Types Of Oscillatory Activities Research Articles

Optical recording of oscillatory activity in the absence of external Ca2+ in the embryonic chick olfactory bulb

We applied 464/1020-site optical recording systems with a voltage-sensitive dye (NK2761) to the embryonic chick olfactory system and detected oscillatory activity in the olfactory bulb (OB) in the absence of synaptic transmission. In embryonic day 8–10 (E8-E10) chick olfactory nerve (N.I)-OB-forebrain preparations, the removal of Ca2+ from the external solution completely blocked the glutamatergic excitatory postsynaptic potential (EPSP) from the N.I to the OB as well as oscillations following the EPSP. However, a novel type of oscillatory activity was detected in the OB with the long-term perfusion of a Ca2+-free solution. The characteristics of oscillatory activity in the Ca2+-free solution differed from those in normal physiological solution. The present results suggest the existence of a neural communication system in the absence of synaptic transmission at the early stage of embryonic development.

Shortest Loops are Pacemakers in Random Networks of Electrically Coupled Axons

High-frequency oscillations (HFOs) are an important part of brain activity in health and disease. However, their origins remain obscure and controversial. One possible mechanism depends on the presence of sparsely distributed gap junctions that electrically couple the axons of principal cells. A plexus of electrically coupled axons is modeled as a random network with bi-directional connections between its nodes. Under certain conditions the network can demonstrate one of two types of oscillatory activity. Type I oscillations (100–200 Hz) are predicted to be caused by spontaneously spiking axons in a network with strong (high conductance) gap junctions. Type II oscillations (200–300 Hz) require no spontaneous spiking and relatively weak (low-conductance) gap junctions, across which spike propagation failures occur. The type II oscillations are reentrant and self-sustained. Here we examine what determines the frequency of type II oscillations. Using simulations we show that the distribution of loop lengths is the key factor for determining frequency in type II network oscillations. We first analyze spike failure between two electrically coupled cells using a model of anatomically reconstructed CA1 pyramidal neuron. Then network oscillations are studied by a cellular automaton model with random network connectivity, in which we control loop statistics. We show that oscillation periods can be predicted from the network’s loop statistics. The shortest loop, around which a spike can travel, is the most likely pacemaker candidate. The principle of one loop as a pacemaker is remarkable, because random networks contain a large number of loops juxtaposed and superimposed, and their number rapidly grows with network size. This principle allows us to predict the frequency of oscillations from network connectivity and visa versa. We finally propose that type I oscillations may correspond to ripples, while type II oscillations correspond to so-called fast ripples.

Consciousness and arousal effects on emotional face processing as revealed by brain oscillations. A gamma band analysis

It remains an open question whether it is possible to assign a single brain operation or psychological function for facial emotion decoding to a certain type of oscillatory activity. Gamma band activity (GBA) offers an adequate tool for studying cortical activation patterns during emotional face information processing. In the present study brain oscillations were analyzed in response to facial expression of emotions. Specifically, GBA modulation was measured when twenty subjects looked at emotional (angry, fearful, happy, and sad faces) or neutral faces in two different conditions: supraliminal (10 ms) vs subliminal (150 ms) stimulation (100 target-mask pairs for each condition). The results showed that both consciousness and significance of the stimulus in terms of arousal can modulate the power synchronization (ERD decrease) during 150–350 time range: an early oscillatory event showed its peak at about 200 ms post-stimulus. GBA was enhanced by supraliminal more than subliminal elaboration, as well as more by high arousal (anger and fear) than low arousal (happiness and sadness) emotions. Finally a left-posterior dominance for conscious elaboration was found, whereas right hemisphere was discriminant in emotional processing of face in comparison with neutral face.

Neuronal mechanisms of the anoxia-induced network oscillations in the rat hippocampus in vitro.

