Bernard Katz was an influential biophysicist whose pioneering work advanced the understanding of how nerve cells communicate. He received the Nobel Prize in Physiology or Medicine in 1970 for his groundbreaking discoveries concerning synaptic transmission. His research illuminated the fundamental processes by which nerve signals are transmitted, shaping the field of neuroscience.
Early Life and Scientific Journey
Bernard Katz was born in Leipzig, Germany, in 1911, into a Jewish family. He pursued his medical education at the University of Leipzig from 1929 to 1934. After completing his medical degree, he left Germany in 1935, seeking refuge from Nazi persecution. He then moved to England and joined University College London (UCL), working under the mentorship of A.V. Hill, a Nobel laureate. Katz earned his Ph.D. in 1938 and received a Carnegie Fellowship, which took him to Australia to collaborate with John Eccles at the Kanematsu Memorial Institute in Sydney.
During his time in Australia, Katz became a naturalized British citizen in 1941 and served as a radar officer in the Royal Australian Air Force throughout World War II. Following the war, he returned to UCL in 1946, resuming his research on the mechanisms of nerve communication. He was appointed Professor of Biophysics and Head of the Biophysics Department at UCL in 1952.
Unraveling Synaptic Communication
Katz’s work focused on the neuromuscular junction, a specialized synapse where a motor neuron transmits signals to a muscle fiber. Working primarily with frog muscle, Katz and his colleagues studied the electrical events at this junction. They observed that when a presynaptic motor neuron was stimulated, it caused a measurable depolarization of the postsynaptic muscle cell membrane, termed the end-plate potential (EPP). This EPP was strong enough to trigger an action potential in the muscle fiber.
Katz and Paul Fatt discovered miniature end-plate potentials (MEPPs) in 1951. These were small, spontaneous depolarizations of the muscle cell membrane that occurred even in the absence of any deliberate stimulation from the presynaptic motor neuron. While EPPs could be as large as 40 to 50 millivolts, MEPPs were considerably smaller, usually less than 1 millivolt in amplitude. Despite their size difference, both EPPs and MEPPs shared similar characteristics, including their sensitivity to drugs that block acetylcholine receptors.
Based on these observations, Katz proposed the “quantal hypothesis” in 1952, which changed understanding of neurotransmitter release. This hypothesis posited that neurotransmitters, rather than being released in a continuous flow, are discharged in discrete packets, or “quanta.” Each MEPP was interpreted as the postsynaptic response to the release of a single quantum of acetylcholine (ACh), the neurotransmitter at the neuromuscular junction. A full EPP, therefore, resulted from the synchronous release of multiple such quanta.
Further experiments by del Castillo and Katz in 1952 demonstrated the role of calcium ions in neurotransmitter release. They found that altering the concentration of calcium in the extracellular fluid affected the size of evoked EPPs but did not change the amplitude of individual MEPPs. This indicated that calcium influx into the presynaptic terminal controls the probability of quantum release, rather than the amount of neurotransmitter within each quantum. Subsequent ultrastructural studies provided physical evidence for this quantal release, showing that neurotransmitters are stored in membrane-bound sacs called synaptic vesicles within nerve terminals, which then fuse with the presynaptic membrane to release their contents.
The Enduring Influence of His Work
Katz’s discoveries provided a framework for understanding synaptic transmission, particularly at the neuromuscular junction. His insight that neurotransmitters are released in discrete quanta changed neurophysiology. This mechanism of nerve cell communication applies broadly to synapses throughout the central nervous system.
Understanding neurotransmitter release, including acetylcholine and calcium’s roles, has had broad implications. This knowledge helps elucidate causes and progression of neurological disorders, especially those affecting nerve-muscle communication. By clarifying the molecular basis of nerve signal transmission, Katz’s work paved the way for new pharmacological agents. These drugs can target neurotransmitter system components, aiding treatment for nervous and mental disturbances.
Beyond direct medical applications, his research also contributed to understanding the effects of substances like organophosphates, used in pesticides and nerve agents, by revealing how easily the complex enzyme cycles involved in neurotransmission could be disrupted. Katz’s experimental approach and enduring hypotheses inspire neurophysiologists. His legacy is recognized through distinctions such as the Bernard Katz Award, established in 1991 by the Biophysical Society, which celebrates significant scientific contributions in biophysics.