Sensory Receptors, Neuronal Circuits for Processing Information

Our ability to perceive both internal bodily signals and the external world relies on a sophisticated system of sensory receptors. These receptors are specialized to detect various stimuli, including touch, sound, light, pain, cold, and warmth. This chapter delves into the fundamental mechanisms by which these sensory stimuli are converted into nerve signals, which are then transmitted to and processed within the central nervous system (CNS).

Types of Sensory Receptors and the Stimuli They Detect

Sensory receptors are broadly classified into five basic types, each designed to detect specific forms of stimuli. This classification is crucial for understanding how the nervous system gathers information from the environment and the body.

Classification of Sensory Receptors

The following table, adapted from the source material, provides a comprehensive classification of sensory receptors based on the stimuli they detect and their anatomical locations:

I. Mechanoreceptors: These receptors detect mechanical compression or stretching of the receptor itself or adjacent tissues.
- Skin Tactile Sensibilities (Epidermis and Dermis):
  - Free nerve endings
  - Expanded tip endings: Merkel's discs, plus several other variants
  - Spray endings: Ruffini's endings
  - Encapsulated endings: Meissner's corpuscles, Krause's corpuscles
  - Hair end-organs
- Deep Tissue Sensibilities:
  - Free nerve endings
  - Expanded tip endings
  - Spray endings: Ruffini's endings
  - Encapsulated endings: Pacinian corpuscles, plus a few other variants
  - Muscle endings: Muscle spindles, Golgi tendon receptors
- Hearing: Sound receptors of the cochlea
- Equilibrium: Vestibular receptors
- Arterial Pressure: Baroreceptors of carotid sinuses and aorta
II. Thermoreceptors: These receptors detect changes in temperature.
- Cold receptors
- Warm receptors
III. Nociceptors (Pain Receptors): These receptors detect physical or chemical damage occurring in the tissues.
- Free nerve endings
IV. Electromagnetic Receptors: These receptors detect light.
- Vision: Rods, Cones
V. Chemoreceptors: These receptors detect chemical changes.
- Taste: Receptors of taste buds
- Smell: Receptors of olfactory epithelium
- Arterial Oxygen: Receptors of aortic and carotid bodies
- Osmolality: Neurons in or near supraoptic nuclei
- Blood CO₂: Receptors in or on the surface of the medulla and in aortic and carotid bodies
- Blood Glucose, Amino Acids, Fatty Acids: Receptors in the hypothalamus

The chapter primarily focuses on the function of peripheral mechanoreceptors to illustrate the general principles of receptor operation. Visual representations of several somatic sensory nerve endings, such as free nerve endings, expanded tip receptors, tactile hairs, Pacinian corpuscles, Meissner's corpuscles, Krause's corpuscles, Ruffini's endings, Golgi tendon apparatus, and muscle spindles, are provided in the source material to aid understanding.

Differential Sensitivity and Modality of Sensation

A fundamental characteristic of sensory receptors is their differential sensitivity. This means that each receptor type is exquisitely sensitive to the specific type of stimulus it is designed to detect, while being almost entirely unresponsive to other forms of stimuli.

Examples of Differential Sensitivity

Rods and Cones of the Eyes: Highly responsive to light, but virtually nonresponsive to normal ranges of heat, cold, pressure on the eyeballs, or chemical changes in the blood.
Osmoreceptors of the Hypothalamus: Detect minute changes in body fluid osmolality but do not respond to sound.
Pain Receptors in the Skin: Almost never stimulated by ordinary touch or pressure, but become highly active when tactile stimuli are severe enough to cause tissue damage.

Modality of Sensation—The "Labeled Line" Principle

Despite the diverse modalities of sensation we experience (e.g., pain, touch, sight, sound), nerve fibers transmit only electrical impulses. The nervous system distinguishes between these modalities through a principle known as the "labeled line principle."

This principle states that each specific type of sensation we perceive is determined by the particular point in the central nervous system where the nerve tract terminates. Regardless of how a nerve fiber is stimulated, the sensation perceived will always correspond to the specific modality associated with its CNS termination point.

