Neuroscience Terms Starting With R
Neuroscience Glossary: R
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Reflex Arc
/ REE-fleks ark / · Latin reflexus (bent back) + arcus (bow, arch)
Reflex Arc is the neural pathway underlying an automatic, involuntary response to a stimulus, consisting minimally of a sensory receptor, an afferent neuron, an integration center, an efferent neuron, and an effector organ.
The simplest reflex arcs are monosynaptic, involving only one synapse between the sensory afferent and the motor efferent neuron, as in the patellar tendon reflex. Most reflexes involve polysynaptic arcs with one or more interneurons between afferent and efferent neurons, allowing multi-step processing and integration with other inputs. Spinal reflex arcs are processed in the spinal cord without requiring input from the brain, enabling faster responses than conscious reactions and freeing higher brain centers for other tasks.
The total conduction time for the patellar reflex is approximately 20 to 30 milliseconds, compared to 150 to 200 milliseconds for a voluntary reaction to the same stimulus.
Spinal reflexes can persist after complete spinal cord injury because the reflex arc circuitry remains intact below the injury level, even when voluntary control from the brain is fully disrupted. Clinicians use this preservation to distinguish upper motor neuron lesions, which typically produce exaggerated reflexes, from lower motor neuron lesions, which abolish them.
Fun Facts About the Nervous System →The reflex arc operates completely independently of the brain in normal function. Descending pathways from the brain continuously modulate the gain and threshold of spinal reflexes, which is why a relaxed muscle produces a brisker tendon jerk than a tense one.
Physicians tap the patellar tendon to test the monosynaptic stretch reflex arc, which travels through the L3 and L4 spinal segments. An absent or exaggerated response can localize pathology to 1 or 2 spinal segments, peripheral nerves, anterior horn cells, or descending motor pathways above that level.
How To Become A Neurologist? →Resting Potential
/ REST-ing poh-TEN-shul / · Old English raestian + Latin potentia (power)
Resting Potential is the stable negative electrical voltage across the neuronal membrane when the cell is not actively signaling, typically around negative 70 millivolts, maintained by ion concentration gradients and selective membrane permeability.
This voltage of approximately negative 70 millivolts arises from the sodium-potassium ATPase continuously pumping three sodium ions out while bringing two potassium ions in, combined with selective membrane permeability that strongly favors potassium over sodium at rest. Intracellular potassium concentration is about 140 millimolar while extracellular concentration is approximately 4 millimolar, a 35-fold gradient that drives outward potassium diffusion and leaves excess negative charge inside from non-permeable intracellular anions. The Goldman-Hodgkin-Katz equation quantitatively relates resting potential to the concentrations and membrane permeabilities of all relevant ions, predicting values close to those measured experimentally.
Rather than remaining perfectly static, the resting potential fluctuates slightly with spontaneous synaptic input and stochastic channel opening, reflecting ongoing cellular activity even in the absence of deliberate signaling.
Alan Hodgkin and Andrew Huxley first measured the resting potential of a squid giant axon (Loligo forbesi) directly in 1939 by inserting a fine electrode into the axon interior, recording a value of approximately negative 60 millivolts and providing the first direct experimental confirmation that a stable transmembrane voltage exists in living neurons.
The resting potential means the neuron is completely inactive between signals. The neuron continuously expends energy through the sodium-potassium pump and receives fluctuating synaptic inputs that cause small voltage changes even when no action potential is being generated.
Hyperkalemia, elevated blood potassium from kidney failure or certain medications, reduces the potassium concentration gradient across neuronal membranes, shifting the resting potential toward zero and making neurons abnormally excitable. Serum potassium above approximately 6.5 millimoles per liter can trigger cardiac arrhythmias by depolarizing cardiac pacemaker cells through exactly this mechanism.
Urinary System Fun Facts →Reuptake
/ ree-UP-tayk / · Latin re- (again) + Old English tacan (to take)
Reuptake is the process by which a presynaptic neuron recaptures released neurotransmitter molecules from the synaptic cleft through specific transporter proteins, terminating the synaptic signal and recycling neurotransmitter for future use.
Transporter proteins for dopamine, serotonin, norepinephrine, and GABA are embedded in the presynaptic membrane and use the inward sodium gradient to drive neurotransmitter back into the terminal against its concentration gradient. Reuptake is the primary mechanism for terminating the actions of monoamine neurotransmitters and is a major target of psychoactive drugs. Cocaine blocks the dopamine transporter and the norepinephrine transporter simultaneously, increasing dopamine and norepinephrine concentrations in the synapse and producing its stimulant and reinforcing effects.
Each transporter protein cycles through a conformational change that binds the neurotransmitter on the extracellular face and releases it intracellularly, completing one transport cycle in roughly 100 to 500 milliseconds.
The antidepressant fluoxetine selectively blocks the serotonin transporter, preventing serotonin reuptake and increasing serotonin concentration in limbic synapses, with therapeutic effects typically emerging after two to four weeks of continued use despite the transporter being blocked within hours of the first dose.
Reuptake is not the only mechanism for clearing neurotransmitters from the synapse. Enzymatic degradation by monoamine oxidase and catechol-O-methyltransferase provides a parallel clearing mechanism for monoamines, and acetylcholine is cleared primarily by enzymatic hydrolysis rather than reuptake at all.
Fun Facts About the Nervous System →Methamphetamine does not block the dopamine transporter the way cocaine does. Instead, it enters the presynaptic terminal through the dopamine transporter and causes reverse transport, producing extracellular dopamine elevations that can exceed baseline several-fold within minutes.