The nervous system operates across a wide spectrum of temporal scales, with processes ranging from the rapid transmission of action potentials to the prolonged modulation of neurotransmitter activity. Understanding the time course of neuronal events is essential for a comprehensive grasp of neural communication, synaptic integration, and the resultant behavioral outputs. This post explores the intricate dynamics of neural processes, including synaptic potentials, neurotransmitter release, signal propagation, and decision-making, offering a detailed analysis of the temporal aspects that govern these functions. By examining each component within the time framework, we can better appreciate the efficiency and complexity of neural interactions and their implications for cognition and behavior.
Excitatory and Inhibitory Postsynaptic Potentials (EPSPs and IPSPs)
An excitatory postsynaptic potential (EPSP) is a subthreshold depolarization that makes the membrane potential (~0.5 mV) less negative and pushes the neuron toward its excitation threshold. EPSPs are produced when neurotransmitters bind to receptors and cause positive sodium ions to enter the cell. A postsynaptic membrane may have tens to thousands of transmitter-gated ion channels at a single synapse. The amount of transmitter released determines how many of these channels will be activated. The size of an EPSP will be a multiple of the number of vesicles, each containing several thousand transmitter molecules.
An inhibitory postsynaptic potential (IPSP) is a hyperpolarization that makes the membrane potential (~ 0.5 mV) more negative and pushes the neuron away from its excitation threshold. At most inhibitory synapses, IPSPs are produced when neurotransmitters like GABA or glycine bind to receptors and cause negative chloride ions to enter the cell. When an inhibitory synapse is closer to the soma than an excitatory synapse, it can counteract positive current flow and decrease the size of the EPSP. This mechanism is called shunting inhibition (Bear, Connors, & Paradiso, 2016). EPSPs and IPSPs are the fundamental units of synaptic communication. These potentials are brief. They begin no sooner than ~0.5 milliseconds after an action potential reaches the axon terminal due to synaptic delay (Breedlove & Watson, 2023). EPSPs last between 10 and 20 milliseconds (Destexhe & Marder, 2004). IPSPs last up to 50 milliseconds (Camera et al., 2006). The duration depends on the type of neurotransmitter and the receptor involved. For example, glutamate binding to AMPA receptors may produce EPSPs lasting around 10 milliseconds, whereas GABAergic IPSPs mediated by GABA-A receptors tend to last slightly longer.
Transit Time from Dendrites to the Axon Hillock
Dendrites are branched structures designed to receive messages from other neurons via axodendritic synapses and send messages to other neurons through dendrodendritic synapses (junctions between the dendrites of two neurons). Dendrites receive thousands of synaptic contacts and have specialized proteins called receptors for neurotransmitters released into the synaptic cleft (Bear, Connors, & Paradiso, 2016). Axodendritic synapse graphic © nobeastsofierce/Shutterstock.com.
An axon hillock is a swelling of the cell body where the axon begins. The journey of an EPSP or IPSP from the dendrite to the axon hillock depends on the neuron's geometry and the dendritic tree's properties. In large pyramidal neurons of the cortex, this distance can vary from a few micrometers to several hundred micrometers. The speed at which these potentials propagate is approximately 0.1 to 1 meter per second. Therefore, the time required for the signal to travel from a distal dendrite to the axon hillock ranges from 1 to 5 milliseconds (Camera et al., 2006; Magee & Johnston, 1997). Graphic by M.alijar3i from the Wikipedia article Axon Hillock.
EPSP and IPSP Integration at the Axon Hillock
The axon hillock integrates incoming synaptic potentials over a short time window, typically around 10-50 milliseconds. This window allows the neuron to sum excitatory and inhibitory inputs to determine whether the threshold for action potential initiation is reached. These potentials' temporal and spatial summation occurs within this brief time frame (Stuart et al., 1997).
Action Potentials
A typical action potential lasts approximately 0.5 to 2 milliseconds (Breedlove & Watson, 2023; Moreno & Parga, 2004; Stuart et al., 1997). During this time, the neuron's membrane potential rapidly depolarizes and then repolarizes.
