The source of action potential in the heart is the pacemaker cells of SA node. But, I am asking about the pacemaker cells in the brain (cerebrum), as in, what is the first cell that switches-on brain circuits?
We have many circuits and several thousands of action potentials all the time in the brain, but the brain do not have ONE pacemarker. Even, we have to put clear that many neurons in the brain, having action potentials at the same time could be a patological state, like an epileptic event.
However, some nucleus have some characteristic of pacemarkers in several parts of the brain, maybe the inferior olive is the most famous, but is not the only one. But take care, the brain does not have ONE pacemarker, if the brain have some similar, they are several nucleus coordinating involved in different circuits, but these nucleus are functionally very different than the pacemarkers of the heart.
Have a look in:
Buzsáki, G. Rhythms of the Brain. Oxford University Press (2006)
Llinás, R. I of the Vortex: From Neurons to Self (MIT Press, Cambridge, MA. 2001).
We have many circuits and several thousands of action potentials all the time in the brain, but the brain do not have ONE pacemarker. Even, we have to put clear that many neurons in the brain, having action potentials at the same time could be a patological state, like an epileptic event.
However, some nucleus have some characteristic of pacemarkers in several parts of the brain, maybe the inferior olive is the most famous, but is not the only one. But take care, the brain does not have ONE pacemarker, if the brain have some similar, they are several nucleus coordinating involved in different circuits, but these nucleus are functionally very different than the pacemarkers of the heart.
Have a look in:
Buzsáki, G. Rhythms of the Brain. Oxford University Press (2006)
Llinás, R. I of the Vortex: From Neurons to Self (MIT Press, Cambridge, MA. 2001).
In addition to above explanation, please note that there are spontaneous release of neurotransmitters, almost in all of the synapses in the brain. If you apply TTX and block all of the action potentials, you can record the synaptic response to these kind of spontaneous release of neurotransmitters, called "Miniature post synaptic potentials". (mPSP). These mPSPs may be excitatory of (MEPSP) or inhibitory (mIPSP). In the post synaptic neurons, these mPSPs integrated and will result to either excitation or inhibition of neuron. Therefore, mPSPs are a good index of neuronal excitability. In some brain areas this excitability is very high, so that in normal situation (without application of TTX) you can record spontaneous action potentials, even if you cut all of the inputs to these areas. Having spontaneous action potential is a characteristic of most of brain neurons. It is somehow difficult to find a neuron without spontaneous activity for a long time.
It must also be noted that some brain areas have important role in producing some rhythmic activities. For example, some hippocampal neurons are involved in producing theta rhythms, or some brain stem nuclei are involved in producing the respiratory rhythms.
Therefore, you can not compare the activity of neurons with that of cardiac muscle cells.
Hello, some neuronal cell could generate spontaneously an AP without receiving synaptic inputs but due to the intrisic exitability mechanismes such as voltage gated ion channels. Neuron is an excitable cell, its excitation is not problematic hovewer inhibition is.
Pacemakers in the brain could be several: for example one possibility is the stimulus i.e. a physical variation in the environment. This could be the cause for generate a sensory-motor transformation to execute for example a movement (e.g. I see a cup of coffe and I program an arm movement to get it). On the other hand another pacemaker could be an intrinsic need of water, or food, which could be another stimulus to activate a sensory-motor transformation to execute another action (e.g. find and take a glass of water).
In the brainstem, numerous studies suggest that preBötzinger complex neurons have bursting pacemaker properties. Actually the preBötzinger Complex is considered as the main site of respiratory rythmogenesis. and some authors believe that this area is the kernel for respiratory rythmogenesis.
The circadian rhythm is generated by pacemakers. The preBotzinger complex contains pacemaker cells, at least in newborn mammals. The sources of action potentials in the brain are sensory neurons (for example, chemosensitive cells in medulla that generate action potentials in response to elevated concentration of carbon dioxide).
The most important thing to note is that heart is a single muscle, and all the muscle fibres constituting the two atria contract almost simultaneously and after a delay, both ventricles (or their muscle fibres) contract simultaneously. This is a periodic event (or quasi periodic, really), which activity is started by an oscillator, i.e. the sino atrial node or more commonly known as the natural cardiac pacemaker.
However, the brain has innumerable, functionally distinct parts and there is no periodic activity anywhere. At any time, there are multiple activities going on inside the 20-odd billion neurons that make up the brain, and it is a complex circuitry. Some of them are triggered by external stimuli reaching the brain through peripheral nerves and many of them also are triggered or inhibited by other neurons, all in the brain.
There are broadly speaking 2 sources of AP for neurons: above-treshold input (sensory stimuly or synchronous neurotransmitter release from presynaptic terminals) or intrinsic action potential generation from the neuron itself. The second can happen due to the balance of ions and channels on the neuron (generally called pacemaker neurons... Purkinje cells, Substantia nigra etc...), but it can also be activated or inactivated by the surrounding environment: neuromodulators that shift the membrane potential of the neuron in or out a window of a voltage that allows the neuron to fire "like" a pacemaker.