Pain Fibers: If a pain fiber is stimulated, the person perceives pain, whether the stimulus is electricity, overheating, crushing of the fiber, or damage to tissue cells at the nerve ending.
Touch Fibers: Stimulation of a touch fiber, by any means, results in the perception of touch because these fibers lead to specific touch areas in the brain.
Sensory Pathways: Fibers from the retina terminate in the vision areas of the brain, fibers from the ear terminate in the auditory areas, and temperature fibers terminate in the temperature areas.

This inherent specificity of nerve fibers for transmitting only one modality of sensation is the essence of the labeled line principle.

Transduction of Sensory Stimuli into Nerve Impulses

All sensory receptors share a common initial response to a stimulus: a change in their membrane electrical potential. This change is termed a receptor potential.

Mechanisms of Receptor Potentials

Receptor potentials can be generated through several distinct mechanisms, generally corresponding to the different types of sensory receptors:

Mechanical Deformation: Stretching the receptor membrane, which opens ion channels.
Application of a Chemical: Chemicals binding to the membrane, which also opens ion channels.
Change in Temperature: Altering the permeability of the membrane.
Electromagnetic Radiation: Such as light acting on retinal visual receptors, which directly or indirectly changes membrane characteristics, allowing ions to flow through channels.

In all these instances, the fundamental cause of the change in membrane potential is an alteration in membrane permeability, which allows ions to diffuse more or less readily across the membrane, thereby changing the transmembrane potential.

Maximum Receptor Potential Amplitude

The maximum amplitude of most sensory receptor potentials is approximately 100 millivolts. This level is achieved only with extremely high-intensity sensory stimuli. This amplitude is comparable to the maximum voltage recorded in action potentials and represents the voltage change when the membrane becomes maximally permeable to sodium ions.

Relation of the Receptor Potential to Action Potentials

When the receptor potential rises above a specific threshold for eliciting action potentials in the nerve fiber attached to the receptor, action potentials are generated. The relationship is such that the greater the receptor potential rises above the threshold level, the higher the frequency of action potentials generated. This is illustrated by a typical graph showing membrane potential over time, where a rising receptor potential eventually crosses a threshold, leading to a series of action potentials.

Receptor Potential of the Pacinian Corpuscle: A Detailed Example

The Pacinian corpuscle serves as an excellent model for understanding receptor function due to its well-defined structure and mechanism of action.

Structure of the Pacinian Corpuscle

As depicted in the source material's figures, the Pacinian corpuscle features a central nerve fiber extending through its core. This central fiber is surrounded by multiple concentric capsule layers. Compression applied anywhere on the outside of the corpuscle will deform this central fiber.

The tip of the central fiber inside the capsule is unmyelinated, but the fiber becomes myelinated (indicated by a blue sheath in diagrams) shortly before it exits the corpuscle to join a peripheral sensory nerve.

Mechanism of Receptor Potential Production

When the Pacinian corpuscle is compressed, a small area of the terminal fiber within the corpuscle is deformed. This deformation causes ion channels in the membrane of the terminal fiber to open, allowing positively charged sodium ions to diffuse into the fiber's interior. This influx of positive charge creates an increased positivity inside the fiber, which is the receptor potential.

This receptor potential, in turn, generates a local circuit of current flow that spreads along the nerve fiber. At the first node of Ranvier, which is located inside the capsule, this local current flow depolarizes the fiber membrane. If this depolarization reaches the threshold, it triggers typical action potentials that are then transmitted along the myelinated nerve fiber towards the central nervous system.

Relation between Stimulus Intensity and the Receptor Potential

Experimental studies on the Pacinian corpuscle, involving progressively stronger mechanical compression, demonstrate a specific relationship between stimulus strength and receptor potential amplitude. The amplitude of the receptor potential increases rapidly at low stimulus strengths but then progressively less rapidly at high stimulus strengths. This characteristic is crucial because it allows the receptor to be highly sensitive to very weak sensory experiences while also having an extensive range of response, preventing it from reaching a maximum firing rate until the sensory experience is extreme.

In parallel, the frequency of repetitive action potentials transmitted from sensory receptors increases approximately in proportion to the increase in receptor potential. Combining these principles, very intense stimulation of a receptor causes progressively smaller additional increases in action potential frequency. This mechanism is applicable to almost all sensory receptors, enabling them to respond across a wide range of stimulus intensities.

