scholarly journals Cortical rhythms are modulated by respiration

2016 ◽  
Author(s):  
Detlef H. Heck ◽  
Samuel S. McAfee ◽  
Yu Liu ◽  
Abbas Babajani-Feremi ◽  
Roozbeh Rezaie ◽  
...  
Keyword(s):  
Phase Transitions ◽  
Cognitive Processing ◽  
Neuronal Activity ◽  
Cognitive Functions ◽  
Barrel Cortex ◽  
Respiratory Rhythm ◽  
Gamma Oscillations ◽  
Cortical Activity ◽  
Cortical Rhythms ◽  
Wide Range

SummaryThe brain generates oscillatory neuronal activity at a broad range of frequencies and the presence and amplitude of certain oscillations at specific times and in specific brain regions are highly correlated with states of arousal, sleep, and with a wide range of cognitive processes. The neuronal mechanisms underlying the generation of brain rhythms are poorly understood, particularly for low-frequency oscillations. We recently reported that respiration-locked olfactory bulb activity causes delta band (0.5-4 Hz) oscillatory neuronal activity in the whisker sensory (barrel) cortex in mice. Furthermore, gamma oscillations (30 – 100Hz), which are widely implicated in cognitive processing, were power-modulated in synchrony with the respiratory rhythm. These findings link afferent sensory activity caused by respiration directly to cortical rhythms associated with cognitive functions. Here we review the related literature and present new evidence to propose that respiration has a direct influence on oscillatory cortical activity, including gamma oscillations, and on transitions between synchronous and asynchronous cortical network states (marked by phase transitions). Oscillatory cortical activity, as well as phase transitions, has been implicated in cognitive functions, potentially linking respiratory phase to cognitive processing. We further argue that respiratory influence on cortical activity is present in most, and possibly in all areas of the neocortex in mice and humans. We furthermore suggest that respiration had a role in modulating cortical rhythms from early mammalian evolution. Early mammals relied strongly on their olfactory sense and had proportionately large olfactory bulbs. We propose that to this day the respiratory rhythm remains an integral element of dynamic cortical activity in mammals. We argue that breathing modulates all cortical functions, including cognitive and emotional processes, which could elucidate the well-documented but largely unexplained effects of respiratory exercises on mood and cognitive function.

scholarly journals Ethanol and the Developing Brain: Inhibition of Neuronal Activity and Neuroapoptosis

2017 ◽  
Vol 24 (2) ◽  
pp. 130-141 ◽  
Author(s):  
Nailya Lotfullina ◽  
Roustem Khazipov
Keyword(s):  
Nmda Receptors ◽  
Neuronal Activity ◽  
Activity Patterns ◽  
Gamma Oscillations ◽  
Cortical Activity ◽  
Neuronal Firing ◽  
Developing Brain ◽  
Pathophysiological Mechanism ◽  
Intracortical Circuits ◽  
Early Activity

Ethanol induces massive neuroapoptosis in the developing brain. One of the main hypotheses that has been put forward to explain the deleterious actions of ethanol in the immature brain involves an inhibition of neuronal activity. Here, we review recent evidence for this hypothesis obtained in the somatosensory cortex and hippocampus of neonatal rodents. In both structures, ethanol strongly inhibits brain activity. At the doses inducing massive neuroapoptosis, ethanol completely suppresses the early activity patterns of spindle-bursts and gamma oscillations in the neocortex and the early sharp-waves in the hippocampus. The inhibitory effects of ethanol decrease with age and in adult animals, ethanol only mildly depresses neuronal firing and induces delta-wave activity. Suppression of cortical activity in neonatal animals likely involves inhibition of the myoclonic twitches, an important physiological trigger for the early activity bursts, and inhibition of the thalamocortical and intracortical circuits through a potentiation of GABAergic transmission and an inhibition of N-methyl-d-aspartate (NMDA) receptors, that is in keeping with the neuroapoptotic effects of other agents acting on GABA and NMDA receptors. These findings provide support for the hypothesis that the ethanol-induced inhibition of cortical activity is an important pathophysiological mechanism underlying massive neuroapoptosis induced by ethanol in the developing brain.

scholarly journals Basal forebrain gating by somatostatin neurons drives cortical activity

