<p>Theories of how EEG arises and propagates itself are still evolving. The EEG at the surface of the cortex reflects the summated activity of ensembles of cells in the form of extracellular current flow. This summated activity is due apparently to synchronously
    activated postsynaptic potentials from vertically oriented pyramidal cells. Thus, the production of Local Field Potentials (LFPs) is what is picked up by the electroencephalograh (i.e. amplifier), and LFPs are observed only as radially-oriented (i.e.
    right-angle) dendrites excitatory action potentials summate in the cortical gyri and sulci.&nbsp;</p>
<p style="text-align: center;"><img src="@@PLUGINFILE@@/axon-potential.png" alt="Figure xx: Action potential occurring along an axon" width="625" height="406" class="img-responsive atto_image_button_middle"><br></p>
<p style="text-align: center;"><span style="font-size: 1rem;">Figure 1: Action potential occurring along an axon</span></p><p style="text-align: center;"><span style="font-size: 1rem;"><p style="text-align: left;"><br></p><p style="text-align: left;">Figuree 2: Purkinje Cell</p><p style="text-align: left;"><img src="@@PLUGINFILE@@/Purkinje%20Cell.jpg" alt="Purkinje Cell" width="459" height="428" class="img-responsive atto_image_button_left">The cerebellum is uniquely difficult to get EEG source from due to the complexity of its folds and the orientation of the neurons:&nbsp;&nbsp;the human cerebellum is more tightly folded than the neocortex with individual folia being 1–2 mm wide (Braitenberg &amp; Atwood,&nbsp;<a href="https://onlinelibrary.wiley.com/doi/full/10.1002/hbm.24951#hbm24951-bib-0005" id="hbm24951-bib-0005R" data-tab="pane-pcw-references">1958</a>)&nbsp; creating difficulty due to convolution.&nbsp; Furthermore, a good portion of the cerebellum is made of Purkinje cells, which&nbsp;are GABAergic inhibitory projection neurons. Their large somata are located in the&nbsp;<b>Purkinje cell layer</b>&nbsp;(PCL) in the adult cerebellum, and aligned like dominos stacked one in front of the other.&nbsp;</p><p style="text-align: left;"><br></p></span></p>
<p>What we see in the EEG is limited to measuring what is occurring at the cortical excitatory pyramidal neurons, which make up about 80% of the human cortex (or 80 billion of the 100 billion). The high density clustering these excitatory pyramidal neurons’
    synapses create high density network nodes, or hubs in the brain, which serve as metaphorical substations for the relay of energy across functional networks in the brain (Hagmann et al., 2008; He et al., 2008). The actions of inhibitory neurons is
    not visible in the EEG, however, inhibitory neurons serve to hyperpolarize action potentials of pyramidal neurons into in-phase and anti-phase dynamics. And balancing of opposing forces, such as excitation and inhibition, often gives rise to rhythmic
    behavior. The mean time difference between&nbsp; the discharges of any two pairs of cells is zero; that is, interneurons discharge synchronously at approximately the same time. And neurons in the inhibitory network will be inhibited at the same time
    and fire simultaneously after inhibition wears off. Discharge and silence will alternate in all parts of the network synchronously (Buszaki, p. 75). On average, all neurons will fire at zero lag time and will be silenced at the same time (p. 76).
    Oscillator networks made from homogenous inhibitory neurons can have a large deteriorating effect on subsequent synchronous discharge of the neurons. This may explain why gamma-frequency oscillations are typically short-lasting, transient events (Buszaki,
    p. 76)</p>
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<p>GABAergic inhibitory neurons can aid to synchronize neurons in a coordinated manner (into cross-frequency phase shift and phase lock) by shifting the membrane potentials of pyramidal neurons.</p>
<p style="text-align: center;"><img src="@@PLUGINFILE@@/pyramidal-neurons.png" alt="Figure xx: Pyramidal Neurons" width="625" height="350" class="img-responsive atto_image_button_middle"><br></p>
<p style="text-align: center;"><span style="font-size: 1rem;">Figure 3: Pyramidal Neurons</span></p>
<p>According to Duffy (1989), excitatory neurotransmitters evoke an electrical change in the excitatory postsynaptic membrane potentials (EPSP), depolarizing the post synaptic membrane and leading eventually to an action potential, while inhibitory neurotransmitters
    result in increased negative charge inside the cell membrane known as the inhibitory postsynaptic potential (IPSP) that hyperpolarizes the cell membrane and inhibits depolarization. Excitatory post synaptic potentials move positive ions (sodium, calcium
    and potassium) down axons and inhibitory post synaptic potentials move negative ions (chlorine) down axons. When recording an EEG, 50% of the data arriving at the site of the electrode is from neurons directly underneath it, and 95% of the data comes
    from within 6 centimeters distance (that’s a circle with a diameter of 2 1/3 inches—big).&nbsp;</p>
<p><span style=""></span></p>
<p>There are two types of connections between synapses: electrical and chemical synapses. Electrical synapses produce very short and high-speed communication (200 nsec to a few msec), which are too short to be measured at the scalp surface, due to filtering
    properties of the skull. However, chemical synapses, which are responsible for the swap of neurotransmitters (small molecules) and neuromodulators (large molecules), produce short duration electrical potentials of 100msec to seconds, which are readable
    via EEG (1 to 300Hz with intra-cerebral electrodes and 1 – 50Hz with scalp electrodes) (Buzsaki, 2006).&nbsp;&nbsp;<span style="font-size: 1rem;">There are “fast synapses” and “slow synapses”. Fast synapses encompass 90% of excitatory synapses, which are modulated with the neurotransmitter glutamate, and 90% of inhibitory synapses, which are modulated by the neurotransmitter GABA. Slow synapses encompass the other 20% are long duration synaptic potentials that last for 100 msec to 1 sec and are modulated by dopamine, acetycholine, serotonin, norepinephrine and histamine (these molecules are within a sub-class of neurotransmitters, called neuromodulators, due to the lack of re-uptake mechanism) (Thatcher, 2012). Fast synapses&nbsp; oscillate at 0 – 80msec and slow synapses oscillate at 100 msec – 1 second), thus the frequencies of 0-80 msec (12.5+ Hz) are ruled by the gaba/glutamate allostasis and the frequencies of 10Hz (100 msec to 1 sec) and under are ruled by the slow synaptic neuromodulators. The frequencies of 10 – 12.5Hz are a blend of fast and slow synapses. If you brain is not producing noephinephrine, your alpha is likely too slow and if you have too much GABA, your alpha is likely too fast.&nbsp;</span></p>