There is not a general on or off mode in the brain. Many neurons fire always, some fire upon sensory stimulus and some fire upon modulation by environmental factors like stress or sleep deprivation. A lot of the coding is not based on the firing but on the timing, regularity and balance between circuits of firing neurons. Some part of the brain have very complex switches that are poorly understood, for instance there are many ways in which glial cells (eg, astrocytes) can modulate the neuronal activity. Even when you sleep your brain is working and producing wave of activity (action potentials). Essentially the brain never stops from the moment it starts to form to the moment you are dead. If you think about it in a "computer" analogy, think of a machine which is always on and running house-keeping routines, I you turn it of there is no more start button. You are dead.
Somehow this comparison between SA node pacemaker and the brain felt to me a bit like asking: " When I push the "start" button my computer starts... now where is the "on" switch of the whole Internet?"
Your question sounds a bit funny to Neuro-workers. You see how much information you have generated with the answers. The way it is posed has a simple answer, see Marco Lanzilotto's, that's a good one. The brain is not a heart. APs in the heart have a totally different function than in the muscle or the brain. In the brain, APs are bits of coded information from outside world and our own body. Thus, the more parsimonious answer to your question as it stands, is that the APs in the brain are initiated by transduction of different types of energy (chemical, luminance, mechanical, etc) in sensory organs to electrochemical energy in neurons. Considering this, you may imagine how many different stimuli can initiate APs.
The action potentials in the brain have many sources...Many come from sensory neurons (retina, muscle stretch, skin, ears, etc.). Others come from neurons giving signals to move a particular muscle in the body. However, many more action potentials come from the brain's continuous flow of information between neurons. For example, during slow-wave (deep) sleep, millions of neurons all over the neocortex are active and fire action potentials in synchrony at a rhythmic pace of about one cycle every two seconds. Therefore, at any one time, whether awake or asleep, there are literally HUNDREDS OF MILLIONS of action potentials carrying information from one place to another within the brain.
Current ideas in computational neuroscience regarding (ISI, STDP http://en.wikipedia.org/wiki/Spike-timing-dependent_plasticity) are just extensions of Adrian’s model (firing rate, 1914 http://en.wikipedia.org/wiki/Edgar_Adrian,_1st_Baron_Adrian).
At this point, you'll understand that the mainstream in computational neuroscience preserves a dogma older than the Turing's paradigm (1936) . Taken from this perspective one may explain why the neurological basis for category formation and many other processes are missing and possibly inaccurately described.
The brain as a whole has its own activity beyond neurons and glia cells. Which is the oscillation. This oscillation of local field potentials as well as cortical potentials along will trigger spontaneous transmitter release and, in some cases, action potentials. So, you don't really need the 'first cell' to trigger the activity of the whole brain activity. Just like when we talk about a living human, we do not ask him which of his 50 trillion cells are the one that switched on his life. There is actually none such thing. A human being is alive not because of any particular single cell. In the same way, the brain does not rely on any single cell to trigger it on.
To add to what Fei Luo wrote, most of the brain's oscillatory activity is subthreshold. At any given time, interconnected networks of interneurons and principal cells are generating subthreshold membrane potential oscillations -- a major contributor to the local field potentials that you detect with extracellular electrodes or EEG -- in multiple, partly interlocking frequency bands such as theta (~4-11 Hz) and gamma (low gamma is roughly 30-40 Hz and high gamma is approximately double that). An increasing body of studies is showing that information is encoded partly in how action potentials are embedded within the phasing of these oscillations. **This is another profound difference between brain and SA node oscillations.** Finally, these subthreshold oscillations also contribute to the cellular excitability leading to action potentials, as APs are more likely during the depolarized phases.
If I can chime in 2 cents to the already excellent answers here. Of course, most, if not all of the excitable neurons have action potentials. The pacemakers, as others have pointed out, are many. But I'd also like to introduce the idea (if someone else has already, sorry) that the 'pacemakers' in the brain often have a different character than the cardiac pacemaker. Whereas the cardiac pacemaker explicitly drives the following activity of the heart, i.e. is a 'true' pacemaker, the nature of pacemakers in the brain more often has the character of shaping ongoing activity. That is to say, that the pacemakers have the effect of shaping other inputs. The inferior olive, for example, tends to synchronize the cerebellum's efferent output in response to afferent input, even if it is not driving that output itself. Likewise, circadian pacemakers tend not to drive activity in the brain as much as they bias the response to other activity in the brain. (added note: I see that Fei Luo and Linda Hermer have already touched on this).
Every single neuron is its own pacemaker. When the conditions around it are just right, it fires. Now, it is the action of all these "free agents" 'NSync (sorry, could not resist) that creates our thoughts and feelings and our very being. That said, perhaps the part of the brain that comes close to what you are talking about is the hippocampus function in memory. It is the address book and trigger of our long term memories. If you lose that, you cannot store new long term memories. Check this out:
In neurons the source of action potential is Na+/K+ ion exchange from one cell to other. Moreover their alteration causes disruption in potential difference between cells.