What is a inhibitory tone when talking about neurons?

What is a inhibitory tone when talking about neurons?

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user @nico used the wordinhibitory toneWhat does that mean?

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Neurons communicate electrochemically. That is, when a signal arrives to a neuron it fires a series of electrical signals, called action potentials. Action potentials are depolarization events that propagate along the neuronal membrane, down to the neuronal terminal. The terminal of a neuron is (with some exceptions) in contact with another neuron, via a structure called synapse. When the depolarization arrives at the terminal, it allows the entry of calcium, which then mediates the release of a chemical substance, a neurotransmitter into the synaptic space. Finally, neurotransmitters act on the postsynaptic neuron, by binding to specific receptors on its cell membrane and can either stimulate it, in which case the postsynaptic neuron will fire more and release more of its neurotransmitter or inhibit it, in which case the opposite happens.

The textbook example of a stimulatory neurotransmitter is glutamate, and the inhibitory one is GABA1.

In various areas of the brain certain neurons are constantly receiving inputs from GABAergic afferents. This means that those neurons are constantly receiving a GABA stimulus that inhibits them, and are thus under a constant inhibitory tone. This will prevent their firing until a sufficiently potent stimulatory stimulus arrives or until the inhibitory tone is somehow released (for instance if the inhibitory GABAergic afferents are themselves inhibited by some of their own afferents).

1note that this is not always true: GABA can also be stimulatory in various situations

Difference Between Excitatory and Inhibitory Neurotransmitters

The main difference between excitatory and inhibitory neurotransmitters is that excitatory neurotransmitters increase the trans-membrane ion flow of the post-synaptic neuron, firing an action potential, whereas inhibitory neurotransmitters decrease the trans-membrane ion flow of the post-synaptic neuron, preventing the firing of an action potential. Furthermore, Type I synapses use excitatory neurotransmitters while Type II synapses use inhibitory neurotransmitters.

Excitatory and inhibitory neurotransmitters are the two types of neurotransmitters or chemical messengers released by the end of the pre-synaptic neurons of the central nervous system.

Key Areas Covered

Key Terms

Action Potential, Excitatory Neurotransmitters, Inhibitory Neurotransmitters, Post-Synaptic Neuron

Losing inhibition with ketamine

Schizophrenia is thought to involve a dysfunction of glutamatergic and GABAergic signaling in the prefrontal cortex, but how these systems interact in the disease has been unclear. Now ketamine, a glutamatergic NMDA receptor antagonist, may provide a mechanism that could link these pathways.

Schizophrenia is a devastating illness, and efforts at developing treatments have been hampered, in part, by a limited understanding of the molecular basis of the disease. It is known that people with schizophrenia exhibit apparent decreases in glutamatergic N-methyl- D -aspartic acid (NMDA) receptor subunit expression and alterations in signaling pathways downstream of the receptor 1 . Similarly, NMDA receptor antagonists, such as ketamine, have long been known to induce psychotic effects that are often indistinguishable from those observed in schizophrenics. Surprisingly, although these antagonists block excitatory glutamatergic transmission at NMDA receptors, they increase overall activity in the intact prefrontal cortex in vivo 2 , perhaps by blocking GABAergic inhibition. Behrens et al. now show that ketamine in fact downregulates a key type of inhibitory neuron in the cortex through a process of superoxidase production and NADPH oxidase signaling 3 . If this mechanism also plays a role in schizophrenia, it could open important new avenues for treating the disease.

Modulation of inhibitory output is key function of antiobesity hormone

Scientists have known for some time that the hormone leptin acts in the brain to prevent obesity, but the specific underlying neurocircuitry has remained a mystery. Now, new research published by Cell Press in the July 14 issue of the journal Neuron reveals neurobiological mechanisms that may underlie the antiobesity effects of leptin.

"Leptin is a hormone that is secreted by fat cells and acts at its receptor in the brain to decrease food intake and promote energy expenditure," explains senior study author Dr. Bradford B. Lowell from Beth Israel Deaconess Medical Center and Harvard Medical School. "However, despite intensive investigation, the underlying mechanisms responsible for this are poorly understood, in part due to incomplete knowledge regarding leptin-responsive neurons."