Adaptation of Receptors

A universal characteristic of all sensory receptors is their ability to adapt, either partially or completely, to a constant stimulus over a period of time. When a continuous sensory stimulus is applied, the receptor initially responds at a high impulse rate, which then progressively slows down until the rate of action potentials decreases to very few or often none at all.

Rates of Adaptation

Receptors exhibit varying rates of adaptation:

Rapid Adaptation:
- Pacinian Corpuscle: Adapts very rapidly, to "extinction" within a few hundredths of a second.
- Hair Receptors: Adapt within a second or so.
Slow Adaptation ("Nonadapting" or "Tonic" Receptors):
- Joint Capsule and Muscle Spindle Receptors: Adapt slowly, requiring hours or days to adapt completely.
- Carotid and Aortic Baroreceptors: Can take up to 2 days to adapt, though some physiologists believe they never fully adapt.
- Chemoreceptors and Pain Receptors: Probably never adapt completely.

The source illustrates these differences with a graph showing impulses per second over time for hair receptors, Pacinian corpuscles, muscle spindles, and joint capsule receptors, clearly demonstrating the rapid decline in firing rate for fast-adapting receptors and the sustained firing for slow-adapting ones.

Mechanisms of Receptor Adaptation

The mechanism of adaptation varies among receptor types:

Eye (Rods and Cones): Adapt by changing the concentrations of their light-sensitive chemicals.
Mechanoreceptors (e.g., Pacinian Corpuscle): Adaptation occurs through two primary mechanisms:
1. Viscoelastic Structure: The Pacinian corpuscle is a viscoelastic structure. When a distorting force is suddenly applied, it is instantly transmitted to the central nerve fiber, eliciting a receptor potential. However, within a few hundredths of a second, the fluid within the corpuscle redistributes, and the receptor potential is no longer elicited, even if the compression continues. This accounts for the rapid adaptation.
2. Accommodation: A slower mechanism involves the nerve fiber itself. Even if the central core fiber remains distorted, the tip of the nerve fiber gradually "accommodates" to the stimulus. This is likely due to the progressive "inactivation" of sodium channels in the nerve fiber membrane, meaning that sodium current flow through these channels gradually ceases. This effect is thought to occur for most cell membrane sodium channels.
These two general mechanisms—structural readjustments in the receptor and electrical accommodation in the terminal nerve fibril—are presumed to apply to other types of mechanoreceptors as well.

Slowly Adapting Receptors: "Tonic" Receptors

Slowly adapting receptors, also known as tonic receptors, continue to transmit impulses to the brain as long as the stimulus is present, often for many minutes or hours. They are crucial for keeping the brain continuously informed about the status of the body and its relationship to its surroundings.

Examples: Receptors of the macula in the vestibular apparatus (for balance), pain receptors, baroreceptors of the arterial tree, and chemoreceptors of the carotid and aortic bodies.

Rapidly Adapting Receptors: "Rate," "Movement," or "Phasic" Receptors

Rapidly adapting receptors, also called rate receptors, movement receptors, or phasic receptors, cannot transmit a continuous signal. Instead, they are stimulated only when the stimulus strength changes, reacting strongly during the change itself. They are essential for detecting rapid changes in tissue deformation but are ineffective for conveying information about constant conditions.

Example: The Pacinian corpuscle excites for a few milliseconds when sudden pressure is applied and again when the pressure is released.

Predictive Function of Rate Receptors

Rate receptors play a vital predictive role. By detecting the rate at which bodily changes occur, the nervous system can anticipate future states and make necessary adjustments.

Semicircular Canals: Receptors in the vestibular apparatus detect the rate of head turning, allowing a person to predict future turns and adjust leg motion to maintain balance.
Joint Rate Receptors: Detect rates of movement of body parts, enabling the nervous system to predict limb positions during activities like running, facilitating anticipatory motor corrections. Loss of this function can severely impair complex movements like running.

Nerve Fiber Classification and Signal Transmission Speed

The nervous system transmits various types of signals, some requiring extremely rapid transmission (e.g., leg position during running) and others tolerating slower transmission (e.g., prolonged aching pain).

Nerve Fiber Characteristics

Nerve fibers vary significantly in diameter, which directly correlates with their conduction velocity. Larger diameter fibers conduct impulses at greater speeds. Conduction velocities range from 0.5 to 120 meters per second.