The absolute refractory period, during which a second action potential cannot be initiated regardless of the stimulus strength, lasts about 1 millisecond (Hodgkin & Huxley, 1952). This period corresponds to the time when voltage-gated sodium channels are inactivated.
The relative refractory period follows the absolute refractory period and lasts around 2 to 4 milliseconds. During this time, generating a new action potential is possible, but a stronger-than-normal stimulus is required due to the membrane being hyperpolarized (Hille, 2001; Moreno & Parga, 2004). Graphic redrawn from Breedlove and Watson (2023).
Action Potential Conduction
Unmyelinated axons, like those found in C fibers responsible for transmitting pain signals, conduct action potentials at speeds of 0.5 to 2 meters per second (Waxman, 1980). Their transmission is slow because of greater internal resistance and delays caused by closely spaced ion channels.
Internal Resistance
A smaller axon diameter also increases internal resistance to ion movement. Conduction speed is proportional to the square root of the axon’s diameter (Hodgkin, 1954).
Closely Spaced Ion Channels
In unmyelinated axons, voltage-gated sodium and potassium channels are distributed along the entire length of the axon, and action potentials must be continuously regenerated at every point along the membrane. This continuous regeneration of the action potential, known as continuous conduction, is slower than the saltatory conduction in myelinated axons (Waxman & Bennett, 1972).
In myelinated axons, ion channels are concentrated at the nodes of Ranvier, and the action potential "jumps" from node to node, allowing for faster transmission. This spacing of ion channels reduces the number of points where the action potential needs to be regenerated, leading to quicker propagation.
Due to saltatory conduction, action potentials travel more quickly in myelinated axons than in unmyelinated ones.
Action potential video © viktorov.pro/Shutterstock.com.
In myelinated axons, such as those in the corticospinal tract, action potentials travel at 70 to 120 meters per second. Action potential conduction graphic © Dee-sign/Shutterstock.com.
Sensory Signal Transmission
The distance from the toe to the somatosensory cortex is approximately 1 to 1.5 meters. In myelinated fibers, such as those in the somatosensory pathway, the conduction velocity is around 100 meters per second. Therefore, a signal takes about 20 to 30 milliseconds to travel from the toe to the somatosensory cortex (Huang & Doiron, 2016; Lucey & Waxman, 1978). In contrast, slower unmyelinated fibers transmitting pain signals would take around 500 to 2,000 milliseconds for the same journey (Perl, 1992).
Motor Signal Transmission
Similarly, motor signals from the motor cortex to the muscles in the toe travel along myelinated corticospinal axons at a speed of 70 to 120 meters per second. The transmission time for this motor command is approximately 10 to 20 milliseconds, similar to that of somatosensory signals (Porter & Lemon, 1993).
Hormone Signaling
Peptide Hormones
Peptide hormones exert their effects at their receptors over a period ranging from seconds to minutes, and their actions typically last minutes to hours. This is because peptide hormones, such as insulin, glucagon, and growth hormone, bind to membrane-bound receptors on the surface of target cells, triggering signal transduction pathways inside the cell (Evans et al., 2001; Gore, 2014).
Once a peptide hormone binds to its receptor, it activates intracellular signaling cascades, often involving second messengers like cyclic AMP (cAMP) or calcium ions. These signaling pathways lead to rapid changes in cellular activity, such as enzyme activation or inhibition, ion channel activity changes, or gene expression alterations (Gore, 2014; Lodish et al., 2000).
Since these processes rely on rapid signal transmission rather than changes in gene transcription (as seen with steroid hormones), the effects of peptide hormones tend to be faster but often shorter-lived than those of steroid hormones. The duration of action depends on factors like the hormone's half-life in the bloodstream, receptor desensitization, and feedback mechanisms (Beato et al., 1995; Evans et al., 2001). Endocrine system graphic © Alexander_P/Shutterstock.com.
Steroid Hormones
Steroid hormones exert their effects on their receptors over a period of hours to days, depending on the specific hormone and target tissue. This is because steroid hormones, such as cortisol, estrogen, testosterone, and progesterone, operate through intracellular receptors that initiate changes in gene transcription and protein synthesis (Mangelsdorf et al., 1995; Spencer & Deak, 2017). Stress system graphic © GraphicsRF.com/Shutterstock.com.
