Primate Freedom Project - Education, Advocacy, Support Primate Freedom Project - Education, Advocacy, Support
LIFE STORIES
These are life stories of primates held in U.S. primate laboratories. They are based on documents obtained from the labs.
YNPRC
Clint Chimpanzee
Dover Chimpanzee
Sellers Chimpanzee
Tottie Chimpanzee
3566 Rhesus Macaque
PWc2 Rhesus Macaque
Unknown Rhesus Macaque
YN70-119 Chimpanzee
YN73-125 Gorilla
YN74-17 Chimpanzee
YN74-68 Chimpanzee
YN78-109 Chimpanzee
YN79-33 Chimpanzee
YN81-124 Chimpanzee
YN86-37 Squirrel Monkey
ONPRC
13447 Rhesus Macaque
13481 Rhesus Macaque
14326 Rhesus Macaque
20213 Rhesus Macaque
20229 Rhesus Macaque D
20233 Rhesus Macaque
20247 Rhesus Macaque
20253 Rhesus Macaque
20346 Rhesus Macaque
CNPRC
18714 Crab-eating Macaque
20629 Rhesus Macaque
22114 Crab-eating Macaque
23915 Crab-eating Macaque
23954 Squirrel Monkey
23993 Squirrel Monkey
23997 Squirrel Monkey
24005 Squirrel Monkey
24013 Squirrel Monkey
24557 Crab-eating Macaque
24605 Crab-eating Macaque
24974 Rhesus Macaque
24994 Rhesus Macaque
25142 Crab-eating Macaque
25157 Crab-eating Macaque
25205 Crab-eating Macaque
25250 Crab-eating Macaque
25274 Rhesus Macaque
25281 Rhesus Macaque
25412 Crab-eating Macaque
25809 Squirrel Monkey
27276 Crab-eating Macaque
27306 Rhesus Macaque
28092 Crab-eating Macaque
28098 Crab-eating Macaque
28100 Crab-eating Macaque
28104 Crab-eating Macaque
28109 Crab-eating Macaque
28114 Crab-eating Macaque
28545 Squirrel Monkey
28562 Squirrel Monkey
28796 Crab-eating Macaque
30749 Crab-eating Macaque
30755 Crab-eating Macaque
30813 Rhesus Macaque
30914 Rhesus Macaque
30916 Rhesus Macaque
30983 Rhesus Macaque
31031 Rhesus Macaque
34273 Crab-eating Macaque
34274 Crab-eating Macaque
34275 Crab-eating Macaque
34276 Crab-eating Macaque
34278 Crab-eating Macaque
34279 Crab-eating Macaque
34280 Crab-eating Macaque
34281 Crab-eating Macaque
WNPRC
cj0233 Common Marmoset
cj0453 Common Marmoset D
cj0495 Common Marmoset
cj0506 Common Marmoset
cj1654 Common Marmoset
Piotr Rhesus Macaque
rhaf72 Rhesus Macaque
rhao45 Rhesus Macaque
Rh1890 Rhesus Macaque
R80180 Rhesus Macaque
R87083 Rhesus Macaque
R89124 Rhesus Macaque
R89163 Rhesus Macaque
R90128 Rhesus Macaque
R91040 Rhesus Macaque
R93014 Rhesus Macaque
S93052 Rhesus Macaque
R95054 Rhesus Macaque D
R95065 Rhesus Macaque D
R95076 Rhesus Macaque D
R95100 Rhesus Macaque
R96108 Rhesus Macaque
R97041 Rhesus Macaque
R97082 Rhesus Macaque
R97111 Rhesus Macaque
Response from Jordana Lenon, public relations manager for WNPRC. Citizens' requests Lenon refused to answer.
WANPRC
A03068 Rhesus Macaque
A98056 Pig-tailed Macaque
A92025 Baboon
F91396 Pig-tailed Macaque D
J90153 Pig-tailed Macaque
J90266 Pig-tailed Macaque
J90299 Crab-eating Macaque
J91076 Pig-tailed Macaque D
J91386 Pig-tailed Macaque D
J91398 Pig-tailed Macaque D
J92068 Pig-tailed Macaque
J92349 Pig-tailed Macaque D
J92476 Pig-tailed Macaque
UCLA
B15A Vervet
788E Rhesus Macaque
9382 Vervet
1984-016 Vervet
1991-016 Vervet
1992-015 Vervet
1994-014 Vervet
1994-046 Vervet
1994-087 Vervet
1995-046 Vervet
1995-101 Vervet
1996-022 Vervet
UTAH
MCY24525 Crab-eating Macaque
MCY24540 Crab-eating Macaque
OIPM-007 Crab-eating Macaque
MCY24525 Crab-eating Macaque
MCY24540 Crab-eating Macaque
UNC-Chapel Hill
3710 Squirrel Monkey
APF
Ashley Chimpanzee
Karla Chimpanzee
Tyson Chimpanzee
Snoy Chimpanzee
Maurice p1 Maurice p2 Chimpanzee
Hercules Chimpanzee
Jerome Chimpanzee
Ritchie Chimpanzee
Rex Chimpanzee
Topsey Chimpanzee
B.G. Chimpanzee
Dawn Chimpanzee
BamBam Chimpanzee
Dixie Chimpanzee
Ginger Chimpanzee
Kelly Chimpanzee
Lennie Chimpanzee
Kist Chimpanzee
Peg Chimpanzee
Aaron Chimpanzee
Chuck Chimpanzee
James Chimpanzee
Alex Chimpanzee
Muna Chimpanzee
Wally Chimpanzee
#1028 Chimpanzee
Lippy Chimpanzee
#1303 Chimpanzee
#CA0127 Chimpanzee
Shane Chimpanzee
LEMSIP
196 Baboon
The Fauna Foundation Chimpanzees
Center for Biologics Evaluation
Univ. of Alabama - Birmingham