Previous studies by Dr. Lowell's group and others pinpointed a region of the brain called the arcuate nucleus as the site of key components related to the control of obesity. In particular, pro-opiomelanocortin (POMC) neurons, which have been shown to play a key role in appetite suppression, reside in this region. Although many POMC neurons express receptors for leptin, direct action of leptin on POMC neurons has not been shown to play a large role in controlling body weight. This suggests that there are likely to be other leptin-responsive neurons that are critical for leptin's antiobesity actions.

In the current study, Dr. Lowell and colleagues took a new approach for identifying these "unidentified" body weight-regulating neurons and investigated whether leptin's effects are mediated primarily by excitatory (glutamate) or inhibitory (GABA) neurons. "Remarkably, we found that leptin's antiobesity effects are mediated predominantly by GABA neurons and that glutamate neurons play only a small role," says Dr. Linh Vong, a first author on the study. Importantly, the GABA neurons are "upstream" of the POMC neurons and, in response to leptin, the GABA neurons are less active. Conversely, a reduction in leptin levels, such as occurs with fasting, increases the activity of these GABA neurons.

Taken together, the findings suggest that modulation of GABA output is a key aspect of leptin action. "Leptin working directly on GABA neurons reduces inhibitory tone to POMC neurons," concludes Dr. Lowell. "As POMC neurons prevent obesity, their disinhibition by leptin action on upstream GABA neurons likely mediates, at least in part, leptin's antiobesity effects. Further, indirect regulation of POMC neurons by leptin reconciles the known important role of POMC neurons in regulating body weight with the relatively unimportant role played by direct action of leptin on POMC neurons."

Corticofugal amplification of facilitative auditory responses of subcortical combination-sensitive neurons in the mustached bat

Recent studies on the bat's auditory system indicate that the corticofugal system mediates a highly focused positive feedback to physiologically "matched" subcortical neurons, and widespread lateral inhibition to physiologically "unmatched" subcortical neurons, to adjust and improve information processing. These findings have solved the controversy in physiological data, accumulated since 1962, of corticofugal effects on subcortical auditory neurons: inhibitory, excitatory, or both (an inhibitory effect is much more frequent than an excitatory effect). In the mustached bat, Pteronotus parnellii parnellii, the inferior colliculus, medial geniculate body, and auditory cortex each have "FM-FM" neurons, which are "combination-sensitive" and are tuned to specific time delays (echo delays) of echo FM components from the FM components of an emitted biosonar pulse. FM-FM neurons are more complex in response properties than cortical neurons which primarily respond to single tones. In the present study, we found that inactivation of the entire FM-FM area in the cortex, including neurons both physiologically matched and unmatched with subcortical FM-FM neurons, on the average reduced the facilitative responses to paired FM sounds by 82% for thalamic FM-FM neurons and by 66% for collicular FM-FM neurons. The corticofugal influence on the facilitative responses of subcortical combination-sensitive neurons is much larger than that on the excitatory responses of subcortical neurons primarily responding to single tones. Therefore we propose the hypothesis that, in general, the processing of complex sounds by combination-sensitive neurons more heavily depends on the corticofugal system than that by single-tone sensitive neurons.


The reciprocal inhibitory exchange between the major ascending monoaminergic arousal groups and the sleep-inducing VLPO acts as a feedback loop when monoamine nuclei discharge intensively during wakefulness, they inhibit the VLPO, and when VLPO fire rapidly during sleep, block the discharge of the monoamine cell groups [98]. This relationship is described as a bistable, 𠇏lip-flop” circuit, in which the two halves of the circuit strongly inhibit each other to produce two stable discharge patterns – on or off (Fig. ​ 3 3 ). Intermediate states that might be partially “on and off” are resisted. This model helps clarify why sleep-wake transitions are relatively abrupt and mammals spend only about 1% to 2% of the day in a transitional state [99]. Hence, changes between sleep and arousal occur infrequently and rapidly. As will be described below, the neural circuitry forming the sleep switch contrasts with homeostatic and circadian inputs, which are continuously and slowly modified [98].