After steroid hormones diffuse across the cell membrane, they bind to intracellular receptors in the cytoplasm or nucleus. This hormone-receptor complex then interacts with DNA to regulate gene expression, producing specific proteins. Since this process involves changes at the genetic level, the effects tend to be long-lasting compared to other hormones (like peptide hormones), which act more rapidly but with shorter duration (Spencer & Deak, 2017).
In some cases, steroid hormones can also exert faster non-genomic effects, occurring within minutes. Membrane-bound receptors mediate these effects and involve intracellular signaling pathways, but these rapid effects are typically short-lived compared to the genomic actions (Beato et al., 1995; Spencer & Deak, 2017).
Neurotransmitter Release and Binding
Once released into the synaptic cleft, neurotransmitter molecules diffuse across the gap to bind to their receptors. Diffusion occurs within approximately 1 millisecond (Bouteiller et al., 2011; Fatt & Katz, 1951). Synapse animation without sound © 3Dme Creative Studio/Shutterstock.com.
Once bound, the neurotransmitter remains attached to the receptor for a variable period, typically between 1 and 2 milliseconds, before either being metabolized or undergoing reuptake. Synapse graphic © SciePro/Shutterstock.com.
Electrical Synapses
Electrical synapses, also known as gap junctions, enable bidirectional direct transmission of electrical signals between neurons. These synapses are extremely fast, with signal transmission occurring almost instantaneously, typically within less than 1 millisecond (Bennett & Zukin, 2004). This rapid transmission occurs because electrical synapses involve the direct flow of ions between cells, bypassing the slower chemical synaptic processes. Gap junction illustration © VectorMine/Shutterstock.com.
Retrograde Transmission
Retrograde transmission in a human neuron refers to the process by which signaling molecules, such as endocannabinoids or nitric oxide, are released from the postsynaptic neuron and travel back to the presynaptic neuron to modulate its activity. This type of transmission typically takes place within a few milliseconds to seconds, depending on the specific signaling molecules involved.
Endocannabinoids (e.g., anandamide and 2-AG) are synthesized in the postsynaptic neuron in response to increased intracellular calcium levels. Once released, they can diffuse across the synapse and bind to CB1 receptors on the presynaptic neuron. This process typically occurs within a few hundred milliseconds to seconds, as endocannabinoids are lipid-soluble and diffuse rapidly (Kano et al., 2009). Graphic retrieved from Integrative Pharmacology.
Nitric oxide (NO) is a gaseous neurotransmitter that diffuses almost instantly after its production in the postsynaptic neuron. NO can cross cell membranes without needing a receptor and quickly affects the presynaptic neuron, typically within milliseconds (Garthwaite, 2008).
While the transmission occurs within milliseconds to seconds, the effects of retrograde signaling—such as inhibiting neurotransmitter release or long-term synaptic plasticity—can sometimes last for seconds to minutes or even longer.
Ectopic Transmission
Ectopic neurotransmission refers to the release of neurotransmitters from sites outside traditional synapses, such as along the axon or from dendrites, and their subsequent action on receptors away from the synaptic cleft. In the human nervous system, ectopic neurotransmitter release can take a few milliseconds to seconds to travel to its target receptor, depending on several factors, such as the distance from the release site and the nature of the diffusion process. Graphic adapted from the American Scientist.
Another example is neurotransmitter release from swellings in axon walls called axonal varicosities.
Neurotransmitter release from ectopic sites occurs rapidly, typically within milliseconds after the necessary depolarization or signaling event, similar to classical synaptic transmission.
After release, the neurotransmitters must diffuse through the extracellular space to reach their target receptors. This diffusion is generally slower than in traditional synaptic transmission, where neurotransmitters travel across a very narrow synaptic cleft. Diffusion across larger distances in ectopic transmission can take anywhere from milliseconds to seconds, depending on the proximity of the receptor sites (Zoli et al., 1999).
