The brain is not one organ doing one job. It is a set of regions that each specialise, and that talk to each other all the time through bundles of nerve fibres.
86 billionneurons, plus about as many support (glial) cells [2]
80 %of all neurons sit in the small cerebellum at the back [2]
What you see in the app
The brain in Brain Energy is drawn midsagittal: cut straight down the middle between the two halves and seen from the inside. This view shows the deep parts (thalamus, hypothalamus, brainstem) that are hidden when you look at the outside of the brain. Front is on the left, back on the right.
The main parts
Part
What it mainly does
Neurons
Cerebrum (cerebral cortex)
The large, folded outer layer: thinking, senses, movement, language, memory. Split into four lobes on each side.
Connected spaces filled with cerebrospinal fluid that cushions the brain. No neurons.
0
"—" = no single reliable count. The Regions tab gives each region's count, its source and how sure it is.
Regions work as teams
Most abilities need several regions at once. Remembering a face uses vision (occipital), recognition (temporal), memory (hippocampus) and emotion (amygdala). In the app these teams are called systems (limbic, motor, visual, default mode), and the Functions list shows which regions take part in each function.
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Try it: open the Regions view, click a region to read about it, double-click to split it into its parts, or pick a system on the left.
Sources
Raichle ME, Gusnard DA (2002). Appraising the brain's energy budget. Proc Natl Acad Sci USA 99:10237-10239 · PubMed · DOI
Azevedo FA, Carvalho LR, Grinberg LT, et al., Herculano-Houzel S (2009). Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain. J Comp Neurol 513:532-541 · DOI
Aboitiz F, Scheibel AB, Fisher RS, Zaidel E (1992). Fiber composition of the human corpus callosum. Brain Res 598:143-153 · DOI
Page KA, Arora J, Qiu M, Relwani R, Constable RT, Sherwin RS (2009). Small decrements in systemic glucose provoke increases in hypothalamic blood flow prior to the release of counterregulatory hormones. Diabetes 58:448-452 · DOI
Neurons are the brain's signalling cells. Each one collects signals from others, decides whether to fire, and passes its own signal on through thousands of tiny contact points called synapses.
A simplified neuron. Real neurons have many more branches.
The parts of a neuron
Dendrites — branching inputs that receive signals from other neurons.
Cell body (soma) — holds the nucleus and adds up the incoming signals.
Axon — a single output cable, sometimes very long, that splits into many branches. Many axons are wrapped in myelin, a fatty insulation that makes signals travel much faster.
Axon terminals — the branch endings, filled with small bubbles (vesicles) of neurotransmitter.
How a signal is passed on
Firing. When enough input arrives, the neuron fires an action potential: a brief electrical pulse made by sodium ions rushing in, then potassium ions flowing out.
Down the axon. The pulse runs along the axon and into every branch.
At the synapse. The pulse makes vesicles release neurotransmitter (for example glutamate) into a tiny gap, the synaptic cleft.
Next neuron. The neurotransmitter binds receptors on the next neuron's dendrite and nudges it towards firing (or away from it, for inhibitory synapses).
Reset. Pumps push the ions back and the neurotransmitter is cleared and recycled. This clean-up is what costs most of the energy (see Energy Demands).
~150 trillionsynapses in the human neocortex alone [1]
thousandsof synapses on a typical cortical neuron
1 : 1neurons to glial cells in the whole brain [2]
The support cells (glia)
Astrocytes look after the space around synapses, take up glucose from the blood and pass fuel (lactate) to neurons [3]. Oligodendrocytes make myelin. Microglia are the brain's immune cells and clean up damage.
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Try it: open the Neurons view and press Start signals to watch impulses run down axons and across synapses. Zoom in and click a neuron to see everything it connects to.
Sources
Pakkenberg B, Pelvig D, Marner L, et al. (2003). Aging and the human neocortex. Exp Gerontol 38:95-99 · PubMed · DOI
Azevedo FA, Carvalho LR, Grinberg LT, et al., Herculano-Houzel S (2009). Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain. J Comp Neurol 513:532-541 · DOI
Magistretti PJ, Allaman I (2015). A cellular perspective on brain energy metabolism and functional imaging. Neuron 86:883-901 · DOI
The brain's wiring is not fixed. Connections get stronger, weaker, new ones form and unused ones are removed — this is how we learn and remember, and how the brain can partly recover after injury.