A schematic diagram of the flip-flop switch model. Adapted from Saper 2005, pg 1259 [99].

Despite the bistability of the on/off feedback loop, if either side is weakened or injured, unwanted instability can occur during both sleep and wake states, irrespective of which side is damaged. For instance, animals with VLPO lesions experience a 50% to 60% reduction in NREM and REM sleep time and wake up frequently during their sleep cycle [52]. Rapid sleep-wake cycling also is common in the elderly [6], who have fewer VLPO neurons [36]. These findings suggest that when the self-reinforcing properties of the circuitry are weakened, individuals shift back and forth between sleep and wakefulness more frequently as well.

Somatosensory neurons constantly provide information about the body's current state (e.g. temperature, pain, pressure, position, etc.) this constant influx of information is subject to modulation to enhance or diminish stimuli (see also: gate control theory and gain control-biological). Because there are unlimited stimuli at any given point to feel, it is imperative that these signals are appropriately filtered and compressed. To diminish certain stimuli, primary afferents receive inhibitory input (likely from GABA, but could also be glycine [2] ) to reduce their synaptic output. Impaired presynaptic inhibition has been implicated in many neurological disorders, such as chronic pain, epilepsy, autism, and fragile-X syndrome. [3] [4] [5] [6] [7]

The biophysical mechanism of presynaptic inhibition remains controversial. The presynaptic terminal has a distinct ionic composition that is high in chloride concentration which is largely due to cation-chloride cotransporters. [8] Typically when GABA receptors are activated, it causes a chloride influx, which hyperpolarizes the cell. However, due to the high concentration of chloride at the presynaptic terminal and its altered reversal potential, GABA receptor activation actually causes a chloride efflux, and a resulting depolarization. This phenomenon is called primary afferent depolarization (PAD). Despite the depolarized potential, this still results in a reduction of neurotransmitter release and thus is still inhibition. There are three hypotheses which propose mechanisms behind this paradox: [9] [10] [11] [12] [13] [14] [15] [16] [17]

  1. The depolarized membrane causes inactivation of voltage-gated sodium channels on the terminals and therefore the action potential is prevented from propagating
  2. Open GABA receptor channels act as a shunt, whereby current flows out of instead of concluding at the terminals
  3. The depolarized membrane causes inactivation of voltage-gated calcium channels, preventing calcium influx at the synapse (which is imperative for neurotransmission).

1933: Grasser & Graham observed depolarization that originated in the sensory axon terminals [18]

1938: Baron & Matthews observed depolarization that originated in sensory axon terminals and the ventral root [19]

1957: Frank & Fuortes coined the term "presynaptic inhibition" [20]

1961: Eccles, Eccles, & Magni determined that the Dorsal Root Potential (DRP) originated from depolarization in sensory axon terminals [21]

Brakes in the brain:

Autism is extremely heterogeneous, genetically and behaviorally. As a result, constructing a unifying theory of the condition remains difficult. One intriguing idea is that autism arises from too much excitation relative to inhibition of neuronal activity.

Early support for a so-called signaling imbalance in autism comes from the observation that many people with autism also have epilepsy. Recordings of electrical activity during sleep in the brains of children with autism also suggest that 50 to 70 percent of these children have hyperexcitable neural networks 1 .

Postmortem studies of people with autism suggest these effects are due to decreased signaling of cells via the inhibitory molecule gamma-aminobutyric acid (GABA). For example, the cerebral cortex (outer portion of the brain) in those with autism contains low levels of enzymes that synthesize GABA 2 . Some evidence suggests that levels of receptors for GABA are also unusually low in the brains of people with autism 3 .

Consistent with these studies, mutations linked to autism can abolish inhibitory signals in mice. Tuberous sclerosis, a syndromic form of autism, arises from dysfunction of the TSC1 gene. Mice lacking the gene show a deficit in signaling at inhibitory synapses in the hippocampus and are susceptible to seizures.