2017 ◽  
Author(s):  
Nelson Espinosa ◽  
Alejandra Alonso ◽  
Cristian Morales ◽  
Pablo Fuentealba
Keyword(s):  
Cognitive Processing ◽  
Basal Forebrain ◽  
Cell Types ◽  
Gamma Oscillations ◽  
Cortical Activity ◽  
Somatostatin Cells ◽  
Behavioral Evidence ◽  
Somatostatin Neurons ◽  
And Behavior

AbstractThe basal forebrain provides modulatory input to the cortex regulating brain states and cognitive processing. Somatostatin-expressing cells constitute a local GABAergic source known to functionally inhibit the major cortically-projecting cell types. However, it remains unclear if somatostatin cells can regulate the basal forebrain’s synaptic output and thus control cortical dynamics. Here, we demonstrate in mice that somatostatin neurons regulate the corticopetal synaptic output of the basal forebrain impinging on cortical activity and behavior. Optogenetic inactivation of somatostatin neurons in vivo increased spiking of some basal forebrain cells, rapidly enhancing and desynchronizing neural activity in the prefrontal cortex, inhibiting slow rhythms and increasing gamma oscillations. Locomotor activity was specifically increased in quiescent animals, but not in active mice. Altogether, we provide physiological and behavioral evidence indicating that somatostatin cells are pivotal in gating the synaptic output of the basal forebrain, thus indirectly controlling cortical operations via both cholinergic and non-cholinergic mechanisms.

scholarly journals Cortical regulation of dopaminergic neurons: role of the midbrain superior colliculus

2014 ◽  
Vol 111 (4) ◽  
pp. 755-767 ◽  
Author(s):  
C. Bertram ◽  
L. Dahan ◽  
L. W. Boorman ◽  
S. Harris ◽  
N. Vautrelle ◽  
...  
Keyword(s):  
Superior Colliculus ◽  
Neuronal Activity ◽  
Dopaminergic Neurons ◽  
Barrel Cortex ◽  
Sensory Information ◽  
Complex Stimulus ◽  
Stimulus Properties ◽  
Pulse Trains ◽  
Wide Range

Dopaminergic (DA) neurons respond to stimuli in a wide range of modalities, although the origin of the afferent sensory signals has only recently begun to emerge. In the case of vision, an important source of short-latency sensory information seems to be the midbrain superior colliculus (SC). However, longer-latency responses have been identified that are less compatible with the primitive perceptual capacities of the colliculus. Rather, they seem more in keeping with the processing capabilities of the cortex. Given that there are robust projections from the cortex to the SC, we examined whether cortical information could reach DA neurons via a relay in the colliculus. The somatosensory barrel cortex was stimulated electrically in the anesthetized rat with either single pulses or pulse trains. Although single pulses produced small phasic activations in the colliculus, they did not elicit responses in the majority of DA neurons. However, after disinhibitory intracollicular injections of the GABAA antagonist bicuculline, collicular responses were substantially enhanced and previously unresponsive DA neurons now exhibited phasic excitations or inhibitions. Pulse trains applied to the cortex led to phasic changes (excitations to inhibitions) in the activity of DA neurons at baseline. These were blocked or attenuated by intracollicular administration of the GABAA agonist muscimol. Taken together, the results indicate that the cortex can communicate with DA neurons via a relay in the SC. As a consequence, DA neuronal activity reflecting the unexpected occurrence of salient events and that signaling more complex stimulus properties may have a common origin.

scholarly journals Effects of optogenetic stimulation of basal forebrain parvalbumin neurons on Alzheimer’s disease pathology

2020 ◽  
Author(s):  
Caroline A Wilson ◽  
Sarah Fouda ◽  
Shuzo Sakata
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Activity ◽  
Cognitive Functions ◽  
Basal Forebrain ◽  
Gamma Oscillations ◽  
Cortical Region ◽  
Amyloid Burden ◽  
Sensory Stimuli ◽  
40 Hz