Univ. of Minnesota

00FP8 Long-tailed Macaque
312E Rhesus Macaque
9711B Rhesus Macaque
99IP61 Long-tailed Macaque
CDC-Column E 2002

 

The Rewards of Repetitive Cruelty:

A look at Stuart Zola-Morgan, the director of the Yerkes Regional Primate Research Center, and the implied public message in his appointment.

Rick Bogle
August 1, 2001

A researcher was studying grasshoppers. She sat a grasshopper on the sterile white counter and said, "Jump grasshopper! Jump!"

She carefully recorded the distance the insect had jumped, and pulled off one of the grasshopper's legs. Then, once again, "Jump grasshopper! Jump!"

Another measurement, another recording, and another leg; "Jump grasshopper! Jump!"

This went on again and again.

One leg left. "Jump grasshopper! Jump!" the researcher sternly demanded. She recorded: "Grasshopper with one leg: .002cm"

Finally, the grasshopper is lying on the counter, on her back with no legs. "Jump grasshopper! Jump!" Nothing. Disappointed, this time slapping the table next to the twitching critter, the researcher screamed as loudly as she could, "Jump grasshopper! Jump!"

And she records: Grasshopper with no legs: Cannot hear."

Anonymous old joke

Yerkes may be the best known and perhaps the most prestigious primate-based research facility in the nation. The decisions made concerning Yerkes’ choice of research and directorship is closely watched by the National Institutes of Health (NIH) and the rest of the vivisecting community. The person chosen for the position probably has the approval of the senior NIH staff. The choice of director may be viewed as a statement by the NIH regarding what research methods are desirable. The director’s own research will be seen as an example of high caliber research and will set the tone as he assumes the role of spokesperson for this flagship facility. Of interest is the fact that the previous director, Tom Insel, lost his position after being caught in less than factual statements on national television as he tried to discredit a child who had an encounter with an escaped monkey on her front porch. This public relations blunder, coupled with the cover-up surrounding the death a young lab worker at the facility, was too large an embarrassment for Yerkes and NIH. Insel was “reassigned.”