A detailed diagram in the source material illustrates the physiological classifications and functions of nerve fibers, showing their diameter, conduction velocity, and associated sensory and motor functions.

General Classification of Nerve Fibers

Nerve fibers are broadly divided into two main types:

Type A Fibers: These are typical large and medium-sized myelinated fibers found in spinal nerves. They are further subdivided into α, β, γ, and δ fibers.
Type C Fibers: These are small, unmyelinated nerve fibers that conduct impulses at low velocities. Type C fibers constitute over half of the sensory fibers in most peripheral nerves and include all postganglionic autonomic fibers.

The diagram provides specific details for each subtype, including their diameter, conduction velocity, and associated sensory functions (e.g., muscle spindle primary/secondary endings, hair receptors, vibration, high discrimination touch, deep pressure, pricking pain, crude touch, tickle, aching pain, cold, warmth) and motor functions (e.g., skeletal muscle type Aα, muscle spindle type Aγ, sympathetic type C).

Large myelinated fibers can transmit impulses at velocities up to 120 m/sec, covering a distance longer than a football field in 1 second.
The smallest fibers transmit impulses as slowly as 0.5 m/sec, taking about 2 seconds to travel from the big toe to the spinal cord.

Alternative Classification Used by Sensory Physiologists

Due to challenges in distinguishing certain fiber types with recording techniques, sensory physiologists often use an alternative classification:

Group Ia Fibers: Originate from the annulospiral endings of muscle spindles. They average about 17 micrometers in diameter and are classified as Aα-type A fibers.
Group Ib Fibers: Originate from Golgi tendon organs. They average about 16 micrometers in diameter and are also Aα-type A fibers.
Group II Fibers: Originate from most discrete cutaneous tactile receptors and the flower-spray endings of muscle spindles. They average about 8 micrometers in diameter and are classified as Aβ- and Aγ-type A fibers.
Group III Fibers: Carry temperature, crude touch, and pricking pain sensations. They average about 3 micrometers in diameter and are classified as Aδ-type A fibers.
Group IV Fibers: Unmyelinated fibers carrying pain, itch, temperature, and crude touch sensations. They range from 0.5 to 2 micrometers in diameter and are classified as C fibers.

Transmission of Signal Intensity: Spatial and Temporal Summation

The intensity of a signal, such as the intensity of pain, must be conveyed to the central nervous system. This is achieved through two primary mechanisms: spatial summation and temporal summation.

Spatial Summation

Spatial summation involves transmitting increasing signal strength by activating a progressively greater number of parallel nerve fibers. The source illustrates this phenomenon using pain fibers innervating a section of skin.

Receptor Field: Each pain fiber arborizes into hundreds of minute free nerve endings, covering an area of skin up to 5 centimeters in diameter. The density of these endings is highest in the center of the field and diminishes towards the periphery.
Overlap: The arborizing fibrils from different pain fibers often overlap.
Stimulation Pattern: A pinprick typically stimulates endings from many different pain fibers simultaneously. A pinprick in the center of a fiber's receptive field causes a greater degree of stimulation for that fiber due to the higher density of nerve endings.
Signal Spread: A weak stimulus might only strongly stimulate a single nerve fiber in the center of a nerve bundle, with several adjacent fibers weakly stimulated. As the stimulus becomes moderate or strong, progressively more nerve fibers are stimulated, and the signal spreads to a larger number of fibers. This process effectively conveys increasing signal strength.

Temporal Summation

Temporal summation is the second mechanism for transmitting signals of increasing strength. It involves increasing the frequency of nerve impulses transmitted along a single nerve fiber. The source provides a diagram showing how a changing signal strength (represented by a continuous curve) is translated into a frequency-modulated series of discrete nerve impulses, where higher signal strength corresponds to a higher frequency of impulses.

Transmission and Processing of Signals in Neuronal Pools

The central nervous system (CNS) is organized into thousands to millions of neuronal pools, which can range from a few neurons to vast numbers (e.g., the entire cerebral cortex). Other examples include the basal ganglia, thalamus, cerebellum, mesencephalon, pons, medulla, and the dorsal gray matter of the spinal cord.

Each neuronal pool possesses a unique organization that allows it to process signals in its own distinct way, contributing to the multitude of functions of the nervous system. Despite their functional differences, these pools share many similar principles of operation.