"Cells that fire together, wire together"
In 1949 Donald Hebb proposed that when one neuron repeatedly helps to fire another, the connection between them grows stronger [1]. The popular summary is "cells that fire together, wire together".
Four kinds of change
Stronger or weaker synapses
Repeated use makes a synapse respond more strongly for hours to weeks (long-term potentiation, LTP, first shown in 1973) [2]; little use weakens it (long-term depression, LTD).
New and lost connections
Small dendrite bumps called spines, where most excitatory synapses sit, appear and disappear with experience [3].
Faster cables
Practice can change myelin, tuning how fast signals travel along axons [4].
New neurons?
Whether adults keep making new neurons in the hippocampus is still debated: some studies find almost none [5], others find it continues into old age [6].
Learning costs energy
Building and keeping connections uses energy. In fruit flies, forming long-term memory shortens survival when food is cut off [7], and starving flies switch off costly long-term memory to save energy [8]. The brain's budget per neuron is roughly fixed [9], so plasticity has to fit inside it.
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Try it: in the Neurons view press + Neuroplasticity: each neuron grows a new axon branch towards a neighbour, which grows a dendrite to meet it, and a synapse forms.
Sources
Hebb DO (1949). The Organization of Behavior: A Neuropsychological Theory. Wiley, New York (book)
Bliss TV, Lømo T (1973). Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. J Physiol 232:331-356 · DOI
Holtmaat A, Svoboda K (2009). Experience-dependent structural synaptic plasticity in the mammalian brain. Nat Rev Neurosci 10:647-658 · DOI
Fields RD (2015). A new mechanism of nervous system plasticity: activity-dependent myelination. Nat Rev Neurosci 16:756-767 · DOI
Sorrells SF, Paredes MF, Cebrian-Silla A, et al. (2018). Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults. Nature 555:377-381 · DOI
Boldrini M, Fulmore CA, Tartt AN, et al. (2018). Human hippocampal neurogenesis persists throughout aging. Cell Stem Cell 22:589-599 · DOI
Mery F, Kawecki TJ (2005). A cost of long-term memory in Drosophila. Science 308:1148 · DOI
Plaçais PY, Preat T (2013). To favor survival under food shortage, the brain disables costly memory. Science 339:440-442 · DOI
Herculano-Houzel S (2011). Scaling of brain metabolism with a fixed energy budget per neuron: implications for neuronal activity, plasticity and evolution. PLoS One 6:e17514 · DOI
For its size the brain is the most expensive organ in the body. It runs non-stop, day and night, and it has almost no fuel stored.
2 % → 20 %2 % of body weight uses about 20 % of the body's energy and oxygen at rest [1]
~20 Wroughly the power of a dim light bulb (20 % of a resting body's ~100 W)
~10 sto lose consciousness when blood flow to the brain stops [2]
What it runs on
Normally the brain burns glucose (blood sugar) with oxygen, both delivered by blood [3]. It stores very little — a small amount of glycogen in astrocytes — so it depends on a steady supply. During long fasting the liver makes ketone bodies, which can supply most of the brain's fuel [4]. The body protects the brain's supply before other organs, sometimes called the "selfish brain" [5].
Where the energy goes
Most of it pays for signalling. Every action potential and every synaptic signal lets ions leak across the membrane, and pumps (above all the sodium–potassium pump) must spend ATP to push them back. In grey matter the biggest costs are action potentials and synaptic transmission; keeping neurons at rest and housekeeping cost less [6, 7].
Housekeeping (making proteins and lipids, moving cargo)
smaller
Exact shares differ between studies and species [6, 7].
Not every region is equal
Regions differ in how much energy they use and in how well they cope when supply drops. In hypoglycemia, for example, the brainstem and cerebellum are spared while parts of the cortex and the hippocampus are damaged [8].