The choice of Stuart Zola-Morgan to head Yerkes makes two strong interrelated statements. The first concerns the nature, quality and methodology of research that NIH finds worthy of high reward and showcasing. The second concerns the public face being put on the research occurring in the nation’s taxpayer-funded primate-based experimental programs. This second reason for choosing Zola-Morgan is directly related to the escalating battle between those suckling at the public teat who are engaged in research that is being increasingly questioned on grounds of ethics and efficacy and those calling the research into question. Zola-Morgan’s research will be examined first.

Stuart Zola-Morgan has spent the last twenty years destroying various parts of monkeys’ brains and then testing them to determine whether they could still learn and whether they could remember what they had already learned.

Zola-Morgan explains his research:

The resolution of many issues surrounding the neuropsychology of memory depends significantly on knowing the specific brain structures that, when damaged, cause amnesia. During the course of our work, we have successfully established a model of human amnesia in the monkey, and we have been able to identify a neural system of memory in the temporal lobe that includes the hippocampal region (i.e., dentate gyrus, the hippocampus proper, and subicular complex) and adjacent cortical regions, i.e., entorhinal, perirhinal, and parahippocampal cortices. Identification of the specific sites important for memory has opened the way for more detailed neurobiological investigations. Our work is relevant to issues of how memory is organized in the brain and to issues of memory impairment associated with a wide range of human conditions, e.g., aging, Alzheimer's disease, and stroke.1

Zola-Morgan’s initial premise is illogical. Though damaging an area of the brain associated with memory may result in amnesia, it is illogical to assume that any amnesia arising from any brain injury is an indication that the area damaged is involved in a direct way with the phenomena of memory. Consider a much simpler system: an automobile.

Someone seeking to understand how an automobile works could, following Zola-Morgan’s methods, destroy various components of a car, the key for instance, and make various inferences. A naïve observer might come to the conclusion that the key is a critical component. Deep and careful study of the key itself would offer little insight into the mechanics of internal combustion engines or modern transmissions. The same observer might come to the conclusion that the seatbelt interlock is important for the car to function when in actuality, the seatbelt, the key, the gear shift lever, the parking brake, and other peripheral devices are only marginally associated with the basic functions of an automobile.

Further, even if one did determine that destroying the spark plugs, for instance, interfered with the operation of the engine, one would have little understanding of what the spark plugs do, or of course, how to repair them once they were destroyed. In fact, Zola-Morgan has acknowledged as much. The degree of memory loss in humans due to brain injury is directly related to the size as much as the location of the injury. In other words, if you have a small injury you don’t lose as much memory as you would if you had a larger injury. This suggests that memory may be a widely dispersed dynamic phenomena rather than a storing of experiences in discrete neural compartments. Zola-Morgan says:

One idea that has emerged from this work is that the severity of memory impairment might increase as more components of the medial temporal lobe are damaged. We have evaluated this idea directly by examining behavioral data from 30 monkeys (ten normal monkeys and 20 monkeys with bilateral lesions involving structures within the medial temporal lobe) that have completed testing on our standard memory battery during the last 10 years. The main finding was that the severity of memory impairment depended on the locus and extent of damage to the medial temporal lobe. Specifically, damage limited to the hippocampal region produced a mild memory impairment. More severe memory impairment was produced when the damage was increased to include the adjacent entorhinal and parahippocampal cortices (the H+ lesion). Finally, memory impairment was even more severe when the H+ lesion was extended forward to include the anterior entorhinal cortex and the perirhinal cortex (H++ lesion). Taken together, these findings suggest that, whereas damage to the hippocampal region produces measurable memory impairment, a substantial part of the severe memory impairment produced by large medial temporal lobe lesions in humans and monkeys can be attributed to damage to entorhinal, perirhinal, and parahippocampal cortices adjacent to the hippocampal region.2