Relaying of Signals Through Neuronal Pools: Excitation, Facilitation, and Inhibition

Organization of Neurons for Relaying Signals

A schematic diagram of a neuronal pool shows input fibers on the left and output fibers on the right. Each input fiber typically divides hundreds to thousands of times, providing numerous terminal fibrils that spread into a large area within the pool. These terminals synapse with the dendrites or cell bodies of the neurons in the pool. The dendrites themselves also arborize extensively.

The area of neurons stimulated by an incoming nerve fiber is called its stimulatory field. The highest concentration of terminals from an input fiber is on the nearest neurons in its field, with progressively fewer terminals on neurons farther away.

Threshold and Subthreshold Stimuli—Excitation or Facilitation

A single excitatory presynaptic terminal typically does not cause an action potential in a postsynaptic neuron. Instead, a large number of input terminals must discharge on the same neuron, either simultaneously or in rapid succession, to cause excitation.

Excitatory (Suprathreshold) Stimulus: An input fiber provides enough terminals to cause a neuron to discharge. The stimulus to this neuron is considered excitatory or suprathreshold because it exceeds the threshold required for excitation.
Subthreshold (Facilitating) Stimulus: An input fiber may contribute terminals to other neurons, but not enough to cause their excitation. However, the discharge of these terminals makes these neurons more likely to be excited by signals from other incoming nerve fibers. These stimuli are considered subthreshold, and the neurons are said to be facilitated.

In a more realistic representation of a neuronal pool, each input nerve fiber provides massive numbers of branching terminals to hundreds or thousands of neurons in its distribution field. The central portion of this field, where all neurons are stimulated by the incoming fiber, is called the discharge zone (or excited zone or liminal zone). The areas to each side, where neurons are facilitated but not excited, are called the facilitated zone (or subthreshold zone or subliminal zone).

Inhibition of a Neuronal Pool

Some incoming nerve fibers can inhibit neurons rather than exciting them. This mechanism is the opposite of facilitation. The entire field of inhibitory branches is called the inhibitory zone. The degree of inhibition is greatest in the center of this zone due to the large number of endings and progressively decreases towards its edges.

Divergence of Signals Passing Through Neuronal Pools

Divergence is a phenomenon where a weak signal entering a neuronal pool excites a far greater number of nerve fibers leaving the pool. This serves two distinct purposes:

Amplifying Type of Divergence: An input signal spreads to an increasing number of neurons as it passes through successive orders of neurons in its pathway. This type of divergence is characteristic of the corticospinal pathway, where a single large pyramidal cell in the motor cortex can excite as many as 10,000 muscle fibers under highly facilitated conditions.
Divergence into Multiple Tracts: The signal is transmitted in two directions from the pool to separate areas. For example, information transmitted up the dorsal columns of the spinal cord takes two courses in the lower part of the brain: one to the cerebellum and another through the lower regions of the brain to the thalamus and cerebral cortex. Similarly, in the thalamus, sensory information is relayed to both deeper structures of the thalamus and discrete regions of the cerebral cortex.

Diagrams illustrate these two types: divergence within the same tract (amplification) and divergence into multiple tracts.

Convergence of Signals in Neuronal Pools

Convergence refers to the phenomenon where signals from multiple inputs unite to excite a single neuron. This is crucial because a single action potential from one input terminal almost never excites a neuron. Instead, action potentials converging on the neuron from multiple terminals provide enough spatial summation to bring the neuron to the threshold for discharge.

Convergence can occur in two ways:

Convergence from a Single Source: Multiple terminals from a single incoming fiber tract terminate on the same neuron.
Convergence from Multiple Separate Sources: Input signals (excitatory or inhibitory) from various sources converge onto a single neuron. For instance, interneurons of the spinal cord receive converging signals from peripheral nerve fibers, propriospinal fibers (from other cord segments), corticospinal fibers (from the cerebral cortex), and other long pathways descending from the brain. These signals then converge on anterior motor neurons to control muscle function.

Convergence allows for the summation of information from different sources, resulting in a summated effect of all the different types of information. It is a vital mechanism by which the central nervous system correlates, summates, and sorts diverse information.