1. A spindle of fast network oscillations precedes the ischaemia-induced rapid depolarisation in the rat hippocampus in vivo. However, this oscillatory pattern could not be reproduced in slices and the underlying mechanisms remain poorly understood. We have found that anoxia-induced network oscillations (ANOs, 20-40 Hz, lasting for 1-2 min) can be reproduced in the intact hippocampi of postnatal day P7-10 rats in vitro, and we have examined the underlying mechanisms using whole-cell and extracellular field potential recordings in a CA3 pyramidal layer. 2. ANOs were generated at the beginning of the anoxic depolarisation, when pyramidal cells depolarised to subthreshold values. Maximal power of the ANOs was attained when pyramidal cells depolarised to -56 mV; depolarisation above -47 mV resulted in a depolarisation block of pyramidal cells and a waning of ANOs. 3. A multiple unit activity in extracellular field recordings was phase locked to the negative and ascending phases of ANOs. Pyramidal cells recorded in current-clamp mode generated action potentials with an average probability of about 0.05 per cycle. The AMPA receptor-mediated EPSCs and the GABA receptor-mediated IPSCs in CA3 pyramidal cells were also phase locked with ANOs. 4. ANOs were prevented by tetrodotoxin and glutamate receptor antagonists CNQX and APV, and were slowed down by the allosteric GABA(A) receptor modulator diazepam. In the presence of the GABA(A) receptor antagonist bicuculline, ANOs were transformed to epileptiform discharges. 5. In the presence of the A1 adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), the anoxia induced an epileptiform activity and no ANOs were observed. 6. In normoxic conditions, a rise of extracellular potassium to 10 mM induced an epileptiform activity. Increasing extracellular potassium in conjunction with a bath application of the adenosine A1 receptor agonist cyclopentyladenosine induced oscillations similar to ANOs. 7. Multisite recordings along the septo-temporal hippocampal axis revealed that ANOs and anoxic depolarisation originate in the temporal part, and propagate towards the septal pole at a speed of 1.9 mm x min(-1). 8. ANOs were observed starting from P7, i.e. at a developmental stage when the effects of GABA change from depolarisation to hyperpolarisation. 9. These results suggest that the synchronisation of anoxia-induced oscillations relies on synaptic mechanisms; that the inhibition by GABA and adenosine sets the tune for a generation of oscillations and prevents an epileptiform activity; and that a synchronous GABAergic inhibition is instrumental in a phase locking neuronal activity similarly to other types of oscillatory activities in the gamma frequency range.

Two types of intrinsic oscillations in neurons of the lateral and basolateral nuclei of the amygdala.

Intracellular recordings in the guinea pig and cat basolateral amygdaloid (BL) complex maintained as slices in vitro revealed that a subpopulation of neurons (79%) in the lateral (AL) and basolateral (ABl) nuclei generated two types of slow oscillations of the membrane potential upon steady depolarization from resting potential. The cells were of a stellate or pyramidal-like shape and possessed spiny dendrites and an axon leaving the local synaptic environment, and thus presumably represented projection neurons. Similar oscillatory activity was observed in projection neurons of the cat AL nucleus recorded in vivo. Oscillatory activity with a low threshold of activation (low-threshold oscillation, LTO) appeared as rhythmic deflections (amplitudes, 2-6 mV) of the membrane potential positive to -60 mV. Fast Fourier transformation (FFT) demonstrated a range of frequencies of LTOs between 0.5 and 9 Hz, with >80% occurring at 1-3.5 Hz and an average at 2.3 +/- 1.1 Hz. LTOs were more regular after pharmacological blockade of synaptic transmission and were blocked by tetrodotoxin (TTX). Blockade of LTOs and Na+ spikes revealed a second type of oscillatory activity (high-threshold oscillation, HTO) at depolarizations beyond -40 mV, which was capable of triggering high-threshold spikes. HTOs ranged between 1 and 7.5 Hz, with >80% occurring at 2-6 Hz and an average at 5.8 +/- 1.1 Hz. HTOs vanished at a steady membrane polarization positive to -20 mV. Current versus voltage relations obtained under voltage-clamp conditions revealed two regions of negative slope conductance at -55 to -40 mV and at around -30 mV, which largely overlapped with the voltage ranges of LTOs and HTOs. TTX abolished the first region of negative slope conductance (-55 to -40 mV) and did not significantly influence the second region of negative slope conductance. Neuronal responses to maintained depolarizing current pulses consisted of an initial high-frequency discharge (up to 100 Hz), the frequency of which depended on the amplitude of the depolarizing current pulse, followed by a progressive decline ("adaptation") toward a slow-rhythmic firing pattern. The decay in firing frequency followed a double-exponential function, with time constants averaging 57 +/- 28 ms and 3.29 +/- 1.85 s, and approached steady-state frequencies at 6.3 +/- 2.9 Hz (n = 17). Slow-rhythmic firing remained at this frequency over a wide range of membrane polarization between approximately -50 and -20 mV, although individual electrogenic events changed from Na+ spikes and underlying LTOs to high-threshold spikes and underlying HTOs. Rhythmic regular firing was only interrupted at an intermediate range of membrane polarization by the occurrence of spike doublets. In conclusion, the integrative behavior of a class of neurons in the BL complex appears to be largely shaped by the slow-oscillatory properties of the membrane. While LTOs are likely to synchronize synaptic signals near firing threshold, HTOs are a major determinant for the slow steady-state firing patterns during maintained depolarizing influence. These intrinsic oscillatory mechanisms, in turn, can be assumed to promote population activity at this particular frequency, which ranges well within that of the limbic theta (Theta) rhythm and the delta (delta) waves in the electroencephalogram during slow-wave sleep.