Most troubling is the fact that Zola-Morgan is not destroying various parts of a car; he is methodically destroying parts of living monkeys’ brains. To fully understand the unsettling nature of Zola-Morgan’s experiments, it is necessary to first understand who his victims are. Monkeys have been increasingly understood to possess complex minds and emotions. Monkeys are used in experiments specifically because they are capable of abstract thought3, display emotion4, exhibit altruism5, and maintain highly complex social relationships6. These well-known characteristics should compel a basic ethical and moral reconsideration of the experimental manipulations of these beings, but the contrary is true among the primate experimentation community. The close similarities of the most fundamental aspects of human-ness and monkey-ness – mind and emotion – have been magnets for exploitation by those without moral rudders; Zola-Morgan is an exemplar of this phenomena.

Early in Zola-Morgan’s career he began destroying parts of monkeys’ brains and pointing out that the resultant impairments were similar to impairments seen in humans with similar brain damage. In 1981, he wrote:

…in the first of two experiments, we compared the behavioral effects of inferotemporal cortical lesions with those of either hippocampus, entorhinal area, or fornix, using a visual concurrent discrimination task. Monkeys with either hippocampal or entorhinal ablations were impaired, while those with fornix sections were not. However, ablations of hippocampus included inadvertent damage of the inferotemporal cortex. Therefore, in the second experiment, behavioral effects of inferotemporal lesions were compared with those of hippocampus (without additional inferotemporal damage) on the concurrent task in both visual and tactual modalities. In the visual mode, monkeys with hippocampal removals were as impaired as those with inferotemporal ablations. In the tactual mode, however, hippocampal, but no inferotemporal, ablations were followed by a deficit. Our results, taken together with other existing evidence, emphasize the role of the hippocampus in mediating associative learning in more than one modality. These results, obtained with non-human primates, are in line with clinical findings.7

From this passage it is clear that Zola-Morgan’s methods are less than precise. He says, “ablations of hippocampus included inadvertent damage of the inferotemporal cortex.” Indeed, this messiness and imprecision suggest that his results are suspect. In 1991, Zola-Morgan as much as admitted that variation between individual monkey’s brain physiology makes precision in locating brain structures problematic. He wrote:

A technique is described for producing accurate stereotaxic lesions of the hippocampus in monkeys. This technique overcomes the problem that the size and shape of the brain can vary considerably from monkey to monkey. Magnetic resonance imaging (MRI) is used to create an individual brain atlas for each monkey. The atlas is then used to derive coordinates for making stereotaxic radio frequency lesions of the hippocampus.8

Yerkes and the rest of the NIH Regional Primate Research Center system make the claim that they are sacrificing monkeys for the sake of human health. Yerkes explains its mission:

Long recognized as one of the leading centers for biomedical and behavioral research with non-human primates, Yerkes is focused on the following goal(s):

To conduct a research program focused on scientific problems relevant to human health and the mission of the National Institutes of Health9

So it must be assumed that Yerkes and NIH see Zola-Morgan’s research as fitting neatly into, perhaps exemplifying, this goal. Is Zola-Morgan’s research actually relevant to human health? Of course he says it is when he makes the claim: “Our work is relevant to issues of how memory is organized in the brain and to issues of memory impairment associated with a wide range of human conditions, e.g., aging, Alzheimer's disease, and stroke.”10 But this claim requires substantiation.

Zola-Morgan has investigated the loss of tactile amnesia in monkeys whose brains he has injured. Tactile memory or amnesia refers to the recollection (or loss of ability to recollect) of the physical feel of an object. In other words, when you feel a coin in your pocket do you remember that it is a coin? Is this question relevant to human health?