For example, if an ectopic release occurs a significant distance from the receptor, the delay in signal transmission may last several hundred milliseconds to a few seconds. In contrast, in cases where the release site is relatively close to the receptor, this process can occur much more quickly.
Receptor Activation
Ionotropic Receptors
A neurotransmitter activates an ionotropic receptor very quickly, typically within 1 millisecond of binding to the receptor (Fatt & Katz, 1951). Ionotropic receptors are ligand-gated ion channels, and when the neurotransmitter binds, it causes a conformational change in the receptor, allowing ions to flow through the channel almost immediately. Ionotropic receptor graphic © Ph-HY/Shutterstock.com.
An ionotropic receptor's activation duration depends on the neurotransmitter and receptor type. For example, glutamate binding to AMPA receptors typically results in channel opening that lasts for 1-5 milliseconds (Dingledine et al., 1999), while GABA binding to GABA-A receptors may result in a slightly longer inhibitory postsynaptic potential (IPSP) lasting about 10-20 milliseconds (Destexhe & Marder, 2004). The brief activation allows for rapid signaling, which is essential for fast synaptic transmission. GABA ionotropic receptor graphic © Designua/Shutterstock.com.
Metabotropic Receptors
G-protein-coupled receptors (also called metabotropic receptors; GPCRs) are proteins that convert signals from NTs and drugs into intracellular messages. Activating G-proteins within a neuron's interior can result in synthesizing second messengers that modulate its actions. Second messengers can alter cell division and differentiation, energy conversion and utilization, membrane potential, and ion channels.
A neurotransmitter's activation of metabotropic receptors is slower than that of ionotropic receptors. A neurotransmitter typically takes several hundred milliseconds to a few seconds to activate a metabotropic receptor (Hille, 2001). This delay occurs because metabotropic receptors are G-protein-coupled receptors (GPCRs) that trigger intracellular signaling cascades rather than directly opening ion channels. Metabotropic receptor graphic © Ph-HY/Shutterstock.com.
Once activated, the effects of metabotropic receptor signaling can last much longer than ionotropic receptors, ranging from several seconds to minutes or even longer. This prolonged duration is due to the involvement of second messengers and the amplification of signals within the cell. For example, activating metabotropic glutamate receptors (mGluRs) can last from seconds to minutes, depending on the specific receptor subtype and the intracellular pathways involved (Conn & Pin, 1997).
Receptor Downregulation and Upregulation
Downregulation occurs when receptors are prolonged or excessively stimulated, decreasing receptor number or sensitivity. For example, chronic exposure to high levels of a neurotransmitter or agonist (such as serotonin in the case of SSRIs) can lead to downregulation of its receptors, which may take several hours to days to develop (Stahl, 2013). The downregulation of beta-adrenergic receptors following chronic stimulation can also take a few days (Lohse et al., 1990).
Upregulation occurs when receptor stimulation is reduced, leading to an increase in receptor number or sensitivity. This process also occurs over a similar time frame of hours to days. For example, following chronic blockade of dopamine D2 receptors (as seen with antipsychotic use), upregulation may occur within a few days as the system compensates for reduced receptor activity (Samaha et al., 2007). Graphic adapted from Julien et al. (2023).
Neurotransmitter Deactivation
Reuptake
After neurotransmitters interact with their receptors, reuptake mechanisms remove them from the synaptic cleft to terminate the signal. This process typically takes between 10 and 20 milliseconds (Barker & Blakely, 1995). For example, serotonin reuptake in serotonergic synapses occurs in 10-15 milliseconds, but the exact duration can vary based on the neurotransmitter system involved. Graphic © Blamb/Shutterstock.com.
Serotonin-selective reuptake inhibitors (SSRIs) can delay the reuptake of a specific serotonin molecule in the synapse for a variable period, typically ranging from several hundred milliseconds to a few seconds. The exact duration depends on the concentration of the SSRI and its binding affinity to the serotonin transporter (SERT). Once bound, SSRIs inhibit the transporter's function, preventing it from removing serotonin from the synaptic cleft. This delay extends the presence of serotonin in the synapse, allowing it to interact with postsynaptic receptors longer than normal, usually in the millisecond range under typical conditions (Stahl, 2013).
