-a-go-go related K+ currents by endogenous acetylcholine reduces spike-frequency adaptation and network correlation

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Edward D Cui ◽  
Ben W Strowbridge
Keyword(s):  
Late Phase ◽  
Pyramidal Cells ◽  
Spike Frequency ◽  
Spike Frequency Adaptation ◽  
Firing Rates ◽  
Frequency Adaptation ◽  
Rat Neocortex ◽  
Persistent Firing ◽  
K Current

Most neurons do not simply convert inputs into firing rates. Instead, moment-to-moment firing rates reflect interactions between synaptic inputs and intrinsic currents. Few studies investigated how intrinsic currents function together to modulate output discharges and which of the currents attenuated by synthetic cholinergic ligands are actually modulated by endogenous acetylcholine (ACh). In this study we optogenetically stimulated cholinergic fibers in rat neocortex and find that ACh enhances excitability by reducing Ether-à-go-go Related Gene (ERG) K+ current. We find ERG mediates the late phase of spike-frequency adaptation in pyramidal cells and is recruited later than both SK and M currents. Attenuation of ERG during coincident depolarization and ACh release leads to reduced late phase spike-frequency adaptation and persistent firing. In neuronal ensembles, attenuating ERG enhanced signal-to-noise ratios and reduced signal correlation, suggesting that these two hallmarks of cholinergic function in vivo may result from modulation of intrinsic properties.

Hippocampus Retains the Periodicity of Gamma Stimulation In Vivo

2002 ◽  
Vol 88 (5) ◽  
pp. 2349-2354 ◽  
Author(s):  
J. E. Mikkonen ◽  
T. Grönfors ◽  
J. J. Chrobak ◽  
M. Penttonen
Keyword(s):  
Information Acquisition ◽  
Pyramidal Cells ◽  
Gamma Oscillations ◽  
Short Term ◽  
Ca1 Pyramidal Cells ◽  
State Dependent ◽  
Hippocampal Ca1 ◽  
Oscillatory Rhythms ◽  
The Brain

Several behavioral state dependent oscillatory rhythms have been identified in the brain. Of these neuronal rhythms, gamma (20–70 Hz) oscillations are prominent in the activated brain and are associated with various behavioral functions ranging from sensory binding to memory. Hippocampal gamma oscillations represent a widely studied band of frequencies co-occurring with information acquisition. However, induction of specific gamma frequencies within the hippocampal neuronal network has not been satisfactorily established. Using both in vivo intracellular and extracellular recordings from anesthetized rats, we show that hippocampal CA1 pyramidal cells can discharge at frequencies determined by the preceding gamma stimulation, provided that the gamma is introduced in theta cycles, as occurs in vivo. The dynamic short-term alterations in the oscillatory discharge described in this paper may serve as a coding mechanism in cortical neuronal networks.

scholarly journals Reconciling the STDP and BCM Models of Synaptic Plasticity in a Spiking Recurrent Neural Network

2010 ◽  
Vol 22 (8) ◽  
pp. 2059-2085 ◽  
Author(s):  
Daniel Bush ◽  
Andrew Philippides ◽  
Phil Husbands ◽  
Michael O'Shea
Keyword(s):  
Neural Network ◽  
Synaptic Plasticity ◽  
Recurrent Neural Network ◽  
Hebbian Learning ◽  
Spike Timing ◽  
Synaptic Competition ◽  
Firing Rates ◽  
Plasticity Rule ◽  
Asymmetric Learning

Rate-coded Hebbian learning, as characterized by the BCM formulation, is an established computational model of synaptic plasticity. Recently it has been demonstrated that changes in the strength of synapses in vivo can also depend explicitly on the relative timing of pre- and postsynaptic firing. Computational modeling of this spike-timing-dependent plasticity (STDP) has demonstrated that it can provide inherent stability or competition based on local synaptic variables. However, it has also been demonstrated that these properties rely on synaptic weights being either depressed or unchanged by an increase in mean stochastic firing rates, which directly contradicts empirical data. Several analytical studies have addressed this apparent dichotomy and identified conditions under which distinct and disparate STDP rules can be reconciled with rate-coded Hebbian learning. The aim of this research is to verify, unify, and expand on these previous findings by manipulating each element of a standard computational STDP model in turn. This allows us to identify the conditions under which this plasticity rule can replicate experimental data obtained using both rate and temporal stimulation protocols in a spiking recurrent neural network. Our results describe how the relative scale of mean synaptic weights and their dependence on stochastic pre- or postsynaptic firing rates can be manipulated by adjusting the exact profile of the asymmetric learning window and temporal restrictions on spike pair interactions respectively. These findings imply that previously disparate models of rate-coded autoassociative learning and temporally coded heteroassociative learning, mediated by symmetric and asymmetric connections respectively, can be implemented in a single network using a single plasticity rule. However, we also demonstrate that forms of STDP that can be reconciled with rate-coded Hebbian learning do not generate inherent synaptic competition, and thus some additional mechanism is required to guarantee long-term input-output selectivity.