NIH maintains an online database of medical journals:

PubMed, available via the NCBI Entrez retrieval system, was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM), located at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at web sites of participating publishers.11

This database is used by researchers as they seek to ascertain whether their work is redundant and as a source for scientific information. A search for “cancer” results in a list of 1,355,509 citations. This is unsurprising due to the prevalence of the malady and the research effort associated with it. Likewise, “arteriosclerosis” results in over 56,000 citations and “stroke” over 65,000 citations. On the other hand, “amnesia” results in 6,999 (as of July 30, 2001) and “tactile AND amnesia” results in 17 citations.

Of these seventeen citations, seven refer to the temporary and often desirable amnesia associated with anesthesia and sedatives. Of the remaining ten, one is a paper published in 1970, and six others published in the years 1979, 1980, 1982, 1983, 1984, and 1990. A study of rats with experimental brain damage induced tactile amnesia was published in 1991, and single papers in 1993 and 2000.

It must be inferred that the study of tactile amnesia is of little interest in the medical community, not perhaps out of a lack of compassion, but more likely due to the rarity of the condition. Undoubtedly, there must be a few doctors and researchers with an interest in the topic, but its relevance as compared with the major human ailments must be considered to be very low.

It is precisely this inconsequential and logically flawed research that NIH and Yerkes have chosen to highlight by choosing Zola-Morgan to head the most visible of all the nation’s primate laboratories. To gain a better understanding of what it is that Zola-Morgan does in his laboratory one need only consult his published work.12 Excerpts follow:

SUBJECTS

Twenty-eight male cynomolgus monkeys (Macaca fascicularis) were tested, all weighing between 3.1 kg and 5.2 kg at the start of the experiment. Five monkeys received bilateral lesions of the perirhinal cortex (PR group). Five monkeys received bilateral lesions of inferotemporal cortical area TE (TE group). The remaining eighteen monkeys comprised unoperated control groups used in the individual experiments.

SURGERY

Monkeys were anesthetized using Isofluorane gas and placed in a stereotaxic headholder that allowed unobstructed access to the temporal portion of the skull. The temporal muscles were exposed and fully retracted, and the zygomatic arches were removed. Bilateral openings were made in the skull to expose the anterior and ventrolateral portions of the temporal lobe, and the dura was opened. The pial surface over the intended lesions was first cauterized, and the cauterized tissue together with the underlying cortical tissue was then removed by suction using a glass pipette with an angled tip. Cortical tissue was removed slowly until the white matter was visualized. The dura was then sewn, and the wound was closed in anatomical layers.

Prior to the brain surgeries, the monkeys had been trained to reach over a visual barrier and feel an object. If it was the correct object, and they tugged on it thee times, they received a food reward (a raisin). The monkeys learned which objects when tugged on resulted in a food reward.

After their brains were damaged, they were again tested.

BEHAVIORAL TESTING

All testing was conducted in the Wisconsin General Testing Apparatus (WGTA; Harlow and Bromer 1938[13]). In this apparatus, the experimenter and monkey face opposite sides of a testing tray that has three food wells. A sliding opaque door separates the monkey from the testing tray, and a sliding door with a one-way mirror separates the experimenter from the tray. The one-way mirror allows the experimenter to observe the monkey but prevents the monkey from seeing the experimenter. During a trial, the experimenter lowers the one-way mirror and raises the opaque door, allowing the monkey to respond to the objects on the testing tray.

Each operated group was allowed 6-8 weeks of recovery prior to the start of behavioral testing. During four to six daily sessions of pretraining, operated monkeys and control monkeys learned to obtain food by displacing objects that covered any of three food wells located on a stimulus tray in front of the testing chamber.

In summary, the present findings demonstrate the distinct functions of the perirhinal cortex and area TE. The deficits following lesions of area TE are consistent with an impairment of visual perception. Lesions of area TE produced a unimodal visual impairment in visual recognition memory (experiment 1), an impairment in visual recognition even at very short delays (experiment 2), and an impairment in relatively complex visual discrimination learning together with sparing of simple visual object discrimination learning (experiment 3). In contrast, the impairment following perirhinal lesions is best described as a memory impairment. Lesions of perirhinal cortex produced a multimodal impairment in recognition memory (experiment 1), spared short-term memory and impaired long-term memory (experiments 1 and 2), and impaired simple object discrimination learning while sparing more complex visual discrimination learning (experiment 3).

