NOTES TO CHAPTER 1 135looking at similar tissue, he saw something different (DeFelipe 2006; Shepard
1991).
3 For example, in 1890 Weidersheim claimed to observe neural plasticity in his
study of Leptodora hyaline, a crustacean that lived in deep, freshwater lakes in
northern Europe. The crustacean was unusual in being “absolutely transpar-
ent, almost invisible in a glass of water,” as described in Nature in 1897, cited in
DeFelipe 2006). Able to see right into to its living organs, he claimed that cells
in its cerebral ganglion continuously changed their shape in a “slow and flow-
ing” manner (Weidersheim 1890, cited in DeFelipe 2006). Cajal’s student Tanzi
hypothesized that such changes in the ganglia resulted from changes in neurons’
connections with other neurons and, further, that the strengthening of connec-
tions is linked to the consolidation of memories and the learning of motor skills
(DeFelipe 2002, 2006).
4 Pharmacologists and neurophysiologists vigorously debated the mechanisms
of synaptic transmission for decades; only in the 1950s did they agree on Henry
Dale’s chemical explanation involving neurotransmitters, which is still under-
stood to explain most neural communication. Dale, along with Otto Loewi, won
the Nobel Prize in 1936 for their work on acetylcholine as a neurotransmitter, but
many neurophysiologists (most notably John Eccles) rejected chemical transmis-
sion in the central nervous system in favor of an exclusively electrical model of
neural communication. In chemical transmission an electrical charge in the axon
of a neuron, or an “action potential,” stimulates the release of a chemical (such as
acetylcholine or serotonin) from a vesicle in the cell.^ It acts as a neurotransmit-
ter, traveling across the synapse and binding to a receptor on another neuron’s
dendrite. This binding can stimulate an excitatory electrical charge, which in-
creases the likelihood of the second neuron generating its own action potential
and transmitting its signal to yet another cell. (It can also generate an inhibitory
charge, which decreases such likelihood.) In this way chains of electrical con-
nection are created. Beyond neurotransmitters, other neuromodulators (such as
hormones) have also been recognized as influencing synaptic transmission, and
all of these chemicals are thought to influence each other as well. Loewi found
evidence for chemical neurotransmission in his famous frog study, the design of
which came to him in a series of dreams. He removed the beating hearts of two
frogs in vivo, one with the vagus nerve still attached. He changed its rate with
electrical stimulation of the nerve. He was able to change the rate of the other by
applying fluid from the first heart. The neurotransmitting chemical in this fluid
was eventually identified as acetylcholine, which Dale had identified earlier as a
neurotransmitter. The chemical explanation for synaptic transmission competed
with John Eccles’s insistence that transmission is primarily electrical. The Dale-
Eccles debate was highly contentious, reportedly involving public rows (as did
the Golgi- Cajal debate), and it was not until the very end of the 1940s that Eccles
embraced Dale’s position. Until the 1950s, as Dale wrote in notably sexist terms,
chemical transmission was treated “like a lady with whom the neurophysiologist