Enzymatic Deactivation
Enzymatic deactivation typically occurs within milliseconds. For instance, acetylcholinesterase deactivates acetylcholine in synapses, such as the neuromuscular junction, in about 1 millisecond (Fatt & Katz, 1951). Graphic © Designua/Shutterstock.com.
The process can take longer for other neurotransmitters, like dopamine, serotonin, and norepinephrine but generally falls within milliseconds to tens of milliseconds, depending on the enzyme involved. Monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT), which degrade these neurotransmitters, operate on a similar millisecond timescale. However, the exact time may vary depending on the synapse type and neurotransmitter concentration (Houslay & Tipton, 1973).
Decision-Making
Decision-making in the prefrontal cortex is a complex process involving the integration of sensory inputs, memory, and executive functions. Studies using neuroimaging and electrophysiology suggest that the prefrontal cortex takes between 300 milliseconds to seconds to arrive at a decision, depending on the complexity of the task (Grossman & Cohen, 2022; Miller & Cohen, 2001). This can be as fast as 300 milliseconds for simple decisions, while more complex decisions requiring weighing multiple pieces of information may take closer to seconds. This is influenced by the dynamics of neuromodulators, which play a key role in temporal scaling of neuronal dynamics (Grossman & Cohen, 2022).
In one study, EEG changes preceded conscious choices by 5-10 seconds (Soon et al., 2008).
Frontal lobe graphic © ART-ur/Shutterstock.com.
Conclusion
Neural processes occur over a wide range of time scales, from the millisecond precision of ion channel openings to the longer-lasting effects of receptor modulation. These temporal dynamics are critical for coordinating neural communication, synaptic plasticity, and overall brain function. By integrating rapid and slower processes, the nervous system achieves the sophisticated control required for sensory perception, motor coordination, and decision-making. A thorough understanding of these time scales enhances our comprehension of how the brain orchestrates complex behaviors and adapts to environmental demands.
Glossary
absolute refractory period: the phase during which a neuron cannot generate another action potential, regardless of the stimulus strength, typically lasting about 1 millisecond.
action potential: a rapid depolarization and repolarization of the neuronal membrane, lasting 1 to 2 milliseconds, that transmits signals along axons.
axon hillock: the region of a neuron where the cell body transitions into the axon and where action potentials are initiated based on incoming excitatory and inhibitory signals.
axonal varicosities: swellings along the length of an axon where ectopic neurotransmitter release occurs, allowing neurotransmission outside traditional synapses.
continuous conduction: a process in unmyelinated axons where action potentials are propagated along the entire length of the axon membrane. In continuous conduction, the action potential is regenerated at every point along the axon as ion channels open sequentially, allowing for the flow of sodium and potassium ions. This process is slower compared to saltatory conduction in myelinated axons because it requires constant depolarization along the entire membrane.
cortisol: a steroid hormone produced by the adrenal cortex, involved in regulating metabolism, immune response, and stress (often referred to as the "stress hormone").
cyclic AMP (cAMP): a second messenger involved in transmitting signals within cells, particularly in response to hormones like glucagon and adrenaline. It activates certain proteins and enzymes, playing a key role in signal transduction pathways.
decision-making: a cognitive process occurring in the prefrontal cortex, taking between 300 to 800 milliseconds depending on task complexity.
dendrite: branched projections of a neuron that receive signals from other neurons at synapses and convey them toward the axon hillock. depolarization: a change in a neuron's membrane potential where the inside of the cell becomes less negative relative to the outside. This occurs when positively charged ions, such as sodium (Na+), enter the cell, reducing the difference in charge across the membrane. Depolarization moves the membrane potential closer to the threshold for generating an action potential, making the neuron more likely to fire. downregulation: the process by which a neuron decreases the number or sensitivity of its receptors in response to prolonged or excessive stimulation, taking hours to days.
ectopic transmission: the release of neurotransmitters from sites outside traditional synapses, with diffusion times ranging from milliseconds to seconds.