One way to judge the value of a researcher’s work is to look at the number of times it has been referred to in subsequent research by other scientists. If a scientist publishes a paper and no one pays attention, it can mean that others deem the work unimportant. In animal-based studies, it is the norm for researchers to claim that the work they are engaged in will have value for human health at some later date. The paper excerpted above was published at the end of 1999, or a year and a half ago at the time of this writing. To date, according to the journal’s publishers, the paper has been cited in ten subsequent papers.14 Two of those papers are Zola-Morgan citing his own work. Two of the papers have to do with experiments on rats, and five of the papers are by other monkey users. Only one is from a human study, and this is a German clinical study on brain plasticity related to language after cochlear implants.

But perhaps a year and a half is simply too short a time for clinical researchers to have taken note of Zola-Morgan’s work. Another paper15 published over ten years ago has been cited much more frequently. The publisher reports that the paper has been cited forty-one times. Of these: three are Zola-Morgan citing his own work; one is a Guinea pig-based study; two are experiments using cats; ten are rat-based studies; fifteen are by other researchers destroying monkeys’ brains; one is based on an unnamed species; one is a general article rather than a research report; and seven are human related.

Of these seven human related studies, one16 is coauthored by one of Zola-Morgan’s own regular co-authors, David Amaral, himself a monkey brain experimenter at the California RPRC in Davis. The rest cite Zola-Morgan when noting that the parahippocampus may be involved in memory. But none of the clinical papers seem to actually build on Zola-Morgan’s work.

It would be unreasonable to claim that Zola-Morgan’s work has in any way been trail blazing or otherwise exemplary.

Zola-Morgan has, however, blazed a trail to the bank. He explains why he should keep being paid from the public trough:

This is our second competing continuation for a project begun in 1983. Work during the most recent funding period (1987-present) has resulted in 27 publications that lay out the steps that have established an animal model of amnesia in the monkey and in identifying the anatomical components of the medial temporal lobe memory system. These developments allow us to now address a fundamental issue concerning memory function, that is, how individual structures of this system contribute to memory. The present proposal involves detailed behavioral and anatomic analyses of a group of normal monkeys and seven operated groups of monkeys including those with damage to components of the medial temporal lobe memory system and to area TE.17

Over the past decade Zola-Morgan has received nearly $2 million in taxpayer funding: 1992 - $48,203; 1993 - $158,227; 1994 - $156,011; 1995 - $162,657; 1996 - $169,303; 1997 – none listed; 1998 - $306,105; 1999 - $315,128; 2000 - $324,580; 2001 - $334,321.18

The second reason that Zola-Morgan is likely to have been selected to head Yerkes is his strong and outspoken opposition to the critics of vivisection. On Thursday, May 14, 1998, Zola-Morgan testified before the U.S. House of Representatives’ Committee on Science’s National Science Policy Hearing. His talk was titled: Communicating Science and Engineering in a Sound-Bite World. His speech was couched in reasonable terms and he assured the Committee members that his research was helping find answers to Alzheimer's Disease (AD), encephalitis, head trauma, chronic stress and the memory problems associated with aging.

He went on to claim that the reason the public was increasingly critical of using animals in research was due to their “scientific illiteracy.”

He testified:

The claims about animal research and about the process of science in general that were being made by the animal activists seemed not unreasonable on the surface. And because they were not being effectively disputed by the scientific community, the distortions and untruths about science and the scientific process were often accepted without question by the general public Moreover, claims of abuse of animals were often being accepted at face value by the general public and by legislators, who were beginning to generate legislation that would further regulate research using animals.