Neuronal Circuits with Both Excitatory and Inhibitory Output Signals

In some neuronal pools, an incoming signal can simultaneously cause an excitatory output signal in one direction and an inhibitory signal elsewhere. This type of circuit is known as a reciprocal inhibition circuit.

A classic example is the control of antagonistic muscle pairs: an excitatory signal transmitted to one set of neurons causes forward movement of a leg, while an inhibitory signal is transmitted through a separate set of neurons to inhibit the muscles on the back of the leg, preventing them from opposing the forward movement. This circuit is essential for coordinating all antagonistic muscle pairs and is also important in preventing overactivity in various parts of the brain.

The mechanism involves the input fiber directly exciting the excitatory output pathway, but also stimulating an intermediate inhibitory neuron. This inhibitory neuron then secretes a different type of transmitter substance to inhibit the second output pathway from the pool.

Prolongation of a Signal by a Neuronal Pool—"Afterdischarge"

In many instances, a signal entering a neuronal pool can cause a prolonged output discharge, known as afterdischarge, which can last from a few milliseconds to many minutes after the original input signal has ceased. This phenomenon is primarily achieved through two mechanisms:

Synaptic Afterdischarge

When excitatory synapses discharge on the dendrites or soma of a neuron, a postsynaptic electrical potential develops. This potential can last for many milliseconds, especially when long-acting synaptic transmitter substances are involved. As long as this potential persists, it can continue to excite the neuron, causing it to transmit a continuous train of output impulses. Thus, a single instantaneous input signal can result in a sustained signal output (a series of repetitive discharges) lasting for many milliseconds.

Reverberatory (Oscillatory) Circuit as a Cause of Signal Prolongation

One of the most important circuits in the nervous system for signal prolongation is the reverberatory or oscillatory circuit. These circuits are characterized by positive feedback, where the neuronal circuit feeds back to re-excite its own input. Once stimulated, the circuit can discharge repetitively for an extended period.

Several varieties of reverberatory circuits exist, ranging in complexity:

Simplest Circuit: Involves a single neuron where the output neuron sends a collateral nerve fiber back to its own dendrites or soma to restimulate itself. Theoretically, this feedback could sustain discharge for a protracted time.
More Complex Circuits: Involve a few additional neurons in the feedback circuit, introducing a longer delay between the initial discharge and the feedback signal.
Highly Complex Systems: Incorporate both facilitatory and inhibitory fibers impinging on the reverberating circuit. A facilitatory signal enhances the intensity and frequency of reverberation, while an inhibitory signal depresses or stops it.
Parallel Fiber Pathways: Most reverberating pathways consist of many parallel fibers, with terminal fibrils spreading widely at each cell station. The total reverberating signal strength depends on the number of parallel nerve fibers momentarily involved.

Characteristics of Signal Prolongation From a Reverberatory Circuit

The output signals from a typical reverberatory circuit exhibit a characteristic pattern: an input stimulus lasting only a millisecond or so can produce an output lasting for many milliseconds or even minutes. The intensity of the output signal usually increases to a high value early in reverberation, then decreases to a critical point, at which it suddenly ceases entirely. This cessation is primarily caused by fatigue of synaptic junctions in the circuit, which lowers the stimulation of the next neuron below the threshold level, breaking the feedback loop.

The duration of the total signal before cessation can also be controlled by facilitatory or inhibitory signals from other parts of the brain. These patterns are observed in physiological responses, such as the motor nerves exciting a muscle during a flexor reflex after pain stimulation of the foot.

Continuous Signal Output from Neuronal Circuits

Some neuronal circuits are capable of emitting output signals continuously, even without excitatory input signals. This continuous output can arise from two main mechanisms:

Continuous Discharge Caused by Intrinsic Neuronal Excitability

Neurons, like other excitable tissues, can discharge repetitively if their excitatory membrane potential rises above a certain threshold. Many neurons, particularly in the cerebellum and the interneurons of the spinal cord, normally maintain membrane potentials high enough to emit impulses continually. Excitatory signals can increase their firing rate, while inhibitory signals can decrease it, potentially to zero.