The autism-related condition fragile X syndrome is also associated with abnormalities in inhibitory signaling. Last year, researchers found that disruption of the gene PX-RICS, which facilitates the trafficking of a GABA receptor at inhibitory synapses, is linked to Jacobson syndrome, another condition that overlaps with autism. Loss of this gene in mice results in a decrease in GABA signaling and behaviors reminiscent of autism 4 .

There are two types of motor neuron: upper motor neurons and lower motor neurons.

Upper Motor Neurons

Upper motor neurons originate in the motor cortex of the brain or the brain stem and transmit signals from the brain to interneurons and lower motor neurons. These are the main cells that initiate voluntary movement throughout the body by connecting the cerebral cortex to the brain stem or spinal cord.

Lower Motor Neurons

The lower motor neurons are found in the brain stem and spinal cord and are directly responsible for communicating with the effector organs, such as the muscle cells. They receive the signals from upper motor neurons (either directly or via interneurons) and stimulate their activity.

They can be classified as either alpha motor neurons, beta motor neurons, or gamma motor neurons.

  • Alpha motor neurons are responsible for controlling muscle contractions involved in voluntary movement through contracting extrafusal muscle fibers, which make up most of the muscle tissue.
  • Beta motor neurons are less common than alpha and gamma motor neurons and are less well-characterized. However, they are known to stimulate intrafusal muscle fibers (which are found deeper within the muscle).
  • Gamma motor neurons control muscle contraction in response to external forces through the intrafusal fibers. They regulate the muscle response to stretch. For example, the knee-jerk reflex.


EPSP: An EPSP is an electrical charge on the postsynaptic membrane, which is caused by the binding of excitatory neurotransmitters and makes the postsynaptic membrane generate an action potential.

IPSP: An IPSP is an electric charge on the postsynaptic membrane, which is caused by the binding of inhibitory neurotransmitters and makes the postsynaptic membrane less likely to generate an action potential.

EPSP: EPSP stands for Excitatory Postsynaptic Potential.

IPSP: IPSP stands for Inhibitory Postsynaptic Potential.


EPSP: EPSP is caused by the flow of positively-charged ions.

IPSP: IPSP is caused by the flow of negatively-charged ions.

Type of Polarization

EPSP: EPSP is a depolarization.

IPSP: IPSP is a hyperpolarization.

To the Threshold

EPSP: EPSP brings the postsynaptic membrane towards the threshold.

IPSP: IPSP takes the postsynaptic membrane away from the threshold.


EPSP: EPSP makes the postsynaptic membrane more excited.

IPSP: IPSP makes the postsynaptic membrane less excited.

Firing of an Action Potential

EPSP: EPSP facilitates the firing of an action potential on the postsynaptic membrane.

IPSP: IPSP lowers the firing of an action potential on the postsynaptic membrane.


EPSP: EPSP is the result of the opening of the sodium channels.

IPSP: IPSP is the result of the opening of the potassium or chloride channels.

Types of Ligands

EPSP: EPSP is generated by the flow of glutamate or aspartate ions.

IPSP: IPSP is generated by the flow of glycine or GABA.


EPSP and IPSP are the two types of electric charges found on the membrane of the postsynaptic nerve at the synapse. The EPSP is caused by the flow of positively-charged ions into the postsynaptic nerve whereas, the IPSP is caused by the flow of negatively-charged ions into the postsynaptic nerve. The EPSP facilitates the generation of an action potential on the postsynaptic membrane whereas the IPSP inhibit the generation of an action potential. The main difference between EPSP and IPSP is the effect of each type of electric charges on the postsynaptic membrane.


1. “Excitatory postsynaptic potential.” Wikipedia, Wikimedia Foundation, 31 Aug. 2017, Available here. 16 Sept. 2017.
2. “Inhibitory postsynaptic potential.” Wikipedia, Wikimedia Foundation, 30 Aug. 2017, Available here. 16 Sept. 2017.

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