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Try it: the Energy view slows the regions the research says lose out first when energy runs short. Press Start and move the energy-deficiency slider.
Sources
Raichle ME, Gusnard DA (2002). Appraising the brain's energy budget. Proc Natl Acad Sci USA 99:10237-10239 · PubMed · DOI
Rossen R, Kabat H, Anderson JP (1943). Acute arrest of cerebral circulation in man. Arch Neurol Psychiatry 50:510-528 · DOI
Mergenthaler P, Lindauer U, Dienel GA, Meisel A (2013). Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci 36:587-597 · DOI
Owen OE, Morgan AP, Kemp HG, Sullivan JM, Herrera MG, Cahill GF (1967). Brain metabolism during fasting. J Clin Invest 46:1589-1595 · DOI
Peters A, Schweiger U, Pellerin L, et al. (2004). The selfish brain: competition for energy resources. Neurosci Biobehav Rev 28:143-180 · DOI
Attwell D, Laughlin SB (2001). An energy budget for signaling in the grey matter of the brain. J Cereb Blood Flow Metab 21:1133-1145 · DOI
Harris JJ, Jolivet R, Attwell D (2012). Synaptic energy use and supply. Neuron 75:762-777 · DOI
When the brain gets less energy than it needs — or cannot use the fuel it gets — signalling falters first, and if the shortage is severe or long, neurons are damaged.
This page is about everyday, gradual and long-term shortage (hunger, low blood sugar, sleep loss, ageing, poor fuel use). Sudden, critical loss of supply — stroke, cardiac arrest, suffocation — is a different situation and is covered separately under Critical energy loss.
What happens
Pumps fall behind. Without enough ATP the ion pumps cannot keep up, so neurons fire less reliably and synapses weaken.
Higher functions slip first. Attention, judgement and self-control (prefrontal cortex) suffer early in low blood sugar and after sleep loss, while basic functions hold up [1, 2].
Vital centres are protected. The brainstem, which keeps breathing and the heart going, is the most resistant [3].
Damage if it lasts. Severe, prolonged hypoglycemia can kill neurons, above all in the cortex and hippocampus [3]. Long-term, smaller shortfalls are linked to slow decline in ageing and neurodegenerative disease [4].
The brain also adapts: at high altitude it lowers its glucose use [5], in long fasting it switches to ketones [6], and in ageing its glucose use falls while ketone use is kept [4, 7].
Where in the neuron does the shortage hit?
Almost every step of a signal costs energy, so a shortage can weaken it in several places. They are not equally sensitive, though. The synapse fails first; the electrical spike itself is one of the last things to go [8].
The places an energy shortage can act, numbered as in the list below.
1
Do neurons fire less often? Yes — early, partly on purpose
When ATP falls, ATP-sensitive potassium (KATP) channels open and quieten the neuron, a built-in brake that protects it [9]. ATP broken down to adenosine also dampens activity through A1 receptors [10]. In milder, long-term shortage (food restriction in mice) neurons kept their firing rate but saved 29 % of their ATP by using weaker synaptic currents, at the cost of less precise signals [11].
2
Do they fire with less energy, a weaker spike? Not at first — late
A spike is all-or-none: if it fires, it is full size, because it is powered by the sodium and potassium gradients the pumps have already built up, not by fresh ATP. Only when the pumps fall far behind do the gradients run down; spikes shrink, then stop as the neuron depolarises (depolarisation block). In severe shortage this ends in a wave of complete depolarisation spreading through the tissue [12].
3
Is the signal re-amplified less well along the axon? Sometimes — long, thin or fast-firing axons
The spike is regenerated at every node of the axon by sodium channels, and the pumps there must clear the sodium afterwards. Long axons get part of their fuel from the myelin-making oligodendrocytes [13] and can bridge short gaps with glycogen from astrocytes; once that is used up, conduction fails [14]. Failures show up first at high firing rates and at thin branch points.