Continuous Signals Emitted from Reverberating Circuits as a Means for Transmitting Information

A reverberating circuit that does not fatigue sufficiently to stop reverberation can serve as a source of continuous impulses. Excitatory impulses entering such a pool can increase the output signal, while inhibitory impulses can decrease or even extinguish it. This mechanism functions as a "carrier wave" type of information transmission, similar to radio transmitters. The excitatory and inhibitory control signals do not cause the output signal but modulate its changing level of intensity. This system allows for both increases and decreases in signal intensity, providing both positive and negative information. It is utilized by the autonomic nervous system to control functions such as vascular tone, gut tone, degree of iris constriction, and heart rate, where nerve excitatory signals can be increased or decreased by accessory input signals into the reverberating neuronal pathway.

Rhythmical Signal Output

Many neuronal circuits generate rhythmical output signals. A prominent example is the rhythmical respiratory signal originating in the respiratory centers of the medulla and pons, which continues throughout life. Other rhythmical signals, such as those for scratching movements or walking, require input stimuli to initiate them.

Almost all experimentally studied rhythmical signals are found to result from reverberating circuits or a succession of sequential reverberating circuits that feed excitatory or inhibitory signals in a circular pathway from one neuronal pool to the next. Excitatory or inhibitory signals can also modulate the amplitude of the rhythmical signal output. For instance, stimulation of the carotid body due to arterial oxygen deficiency increases both the frequency and amplitude of the respiratory rhythmical output signal.

Instability and Stability of Neuronal Circuits

The extensive interconnectedness of the brain poses a significant challenge: an excitatory signal entering any part of the brain could potentially trigger a continuous, uncontrolled cycle of re-excitation throughout all parts, leading to a mass of uncontrolled reverberating signals that would consume brain circuits and prevent informational signals from being transmitted (esimilar to epileptic seizures). The central nervous system prevents this instability through two basic mechanisms:

Inhibitory Circuits as a Mechanism for Stabilizing Nervous System Function

Two types of inhibitory circuits are widespread in the brain to prevent excessive signal spread:

Inhibitory Feedback Circuits: These circuits return from the termini of pathways back to the initial excitatory neurons of the same pathways. They are present in virtually all sensory nervous pathways and inhibit either the input neurons or intermediate neurons when the termini become overly excited.
Gross Inhibitory Control: Some neuronal pools exert broad inhibitory control over widespread areas of the brain. For example, many basal ganglia neurons exert inhibitory influences throughout the muscle control system.

Synaptic Fatigue as a Means of Stabilizing the Nervous System

Synaptic fatigue refers to the progressive weakening of synaptic transmission with prolonged and intense excitation. This mechanism helps stabilize the nervous system. For instance, successive flexor reflexes elicited by pain stimulation show progressively decremental contraction strength due to fatigue of synapses in the reflex circuit. Shorter intervals between reflexes lead to less intense subsequent responses.

Automatic Short-Term Adjustment of Pathway Sensitivity by the Fatigue Mechanism

This phenomenon allows for automatic short-term adjustment of pathway sensitivity. Overused pathways become fatigued, decreasing their sensitivity, while underused pathways rest and increase their sensitivity. This continuous process of fatigue and recovery moderates the sensitivities of different nervous system circuits, ensuring they operate within an effective range.

Long-Term Changes in Synaptic Sensitivity Caused by Automatic Down-Regulation or Up-Regulation of Synaptic Receptors

Beyond short-term fatigue, the long-term sensitivities of synapses can be dramatically altered through the up-regulation or down-regulation of synaptic receptors.

Mechanism: Receptor proteins are continuously formed by the endoplasmic reticular-Golgi apparatus system and inserted into the synaptic membrane of the receptor neuron.
Down-Regulation: When synapses are overused, an excess of transmitter substance combines with receptor proteins, leading to the inactivation and removal of many receptors from the synaptic membrane. This reduces sensitivity.
Up-Regulation: Conversely, underactivity leads to an increase in available receptor proteins, enhancing sensitivity.

These automatic control mechanisms continually adjust the sensitivity in each circuit to the precise level required for proper function. This is crucial for preventing severe neurological disorders such as continuous muscle cramps, seizures, psychotic disturbances, hallucinations, or mental tension that could arise from abnormally high sensitivities, or depression from abnormally low sensitivities. The automatic controls ensure that circuit sensitivities are readjusted back to controllable ranges of reactivity.

Sensory Receptors and Neuronal Circuits for Processing Information

Sensory Receptors and Neuronal Circuits for Processing Information