electrical synapse: a type of synapse where electrical signals are transmitted directly between neurons via gap junctions, occurring almost instantaneously within 1 millisecond.
endocannabinoids: lipid-based neurotransmitters released from the postsynaptic neuron that modulate presynaptic activity by binding to CB1 receptors, typically within hundreds of milliseconds to seconds.
enzymatic deactivation: The breakdown of neurotransmitters by enzymes, typically occurring within milliseconds, as seen in the deactivation of acetylcholine by acetylcholinesterase.
estrogen: a group of steroid hormones primarily responsible for the development and regulation of the female reproductive system and secondary sexual characteristics. It also plays roles in bone health and cardiovascular function.
excitatory postsynaptic potential (EPSP): a subthreshold depolarization of the postsynaptic membrane, typically lasting 10 to 20 milliseconds.
gamma-aminobutyric acid (GABA): the primary inhibitory neurotransmitter in the brain, involved in IPSPs by allowing chloride ions to enter the cell.
gap junction: a specialized connection between the membranes of two adjacent cells that allows for direct electrical and chemical communication. In neurons, gap junctions form electrical synapses where ions and small molecules can pass freely between cells, enabling the rapid transmission of electrical signals. These synapses facilitate almost instantaneous signal transmission, typically within less than 1 millisecond, and are important for synchronous activity in groups of neurons. Gap junctions consist of channels called connexons, which bridge the gap between the cells' membranes.
gene expression: the process by which the information encoded in a gene is used to synthesize a functional product, typically a protein. Gene expression can be regulated at multiple levels, including transcription, translation, and post-translational modification.
gene transcription: the process by which a segment of DNA is copied into RNA, particularly messenger RNA (mRNA), as the first step in gene expression. Transcription factors and other regulatory proteins control this process.
glucagon: a peptide hormone produced by the pancreas that raises blood glucose levels by promoting the release of glucose from the liver into the bloodstream, opposite to insulin's effects.
growth hormone (GH): a peptide hormone produced by the pituitary gland that stimulates growth, cell reproduction, and regeneration in humans and other animals.
hyperpolarization: a change in a neuron's membrane potential where the inside of the cell becomes more negative relative to the outside. This typically occurs when negatively charged ions, such as chloride (Cl−), enter the cell or when potassium (K+) ions leave the cell. Hyperpolarization moves the membrane potential further from the threshold, reducing the likelihood of generating an action potential.
inhibitory postsynaptic potential (IPSP): a hyperpolarization of the postsynaptic membrane that makes action potential generation less likely, lasting up to 50 milliseconds.
insulin: a peptide hormone produced by the pancreas that regulates blood glucose levels by facilitating glucose uptake into cells, especially muscle and fat cells, for storage or energy use.
ionotropic receptor: a receptor that, upon binding to a neurotransmitter, opens ion channels within 1 millisecond, allowing for rapid synaptic transmission.
metabotropic receptor: a slower-acting receptor that uses G-proteins to initiate intracellular signaling cascades, with effects lasting from seconds to minutes.
millisecond (ms): a unit of time equal to one-thousandth of a second (0.001 seconds). In neuroscience, milliseconds are commonly used to measure the duration of fast neural processes, such as the conduction of action potentials, synaptic transmission, and the activation of ion channels. Many key events in neural communication, such as the transmission of an action potential or the release and binding of neurotransmitters, occur within this short time frame.
myelination: the process by which axons are covered with myelin sheaths, facilitating faster action potential conduction via saltatory conduction.
neurotransmitter: a chemical messenger released by neurons to transmit signals across synapses, with release and binding occurring within 1 millisecond.
nitric oxide (NO): a gaseous neurotransmitter that diffuses freely across cell membranes without needing receptors. It is produced in neurons in response to various signals, including increased intracellular calcium levels. Nitric oxide plays a key role in retrograde signaling, modulating synaptic activity in the presynaptic neuron. It acts rapidly, often within milliseconds, and is involved in vasodilation, neurotransmission, and synaptic plasticity. Unlike typical neurotransmitters, NO is not stored in vesicles but synthesized on demand.