scholarly journals Regional heterogeneity of developing GABAergic interneuron excitation in vivo

2019 ◽  
Author(s):  
Yasunobu Murata ◽  
Matthew T. Colonnese
Keyword(s):  
Synapse Formation ◽  
Critical Role ◽  
Reversal Potential ◽  
Pyramidal Cells ◽  
Gabaergic Neurons ◽  
Network Activity ◽  
Gabaergic Interneuron ◽  
Intact Brain

AbstractGABAergic interneurons are proposed to be critical for early activity and synapse formation by directly exciting, rather than inhibiting, neurons in developing hippocampus and neocortex. However, the role of GABAergic neurons in the generation of neonatal network activity has not been tested in vivo, and recent studies have challenged the excitatory nature of early GABA. By locally manipulating interneuron activity in unanesthetized neonatal mice, we show that GABAergic neurons are indeed excitatory in hippocampus at postnatal-day 3 (P3), and responsible for most of the spontaneous firing of pyramidal cells at that age. Hippocampal interneurons become inhibitory by P7, whereas cortical interneurons are inhibitory at P3 and remain so throughout development. This regional and age heterogeneity is the result of a change in chloride reversal potential as activation of light-gated anion channels expressed in glutamatergic neurons causes firing in hippocampus at P3, but silences it at P7. This study in the intact brain reveals a critical role for GABAergic interneuron excitation in neonatal hippocampus, and a surprising heterogeneity of interneuron function in cortical circuits that was not predicted from in vitro studies.

scholarly journals All-optical electrophysiology reveals brain-state dependent changes in hippocampal subthreshold dynamics and excitability

2018 ◽  
Author(s):  
Yoav Adam ◽  
Jeong J. Kim ◽  
Shan Lou ◽  
Yongxin Zhao ◽  
Daan Brinks ◽  
...  
Keyword(s):  
High Speed ◽  
Near Infrared ◽  
Neuronal Excitability ◽  
Signal To Noise Ratio ◽  
Brain State ◽  
Promising Tool ◽  
State Dependent ◽  
Subthreshold Voltage ◽  
Targeted Gene Expression

AbstractA technology to record membrane potential from multiple neurons, simultaneously, in behaving animals will have a transformative impact on neuroscience research1. Parallel recordings could reveal the subthreshold potentials and intercellular correlations that underlie network behavior2. Paired stimulation and recording can further reveal the input-output properties of individual cells or networks in the context of different brain states3. Genetically encoded voltage indicators are a promising tool for these purposes, but were so far limited to single-cell recordings with marginal signal to noise ratio (SNR) in vivo4-6. We developed improved near infrared voltage indicators, high speed microscopes and targeted gene expression schemes which enabled recordings of supra- and subthreshold voltage dynamics from multiple neurons simultaneously in mouse hippocampus, in vivo. The reporters revealed sub-cellular details of back-propagating action potentials, correlations in sub-threshold voltage between multiple cells, and changes in dynamics associated with transitions from resting to locomotion. In combination with optogenetic stimulation, the reporters revealed brain state-dependent changes in neuronal excitability, reflecting the interplay of excitatory and inhibitory synaptic inputs. These tools open the possibility for detailed explorations of network dynamics in the context of behavior.

scholarly journals The mitochondrial calcium uniporter is crucial for the generation of fast cortical network rhythms

2019 ◽  
Vol 40 (11) ◽  
pp. 2225-2239 ◽  
Author(s):  
Carlos Bas-Orth ◽  
Justus Schneider ◽  
Andrea Lewen ◽  
Jamie McQueen ◽  
Kerstin Hasenpusch-Theil ◽  
...  
Keyword(s):  
Energy Homeostasis ◽  
Pyramidal Cells ◽  
Gamma Oscillations ◽  
Spike Timing ◽  
Mitochondrial Calcium ◽  
Attention And Memory ◽  
Mitochondrial Calcium Uniporter ◽  
Sharp Waves ◽  
Calcium Uniporter

The role of the mitochondrial calcium uniporter (MCU) gene ( Mcu) in cellular energy homeostasis and generation of electrical brain rhythms is widely unknown. We investigated this issue in mice and rats using Mcu-knockout and -knockdown strategies in vivo and in situ and determined the effects of these genetic manipulations on hippocampal gamma oscillations (30–70 Hz) and sharp wave-ripples. These physiological network states require precise neurotransmission between pyramidal cells and inhibitory interneurons, support spike-timing and synaptic plasticity and are associated with perception, attention and memory. Absence of the MCU resulted in (i) gamma oscillations with decreased power (by >40%) and lower synchrony, including less precise neural action potential generation (‘spiking'), (ii) sharp waves with decreased incidence (by about 22%) and decreased fast ripple frequency (by about 3%) and (iii) lack of activity-dependent pyruvate dehydrogenase dephosphorylation. However, compensatory adaptation in gene expression related to mitochondrial function and glucose metabolism was not detected. These data suggest that the neuronal MCU is crucial for the generation of network rhythms, most likely by influences on oxidative phosphorylation and perhaps by controlling cytoplasmic Ca2+ homeostasis. This work contributes to an increased understanding of mitochondrial Ca2+ uptake in cortical information processing underlying cognition and behaviour.