AbstractNeuronal activity can modify Alzheimer’s disease pathology. Although overexcitation of neurons can facilitate disease progression, the induction of cortical gamma oscillations can reduce amyloid load and improve cognitive functions in mouse models. These beneficial effects of gamma oscillations can be caused by either optogenetic activation of cortical parvalbumin-positive (PV+) neurons or 40 Hz repetitive sensory stimuli. However, given the fact that cortical gamma oscillations can be induced by multiple mechanisms, it is still unclear whether other approaches to induce gamma oscillations can also be beneficial. Here we show that optogenetic activation of PV+ neurons in the basal forebrain (BF) increases amyloid burden, rather than reducing it. We applied 40 Hz optical stimulation in the BF of 5xFAD mice by expressing channelrhodopsin-2 (ChR2) in PV+ neurons. After one-hour induction of cortical gamma oscillations over three days, we observed the increase in the concentration of amyloid-β42 in the frontal cortical region, but not amyloid-β40. The density of amyloid plaques also increased in the medial prefrontal cortex and the septal nuclei, both of which are targets of BF PV+ neurons. These results suggest that effects of cortical gamma oscillations on Alzheimer’s disease pathology can be bidirectional depending on their induction mechanisms.Significance StatementAlzheimer’s disease (AD) is the most common cause of dementia. Although numerous molecular targets have been identified, the development of treatment is still a challenge. Accumulating evidence shows that artificial control of neuronal activity can modify AD pathology. In particular, the induction of cortical gamma (~40 Hz) oscillations can ameliorate AD pathology and improve cognitive functions. Here we show that optogenetic activation of parvalbumin-positive (PV+) neurons in the basal forebrain (BF) has opposite effects. By expressing channelrhodopsin-2 (ChR2) in PV+ neurons of an AD mouse model and optically stimulating BF PV+ neurons, we induced gamma oscillations and found increased amyloid burden. These results imply that AD pathology can be modified bidirectionally depending on induction mechanisms of gamma oscillations.

scholarly journals CA2 neuronal activity controls hippocampal low gamma and ripple oscillations

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Georgia M Alexander ◽  
Logan Y Brown ◽  
Shannon Farris ◽  
Daniel Lustberg ◽  
Caroline Pantazis ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Cognitive Functions ◽  
Social Memory ◽  
Experimental System ◽  
Gamma Oscillations ◽  
Neuronal Populations ◽  
Prefrontal Cortical ◽  
Network Oscillations ◽  
Hippocampal Area

Hippocampal oscillations arise from coordinated activity among distinct populations of neurons and are associated with cognitive functions. Much progress has been made toward identifying the contribution of specific neuronal populations in hippocampal oscillations, but less is known about the role of hippocampal area CA2, which is thought to support social memory. Furthermore, the little evidence on the role of CA2 in oscillations has yielded conflicting conclusions. Therefore, we sought to identify the contribution of CA2 to oscillations using a controlled experimental system. We used excitatory and inhibitory DREADDs to manipulate CA2 neuronal activity and studied resulting hippocampal-prefrontal cortical network oscillations. We found that modification of CA2 activity bidirectionally regulated hippocampal and prefrontal cortical low-gamma oscillations and inversely modulated hippocampal ripple oscillations in mice. These findings support a role for CA2 in low-gamma generation and ripple modulation within the hippocampus and underscore the importance of CA2 in extrahippocampal oscillations.

Models of Respiratory Rhythm Generation in the Pre-Bötzinger Complex. I. Bursting Pacemaker Neurons

1999 ◽  
Vol 82 (1) ◽  
pp. 382-397 ◽  
Author(s):  
Robert J. Butera ◽  
John Rinzel ◽  
Jeffrey C. Smith
Keyword(s):  
Membrane Potential ◽  
Respiratory Rhythm ◽  
Rhythm Generation ◽  
Minimal Models ◽  
Dynamic Features ◽  
Bursting Neurons ◽  
Wide Range ◽  
Bötzinger Complex ◽  
Voltage Dependent ◽  
Respiratory Rhythm Generation

A network of oscillatory bursting neurons with excitatory coupling is hypothesized to define the primary kernel for respiratory rhythm generation in the pre-Bötzinger complex (pre-BötC) in mammals. Two minimal models of these neurons are proposed. In model 1, bursting arises via fast activation and slow inactivation of a persistent Na+ current I NaP-h. In model 2, bursting arises via a fast-activating persistent Na+ current INaP and slow activation of a K+ current IKS. In both models, action potentials are generated via fast Na+ and K+currents. The two models have few differences in parameters to facilitate a rigorous comparison of the two different burst-generating mechanisms. Both models are consistent with many of the dynamic features of electrophysiological recordings from pre-BötC oscillatory bursting neurons in vitro, including voltage-dependent activity modes (silence, bursting, and beating), a voltage-dependent burst frequency that can vary from 0.05 to >1 Hz, and a decaying spike frequency during bursting. These results are robust and persist across a wide range of parameter values for both models. However, the dynamics of model 1 are more consistent with experimental data in that the burst duration decreases as the baseline membrane potential is depolarized and the model has a relatively flat membrane potential trajectory during the interburst interval. We propose several experimental tests to demonstrate the validity of either model and to differentiate between the two mechanisms.

