Accessible NIH institutional source: non-REM stages 1–3 and REM. NINDS primary page returned403; use this accessible source.

First page and abstract: arrhythmic, 19-hour and 28-hour mutants; eclosion and individual locomotion; constant-darkness tests.

Public-domain original essay; opening definition and case observations of involuntary movement, posture and gait.

Official institutional anatomy table; ciliary nerves and otic ganglion entries used for mixed-fiber pathways and synapse distinctions.

Robert S. Fisher and colleagues, Epilepsia 55(4), pp. 475–482. ILAE official report. The Summary distinguishes the enduring predisposition from the operational clinical criteria. Official primary PDF: www.ilae.org/guidelines/guidelines-and-reports/a-practical-clinical-definition-of-epilepsy

Thiamin deficiency and Wernicke-Korsakoff syndrome. No dosing or treatment recommendations are reproduced.

Definitions of oppositional defiant disorder and conduct disorder; distinction from occasional developmentally expected behavior.

What is generalized anxiety disorder?; signs and symptoms; diagnosis. No treatment instructions are reproduced.

Opening description of impaired control, functional effects and co-occurring disorders.

Definitions: death, nonfatal attempt and suicidal ideation are distinct outcomes; no prevalence values are imported.

Monocular deprivation is an experimental reduction of normal patterned vision through one eye while the other remains available. It is used to investigate how sensory experience shapes a developing nervous system. In classic cat experiments, researchers closed the eyelids of one eye for a stated interval, then reopened it and compared what the animal could do through each eye.^[ref]

P. B. Dews and colleagues varied both the starting age and duration of deprivation, testing the cats when they were at least a year old. Closure during the first four to six weeks left a lasting reduction in visual acuity. Longer early closure could also impair visually guided paw placement and pattern discrimination. Deprivation beginning at four months or later produced no lasting deficit detectable by their behavioural tests. The comparison identifies a critical period of heightened susceptibility in this species and experimental setting; it does not mean that all forms of adult neuroplasticity disappear.^[ref]

An illuminating feature of the design is its separation of when experience is lost from how long it is lost. A weak response immediately after opening an eye would not alone demonstrate a lasting developmental change; delayed testing and comparison with the other eye make that inference stronger.

A critical period in neural development is a bounded interval in which particular experiences have a strong role in establishing a specified function or circuit organization. Its timing must be stated for a species and a measured outcome. A sensitive period emphasizes heightened susceptibility without necessarily asserting that every later change is impossible.

A classic example comes from monocular deprivation in cats. P. B. Dews and colleagues closed one eye at different ages and for different durations, then compared vision through the two eyes when the animals were at least a year old. Starting deprivation at one month offered little protection against lasting impairment; starting at two months reduced the impairment, and starting at four months or later produced no lasting deficit detectable in their behavioural tests. The age comparison revealed a developmental window rather than merely a short-lived effect of having an eye closed.^[ref]

The design separates age at disruption, duration of disruption, and the function tested. A change in visual acuity and a change in the responses of visual cortex neurons need not have identical recovery profiles. The existence of a critical period for one visual measure does not establish a single deadline for the entire brain, or the absence of adult neuroplasticity.^[ref]

Microtubule-associated protein 2, commonly called MAP2, is a neuronal protein associated with microtubules and strongly enriched in many dendrites. It contributes to organization of the dendritic cytoskeleton. Enrichment makes it useful as an experimental marker, but marker abundance and the full functional identity of a cell compartment are different properties. ^[ref]

In cultured hippocampal neurons, MAP2 immunostaining helped confirm dendritic identity after processes had been followed through development. ^[ref] Combining time-resolved shape changes with a molecular marker is more informative than calling every short process a dendrite. Developmental stage, isoform and preparation conditions also matter when interpreting staining.

An interneuron is a neuron acting within a neural circuit to connect and transform signals between other neurons. Many interneurons have local connections, although the category is defined functionally and includes diverse cell types. An interneuron is not automatically inhibitory: excitatory and inhibitory signalling depend on transmitter, receptor and cellular context. ^[ref]

In a reflex circuit, an inhibitory interneuron can couple activation of one motor pathway to suppression of an opposing one. This gives a concrete computational function: the circuit coordinates two outputs instead of simply forwarding a sensory signal unchanged. Recording one interneuron's activity establishes participation, while changing that activity and measuring the circuit response tests its causal contribution.

A motor neuron is a neuron whose output drives or regulates an effector, commonly muscle. A somatic motor neuron carries action potentials along its axon to a neuromuscular junction, where release of acetylcholine promotes excitation of a muscle fibre. Neural excitation, transmitter release and muscle force are successive steps. ^[ref]

A reflex illustrates the distinction between a sensory input and a motor output: a circuit converts an incoming signal into activity of an efferent neuron. The number and timing of motor-neuron impulses can change force without changing the identity of the contacted muscle. Clinical distinctions between upper and lower motor neurons refer to different positions in a motor pathway, so not every neuron involved in motor control directly innervates muscle.

A sensory neuron carries information about a stimulus toward the central nervous system. Its input can concern the external world or the body's own state. For example, stretching a muscle spindle changes the activity of a sensory neuron; the resulting action potentials help the spinal cord regulate muscle activity through a reflex.^[ref]

Many sensory neurons supplying the body have their soma in a dorsal root ganglion and a branching axon with peripheral and central processes. Thus the soma is not simply an obligatory relay between an input dendrite and an output axon. Other sensory pathways use different arrangements; a sensory function does not specify one universal neuron shape.^[ref]