scholarly journals GABAergic interneurons excite neonatal hippocampus in vivo

2020 ◽  
Vol 6 (24) ◽  
pp. eaba1430 ◽  
Author(s):  
Yasunobu Murata ◽  
Matthew T. Colonnese
Keyword(s):  
Visual Cortex ◽  
Synapse Formation ◽  
Reversal Potential ◽  
Pyramidal Cells ◽  
Gabaergic Neurons ◽  
Network Activity ◽  
Gabaergic Interneuron ◽  
Gabaergic Interneurons ◽  
Early Postnatal Development

GABAergic interneurons are proposed to be critical for early activity and synapse formation by directly exciting, rather than inhibiting, neurons in developing hippocampus and neocortex. However, the role of GABAergic neurons in the generation of neonatal network activity has not been tested in vivo, and recent studies have challenged the excitatory nature of early GABA. By locally manipulating interneuron activity in unanesthetized neonatal mice, we show that GABAergic neurons are excitatory in CA1 hippocampus at postnatal day 3 (P3) and are responsible for most of the spontaneous firing of pyramidal cells at that age. Hippocampal interneurons become inhibitory by P7, whereas visual cortex interneurons are already inhibitory by P3 and remain so throughout development. These regional and age-specific differences are the result of a change in chloride reversal potential, because direct activation of light-gated anion channels in glutamatergic neurons drives CA1 firing at P3, but silences it at P7 in CA1, and at all ages in visual cortex. This study in the intact brain reveals that GABAergic interneuron excitation is essential for network activity in neonatal hippocampus and confirms that visual cortical interneurons are inhibitory throughout early postnatal development.

scholarly journals In Vivo Optogenetic Stimulation of Neocortical Excitatory Neurons Drives Brain-State-Dependent Inhibition

2011 ◽  
Vol 21 (19) ◽  
pp. 1593-1602 ◽  
Author(s):  
Celine Mateo ◽  
Michael Avermann ◽  
Luc J. Gentet ◽  
Feng Zhang ◽  
Karl Deisseroth ◽  
...  
Keyword(s):  
Brain State ◽  
Optogenetic Stimulation ◽  
State Dependent ◽  
Excitatory Neurons ◽  
Dependent Inhibition ◽  
Stimulation Of

scholarly journals Sleep slow-wave oscillations trigger seizures in a genetic epilepsy model of Dravet syndrome

2022 ◽  
Author(s):  
Mackenzie A. Catron ◽  
Rachel K. Howe ◽  
Gai-Linn K. Besing ◽  
Emily K. St. John ◽  
Cobie Victoria Potesta ◽  
...  
Keyword(s):  
Slow Wave ◽  
Epileptic Seizures ◽  
Nrem Sleep ◽  
Dravet Syndrome ◽  
Brain State ◽  
Synaptic Potentiation ◽  
Sleep Period ◽  
State Dependent ◽  
Slow Wave Oscillations

Sleep is the brain state when cortical activity decreases and memory consolidates. However, in human epileptic patients, including genetic epileptic seizures such as Dravet syndrome, sleep is the preferential period when epileptic spike-wave discharges (SWDs) appear, with more severe epileptic symptoms in female patients than male patients, which influencing patient sleep quality and memory. Currently, seizure onset mechanisms during sleep period still remain unknown. Our previous work has shown that the sleep-like state-dependent synaptic potentiation mechanism can trigger epileptic SWDs (Zhang et al., 2021). In this study, using one heterozygous (het) knock-in (KI) transgenic mice (GABAA receptor γ2 subunit Gabrg2Q390X mutation) and an optogenetic method, we hypothesized that slow-wave oscillations (SWOs) themselves in vivo could trigger epileptic seizures. We found that epileptic SWDs in het Gabrg2+/Q390X KI mice exhibited preferential incidence during NREM sleep period, accompanied by motor immobility/ facial myoclonus/vibrissal twitching, with more frequent incidence in female het KI mice than male het KI mice. Optogenetic induced SWOs in vivo significantly increased epileptic seizure incidence in het Gabrg2+/Q390X KI mice with increased duration of NREM sleep or quiet-wakeful states. Furthermore, suppression of SWO-related homeostatic synaptic potentiation by 4-(diethylamino)-benzaldehyde (DEAB) injection (i.p.) greatly decreased seizure incidence in het KI mice, suggesting that SWOs did trigger seizure activity in het KI mice. In addition, EEG delta-frequency (0.1-4 Hz) power spectral density during NREM sleep was significantly larger in female het Gabrg2+/Q390X KI mice than male het Gabrg2+/Q390X KI mice, which likely contributes to the gender difference in seizure incidence during NREM sleep/quiet-wake as that in human patients.

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