4
Do synapses release less effectively? Yes — the first thing to fail
In low oxygen or blood flow, synaptic transmission stops while the neurons themselves are still intact; the failure is mainly presynaptic, in transmitter release [8]. This "electrical silence" is reversible if supply returns in time [15]. Adenosine adds to it by turning release down [10].
5
Do the vesicles regenerate less well? Yes — mainly (a) speed and (c) number
(a) Slower. Pulling vesicles back from the membrane (endocytosis) is the most ATP-hungry step of the vesicle cycle; without local ATP it stalls [16]. In cultured neurons low oxygen cut endocytosis to 44 % and release to 72 % of normal [17].
(b) Less transmitter per vesicle. Likely, but less directly measured: vesicles are filled by a proton pump (V-ATPase) that runs on ATP and leaks constantly, so filling depends on steady energy [18, 19].
(c) Fewer vesicles ready. Yes, during sustained activity: when recycling cannot keep up, the pool of ready vesicles runs down and the synapse fatigues [16, 17].
6
Other effects Clean-up, rhythm, upkeep
Clean-up fails. Glutamate is removed from the synapse by transporters driven by the sodium gradient. In severe shortage they run backwards and release glutamate, overstimulating neurons (excitotoxicity) [20].
Rhythms go first. Fast-firing inhibitory interneurons are among the most energy-hungry cells; the fast brain rhythms they pace (gamma oscillations, important for attention and memory) are especially sensitive [21].
Upkeep is postponed. Cells cut "optional" spending such as making proteins before ion pumping [22], and starved animals switch off costly long-term memory [23].
Calcium and water. Calcium pumps fall behind and calcium builds up inside; sodium pulls water in and cells swell.
Grouped by where the chain breaks: the fuel or oxygen supply, the delivery by blood, the cell's ability to use the fuel, or demand that outstrips supply.
Not enough fuel or oxygen
Low blood sugar (hypoglycemia)
Most often from diabetes medication (insulin) with too little food or extra exercise [1, 3].
Narrowed small arteries and a weaker blood–brain barrier reduce delivery over years [25].
Cells can't use the fuel well
Brain insulin resistance
Linked to type 2 diabetes and Alzheimer's disease [24].
Mitochondrial problems
Inherited mitochondrial diseases, and damage from oxidative stress (see the Toxicity tab) [26, 27].
Vitamin B1 (thiamine) deficiency
Thiamine is needed to burn glucose; lack of it (alcohol misuse, malnutrition, after some stomach surgery) causes Wernicke's encephalopathy [28].
Ageing
The brain's glucose use declines with age and more so in Alzheimer's disease [4].
Demand outstrips supply
Head injury (concussion)
After a blow, neurons need much more energy just as blood flow drops — an "energy crisis" [29].
Sleep loss
After a night without sleep, glucose use falls in prefrontal and parietal areas [2, 30].
Sudden events — stroke, cardiac arrest, suffocation — are listed under Critical energy loss. This is basic educational information, not medical advice. If you are worried about any of these, talk to a doctor.
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Try it: in the Energy view, raise the energy deficiency and watch which regions slow down first; the Toxicity view shows what oxidative damage does inside neurons.