nongenomic effect: a rapid cellular response to steroid hormones that does not involve gene transcription or protein synthesis changes. Membrane-bound receptors mediate these effects and occur within minutes.
peptide hormone: a class of hormones composed of amino acids, such as insulin, glucagon, and growth hormone, that bind to membrane-bound receptors and act through signal transduction pathways to exert their effects.
progesterone: a steroid hormone involved in the menstrual cycle, pregnancy, and embryogenesis. It is produced in the ovaries and plays a key role in preparing the uterus for pregnancy and maintaining gestation.
refractory period: the time following an action potential during which a neuron cannot fire another action potential; the absolute period lasts about 1 millisecond.
relative refractory period: the phase following the absolute refractory period, lasting 2 to 4 milliseconds, during which a neuron can fire another action potential, but a stronger stimulus is required.
retrograde transmission: a process by which postsynaptic neurons send signals back to presynaptic neurons, often through molecules like endocannabinoids, within milliseconds to seconds.
reuptake: the process by which neurotransmitters are removed from the synaptic cleft and taken back into the presynaptic neuron, typically within 10 to 20 milliseconds.
saltatory conduction: the jumping of action potentials from one node of Ranvier to another in myelinated axons, enabling rapid signal transmission.
sensory signal transmission: the process by which sensory information is sent to the brain; for example, signals from the toe take 20 to 30 milliseconds to reach the somatosensory cortex.
serotonin-selective reuptake inhibitors (SSRIs): a class of antidepressants that delay the reuptake of serotonin, allowing it to remain in the synapse longer, typically affecting reuptake by several hundred milliseconds to seconds.
spatial summation: the process by which multiple synaptic inputs from different locations on a neuron’s dendrites or cell body combine their effects to influence the neuron's membrane potential. If enough excitatory postsynaptic potentials (EPSPs) occur simultaneously from different synapses, they can collectively depolarize the neuron to reach the threshold for triggering an action potential. Conversely, inhibitory postsynaptic potentials (IPSPs) from different locations can combine to prevent the neuron from reaching the threshold. Spatial summation allows the neuron to integrate signals from various sources at the same time.
steroid hormone: a type of hormone derived from cholesterol, such as cortisol, estrogen, testosterone, and progesterone. These hormones typically exert long-term effects by regulating gene transcription and protein synthesis through intracellular receptors.
synaptic cleft: the gap between two neurons at a synapse, across which neurotransmitters diffuse to bind to receptors on the postsynaptic membrane.
temporal summation: the process by which multiple synaptic potentials combine over time to influence whether a neuron will fire an action potential.
testosterone: a steroid hormone primarily produced in the testes in males and in smaller amounts in the ovaries in females. It plays a key role in male reproductive development, secondary sexual characteristics, muscle mass, and bone density.
upregulation: the process by which a neuron increases the number or sensitivity of its receptors in response to reduced stimulation, typically taking hours to days.
vesicle: a small membrane-bound sac that stores neurotransmitters and releases them into the synaptic cleft upon the arrival of an action potential.
volume transmission: a type of neurotransmission where signals diffuse over larger areas rather than being confined to a traditional synapse, often seen with ectopic transmission.
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Support Our Friends
Dr. Inna Khazan's BCIA Introduction to biofeedback workshop will be offered in two parts this year.
Part 1 is entirely virtual, consisting of 20 hours (over 5 days) of live online instruction, home-study materials distributed prior to the live workshop, and written instructions for practical lab work to be completed during the week of the workshop or after its completion. Part 1 fulfills BCIA requirements for introduction to biofeedback didactic. Part 1 will take place on Zoom, November 4 - 8, 2024, 12 - 4pm EDT. Tuition is $1395.
Part 2 is optional, and consists of 14 hours (over 2 days) of in-person hands-on practical training using state-of-the-art equipment, designed to help participants be better prepared to start working with clients. Part 2 will take place in Boston on November 11 & 12, 2024, 9am-5pm EDT. Tuition is $395. (Please note that an Introduction to Biofeedback didactic (taken at any previous time, anywhere) is a pre-requisite to the hands-on training).
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