And such legislation would impact on Zola-Morgan’s freedom to scramble monkeys’ brains. He continued:

As a result, in the mid 1980’s I became interested in the issue of communicating science to the general public and to legislators, as well. I was, at that time, Chair of the Animal Subjects Committee at UCSD and I knew that we ranked very high in our science (UCSD is consistently in the top 10 or 12 institutions in the country in terms of grant funding received) and in our humane treatment of animals.

UCSD ranked sixteenth in terms of grant funding in Fiscal 200018. Johns Hopkins was number one with NIH grants totaling over four hundred million dollars. UCSD received one hundred ninety million dollars. In terms of the “humane treatment of animals” facilities are not ranked. This claim was simple posturing before the Congressional Committee. In addition, Zola-Morgan’s position as chair of the Animal Subjects Committee gave him great power to deflect any internal criticism of his own work, and when the committee chair is involved in such blatantly pointless and cruel experiments, it tends to open the door for others who might otherwise be under greater constraints.

A small group of individuals at UCSD began to develop counter arguments to the claims of the activists, and to speak out at animal rights gatherings in San Diego. However, it soon became clear that in terms of educating people about science, it was not the animal rights activists whom we should target. Their views were unlikely to be changed by us. Instead, we determined that we should focus on the general public, and on legislators.

And this is likely at the core of Emory University’s and the NIH’s decision to see Zola-Morgan assume the leadership there. Local anti-cruelty activists have been recently successful in having legislators ask pointed questions of the facility. The need to deflect the likely outcome of acknowledging that you have been wasting millions of dollars and thousands of lives has motivated them to seek out someone with a good track record of pubic relations. And clearly, if Zola-Morgan can spin his own experiments in ways that will mollify lawmakers, Yerkes might assume that he might be able to shield them as well.

But it seems that the Yerkes administration and NIH have failed to do their homework. An anti-cruelty activist from the San Diego area recalls:

During the period around l988-90 there were concerted efforts underway in San Diego to end the contract between UCSD and the county Department of Animal Control. "Pound seizure" had been in place for about 30 years at that point, with UCSD taking hundreds of dogs and cats annually for experimentation. San Diego Animal Advocates and a group called Stop Taking Our Pets went from city council to city council, persuading them to put a clause in their animal control contracts that would forbid the county from selling (or giving away) animals, who were picked up in that city, to the university for research. In a number of cities we were successful. While the cities still contracted with the county for
animal control services, the clause was inserted to protect strays from research.

Zola Morgan and colleague, Dr. Patrick Cleveland from the Veterans Administration Hospital, showed up at these meetings as well, to argue their case that all medical advances on the planet were dependent on the use of pound animals. They specifically insisted that pound animals were preferable to purpose-bred animals because of the desirability of the unknown genetic backgrounds!

During this time frame San Diego Animal Advocates held a big demonstration on what was then known as World Day for Laboratory Animals, in April. We presented a mock "vivisector of the year" award each year to someone from UCSD known for a grisly experiment. Both Zola-Morgan and his buddy Cleveland called our animal rights information line and left messages on the recorder. Each one claimed that he should win the award instead of the other, because he used more animals or did more experiments, or had been doing them longer, etc.

They found this very amusing until we took the tapes to the city council meetings and played them. The first time we brought out the tape recorder, Zola-Morgan was on his feet protesting that it was inappropriate, but it was allowed nevertheless. The callous attitude toward the animals was very apparent and he was very embarrassed and angered. That city was Solana Beach and they passed our proposal that evening.