Attenuation of the Early Gamma Oscillations During the Sensory-Evoked Response in the Neonatal Rat Barrel Cortex

2016 ◽  
Vol 6 (4) ◽  
pp. 575-577 ◽  
Author(s):  
Dmitrii Suchkov ◽  
Mikhail Sintsov ◽  
Lyailya Sharipzyanova ◽  
Roustem Khazipov ◽  
Marat Minlebaev
Keyword(s):  
Barrel Cortex ◽  
Gamma Oscillations ◽  
Evoked Response ◽  
Neonatal Rat ◽  
Sensory Evoked

scholarly journals Theta activity paradoxically boosts gamma and ripple frequency sensitivity in prefrontal interneurons

2021 ◽  
Vol 118 (51) ◽  
pp. e2114549118
Author(s):  
Ricardo Martins Merino ◽  
Carolina Leon-Pinzon ◽  
Walter Stühmer ◽  
Martin Möck ◽  
Jochen F. Staiger ◽  
...  
Keyword(s):  
Low Frequency ◽  
Gamma Oscillations ◽  
Brain State ◽  
Gabaergic Interneurons ◽  
Time Resolved ◽  
Cortical Rhythms ◽  
Brain States ◽  
Fast Spiking ◽  
Fast Oscillations ◽  
Cross Frequency Coupling

Fast oscillations in cortical circuits critically depend on GABAergic interneurons. Which interneuron types and populations can drive different cortical rhythms, however, remains unresolved and may depend on brain state. Here, we measured the sensitivity of different GABAergic interneurons in prefrontal cortex under conditions mimicking distinct brain states. While fast-spiking neurons always exhibited a wide bandwidth of around 400 Hz, the response properties of spike-frequency adapting interneurons switched with the background input’s statistics. Slowly fluctuating background activity, as typical for sleep or quiet wakefulness, dramatically boosted the neurons’ sensitivity to gamma and ripple frequencies. We developed a time-resolved dynamic gain analysis and revealed rapid sensitivity modulations that enable neurons to periodically boost gamma oscillations and ripples during specific phases of ongoing low-frequency oscillations. This mechanism predicts these prefrontal interneurons to be exquisitely sensitive to high-frequency ripples, especially during brain states characterized by slow rhythms, and to contribute substantially to theta-gamma cross-frequency coupling.

scholarly journals Robust Rhythmogenesis in the Gamma Band via Spike Timing Dependent Plasticity

2020 ◽  
Author(s):  
Gabi Socolovsky ◽  
Maoz Shamir
Keyword(s):  
Mean Field ◽  
Rhythmic Activity ◽  
Gamma Oscillations ◽  
Underlying Mechanism ◽  
Spike Timing ◽  
Gamma Band ◽  
Fine Tuning ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Wide Range

Rhythmic activity in the gamma band (30-100Hz) has been observed in numerous animal species ranging from insects to humans, and in relation to a wide range of cognitive tasks. Various experimental and theoretical studies have investigated this rhythmic activity. The theoretical efforts have mainly been focused on the neuronal dynamics, under the assumption that network connectivity satisfies certain fine-tuning conditions required to generate gamma oscillations. However, it remains unclear how this fine tuning is achieved.Here we investigated the hypothesis that spike timing dependent plasticity (STDP) can provide the underlying mechanism for tuning synaptic connectivity to generate rhythmic activity in the gamma band. We addressed this question in a modeling study. We examined STDP dynamics in the framework of a network of excitatory and inhibitory neuronal populations that has been suggested to underlie the generation of gamma. Mean field Fokker Planck equations for the synaptic weights dynamics are derived in the limit of slow learning. We drew on this approximation to determine which types of STDP rules drive the system to exhibit gamma oscillations, and demonstrate how the parameters that characterize the plasticity rule govern the rhythmic activity. Finally, we propose a novel mechanism that can ensure the robustness of self-developing processes, in general and for rhythmogenesis in particular.

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