Sources
Warren RE, Frier BM (2005). Hypoglycaemia and cognitive function. Diabetes Obes Metab 7:493-503 · DOI
Thomas M, Sing H, Belenky G, et al., Redmond D (2000). Neural basis of alertness and cognitive performance impairments during sleepiness. I. Effects of 24 h of sleep deprivation on waking human regional brain activity. J Sleep Res 9:335-352 · DOI
Cunnane SC, Trushina E, Morland C, et al. (2020). Brain energy rescue: an emerging therapeutic concept for neurodegenerative disorders of ageing. Nat Rev Drug Discov 19:609-633 · PubMed · DOI
Hochachka PW, Clark CM, Brown WD, et al., Holden JE (1994). The brain at high altitude: hypometabolism as a defense against chronic hypoxia?. J Cereb Blood Flow Metab 14:671-679 · DOI
Owen OE, Morgan AP, Kemp HG, Sullivan JM, Herrera MG, Cahill GF (1967). Brain metabolism during fasting. J Clin Invest 46:1589-1595 · DOI
Courchesne-Loyer A, Croteau E, Castellano CA, St-Pierre V, Hennebelle M, Cunnane SC (2017). Inverse relationship between brain glucose and ketone metabolism in adults during short-term moderate dietary ketosis. J Cereb Blood Flow Metab 37:2485-2493 · DOI
Hofmeijer J, van Putten MJ (2012). Ischemic cerebral damage: an appraisal of synaptic failure. Stroke 43:607-615 · PubMed · DOI
Yamada K, Ji JJ, Yuan H, et al. (2001). Protective role of ATP-sensitive potassium channels in hypoxia-induced generalized seizure. Science 292:1543-1546 · DOI
Dunwiddie TV, Masino SA (2001). The role and regulation of adenosine in the central nervous system. Annu Rev Neurosci 24:31-55 · DOI
Padamsey Z, Katsanevaki D, Dupuy N, Rochefort NL (2022). Neocortex saves energy by reducing coding precision during food scarcity. Neuron 110:280-296 · DOI
Dreier JP (2011). The role of spreading depression, spreading depolarization and spreading ischemia in neurological disease. Nat Med 17:439-447 · DOI
Fünfschilling U, Supplie LM, Mahad D, et al. (2012). Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity. Nature 485:517-521 · DOI
Brown AM, Ransom BR (2007). Astrocyte glycogen and brain energy metabolism. Glia 55:1263-1271 · DOI
Astrup J, Siesjö BK, Symon L (1981). Thresholds in cerebral ischemia - the ischemic penumbra. Stroke 12:723-725 · DOI
Rangaraju V, Calloway N, Ryan TA (2014). Activity-driven local ATP synthesis is required for synaptic function. Cell 156:825-835 · DOI
Fedorovich S, Hofmeijer J, van Putten MJAM, le Feber J (2017). Reduced synaptic vesicle recycling during hypoxia in cultured cortical neurons. Front Cell Neurosci 11:32 · DOI
Pulido C, Ryan TA (2021). Synaptic vesicle pools are a major hidden resting metabolic burden of nerve terminals. Sci Adv 7:eabi9027 · DOI
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Plaçais PY, Preat T (2013). To favor survival under food shortage, the brain disables costly memory. Science 339:440-442 · DOI
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Sometimes the brain's supply is cut off suddenly and almost completely. These are medical emergencies, and they work very differently from the gradual shortages the rest of Brain Energy is about.
!
Not the focus of this site. Brain Energy is about everyday and long-term energy shortage. This page only outlines critical events so they are not confused with it. In an emergency, call your local emergency number.
What counts as critical
Stroke
A blocked or burst artery cuts off part of the brain. In a major stroke about 1.9 million neurons die every minute until blood flow returns [1].
Cardiac arrest
The heart stops and supply to the whole brain ends; consciousness is lost within about 10 seconds [2].
Suffocation and poisoning
Choking, drowning or carbon-monoxide poisoning stop oxygen reaching the brain.
Hypoglycemic coma
Very low blood sugar for a long time can kill neurons in the cortex and hippocampus [3].
Why it is different
In gradual shortage the brain has time to adapt: it turns firing and synapses down, switches fuel and protects vital regions. In a critical event there is no time. With almost no fuel stored, synapses go silent within seconds, and if blood flow stays very low the pumps stop altogether [4].
Blood flow (normal ≈ 50 mL per 100 g per minute)
What happens
Reversible?
Below ~20
Synapses stop transmitting, EEG goes flat; neurons are silent but intact [4, 5]
Yes, if restored in time
Below ~10
Pumps fail, neurons depolarise in spreading waves, glutamate floods out, calcium builds up [5, 6, 7]
No — neurons die within minutes
Sources
Saver JL (2006). Time is brain - quantified. Stroke 37:263-266 · PubMed · DOI
Rossen R, Kabat H, Anderson JP (1943). Acute arrest of cerebral circulation in man. Arch Neurol Psychiatry 50:510-528 · DOI