On another occasion, San Diego Animal Advocates testified at the county Board of Supervisors meeting about the pound seizure issue. One of the supervisors was Pam Slater, who was very favorable to the abolition of pound seizure, although not opposed to all animal research. After the hearing, Zola-Morgan went up to her and angrily demanded to know why she had been so critical of UCSD research. He said, “You know us – you have worked with us.” (She had been a lab assistant there at one time, unbeknownst to us.) She answered that it was precisely because of what she had seen in Zola-Morgan's own laboratory that she was against pound seizure. I don't know if he used any dogs or cats in his experiments, I think it was mostly primates, but whatever she saw made her unwilling to let former companion animals end up at UCSD.19


The effects of Zola-Morgan’s appointment remain to be seen. What does seem clear is that the vivisecting community has escalated their defense of experimenting on animals. The battle is joined, and now we must all decide whether we stand on the side of kindness and compassion, or with the Zola-Morgans who claim the unfettered right to appease any and every curiosity.

Note: A few years ago Zola-Morgan dropped the -Morgan from his name. He now goes by Stuart M. Zola.





1 From Zola-Morgan's profile at the University of California San Diego homepage: [http://medicine.ucsd.edu/neurosci/the-faculty/zola.html]
2 Zola-Morgan S, Squire LR, Ramus SJ. 1994. Severity of memory impairment in monkeys as a function of locus and extent of damage within the medial temporal lobe memory system. Hippocampus. Aug;4(4):483-95. Comment in: Hippocampus. 1995;5(3):232-9.
3 Wallis J, Anderson K, Miller E. 2001. Single Neurons in prefrontal cortex encode abstract rules. Nature: 953-956.
4 Barbas H. 2000.Connections underlying the synthesis of cognition, memory, and emotion in primate prefrontal cortices. Brain Res Bull. Jul 15;52(5):319-30.
5 Masserman J, Wechkin S, and Terris W. 1964. 'Altruistic' behavior in rhesus monkeys. American Journal of Psychiatry vol. 121. pp. 584-585.]
6 Bachevalier J, Alvarado MC, Malkova L. 1999. Memory and socioemotional behavior in monkeys after hippocampal damage incurred in infancy or in adulthood. Biol Psychiatry. Aug 1;46(3):329-39.
7 Moss M, Mahut H, Zola-Morgan S. 1981. Concurrent discrimination learning of monkeys after hippocampal, entorhinal, or fornix lesions. J Neurosci: Mar;1(3):227-40.
8 Alvarez-Royo P, Clower RP, Zola-Morgan S, Squire LR. 1991. Stereotaxic lesions of the hippocampus in monkeys: determination of surgical coordinates and analysis of lesions using magnetic resonance imaging. J Neurosci Methods: Jul; 38(2-3):223-32.
9 From the Yerkes homepage: [http://www.emory.edu/WHSC/YERKES/about_mission.html].
10 See note 1.
11 PubMed Overview [http://www.ncbi.nlm.nih.gov:80/entrez/query/static/overview.html].
12 Buffalo EA, Ramus SJ, Clark RE, Teng E, Squire LR, Zola MS. 1999. Dissociation Between the Effects of Damage to Perirhinal Cortex and Area TE. Learning and Memory: Vol. 6, No. 6, pp. 572-599, November/December.
13 Harlow H, and Bromer. 1938. A test-apparatus for monkeys. Psychol. Rev: 19: 434-438.
14 Learning and Memory: 6:572-599.
15 Zola-Morgan S, Squire LR, Amaral DG and Suzuki WA. 1989. Lesions of perirhinal and parahippocampal cortex that spare the amygdala and hippocampal formation produce severe memory impairment Journal of Neuroscience: Vol 9, 4355-4370.
16 Corkin S, Amaral DG, González RG., Johnson KA, Hyman BT. 1997. H. M.'s Medial Temporal Lobe Lesion: Findings from Magnetic Resonance Imaging. J. Neurosci: 17: 3964-3979.
17 NIH Grant Number: 5R01MH58933-15; Neurology of Memory. Project Start: 01-Mar-83; Project End: 31-Jan-03. National Institutes of Mental Health (NIMH).
18 National institutes of Health Office of Extramural Research Award Data [http://grants.nih.gov/grants/award/award.htm].
19 Cartmil, J. San Diego Animal Advocates. Private correspondence with the author. August, 2001. 

 


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