Biological extension packet - Animal research testing

Animal model

Try used for non-human animals to demonstrate biological or psychological phenomenon. Localization of function is one phenomenon that has been demonstrated using animal models.

Lesioning of the amygdala in rhesus monkeys (weiskrantz 1956)

In the study, the researcher wants to study the relationship between the amid and emotion early research in the late 1900s had found connections between the temporal elope and emotion. This experiment went on one step further by lesioning the amygdala as a particular part of the temporal lobe that might be connected to emotion. There were two conditions in the experiment, one group of monkeys that had the amygdala lesion the other condition had a different part of the temporal lobe lesion. The results showed that there was damage to the amigos specifically that led to lack of fear in the monkeys. The use of monkeys in the experiment helped to develop the understanding of the role in emotion and fear.

Human study SM case study

The above study provides insight into the role of the Magdala in experiencing emotions like fear more modern human studies have supported this connection like the case study of SMSM has bilateral amygdala damage and cannot feel fear. Researchers have tested this observation by observing her behavior in places like haunted houses, exotic pet stores, and watching scary films by seeing the localization of brain function in the biological approach.

Neuroplasticity

Animal experiments have also been valuable in the study of neuroplasticity the brain’s ability to change as a result of experience or the environment similar to studies on localization the benefit of animals experiments of neuroplastic city is that researchers can control the extraneous variables and isolate the environment factors that they are thinking might have an effect on the developing brain we can control/manipulate the environment. Early animal experience were able to disprove the common belief that human brains were fixed from birth by using rats and putting them in different environments, enriched and deprived researchers like Rosencrans and Benedict were able to show how our brain can change depending on the environment. We grew up in. This has been further demonstrated in human studies that compare naturally occurring environment, variables on the developing brain, including poverty and stress.

Effects of enriched and deprived environments on the brain (Rosenzweig and Bennett 1960s)

The name of the study was to investigate the effects of the environment on the brain, growth and development rats replaced in different cages and lived for 30 to 60 days before they euthanized. A postmortem study was conducted to measure the thickness and heaviness of the brain cortex as well as the amount of acetylcholine receptors and synopsis. Male rats were chosen from different litters to control, genetics and gender, and were randomly allocated to two different conditions in rich condition or the deprived condition. In the EC they were 10 to 12 rats. There was a range of toys at the rats to play with. There’s a group that also received maze training on the other hand in the DC. They were alone in the cage with no toys and just food and water. The results showed the rats living in the EC developed a heavier and thicker brain cortex more specifically the frontal lobes of the rats in the EC were heavier as they had developed more receptors and transmitter associated with learning a memory further studies found that their brain weight of the rats can increase by to 10% and the synapse can increase to about 20% as a result of the EC. The results were quite groundbreaking the time. The researchers were so surprised by the results that they replicate the research numerous times and obtain the same results with the each replication. The study may have provided insight into neurological and cognitive development differences are commonly found in human kids that come from different backgrounds similar results have been found in kids who have come from extremely deprived environments like Romanian kids who grew up in orphanages.

Testosterone

Testosterone is a male sex hormone and is produced in the testes and in female ovaries, but in a lower level, it has been associated with aggression and numerous studies, animals experiments are useful when studying the effects of testosterone on aggressive behavior because they can be conducted an environment where all the extreme variables can be control controlled for what allows researchers to deduce cause-and-effect relationships. The IV level levels of testosterone can be directly manipulated in the effects that have on the DV can be measured. Testosterone has also been linked to social status and can be that status in aggression or linked aggression is needed to maintain high social status.

The Albert et al. (1986)

This study investigated the causal link between testosterone and aggression in alpha male rats. They manipulated the testosterone levels of dominant male rats using castration (testosterone removal) and replacement therapy. The results showed that castration significantly decreased aggressive behaviors (such as lateral attacks and bites) toward nonaggressive intruders, and this decrease was typically accompanied by a loss of social dominance. Crucially, when the castrated rats were given testosterone replacement therapy, their aggression levels returned to normal/baseline. The study concluded that testosterone plays a primary role in inter-male social aggression and is necessary for maintaining high social status in male rats.

Cortisol

Cortisol is a stress hormone that is released from the adrenal gland. It is released in times of stress when

the amygdala activates the HPA axis.

A common finding in people who have experienced chronic (long-term) stress (e.g. those who have PTSD

or suffered severe childhood trauma) is that they have reduced volume in their hippocampus (i.e. their

hippocampus is smaller). Animal studies have been used to see if the reduction in size of the

hippocampus could be a direct result of the release of cortisol.

We again can see that the primary value in animal studies is that they allow researchers to control

extraneous variables and isolate the IV as the only variable affecting the DV. In this case, the IV is cortisol

and the DV is the brain. There is no way that humans would participate in this study because no one

would want to volunteer to be in a study that could potentially damage your brain (and not telling people

of the dangers of such an experiment would be unethical). This is why animal studies are valuable, but

they will also raise ethical considerations

The Sapolsky et al. (1990)

conducted on vervet monkeys, provided key evidence that prolonged exposure to glucocorticoids (GCs), like the stress hormone cortisol, can directly damage the primate hippocampus. The researchers implanted cortisol pellets into one hippocampus and control cholesterol pellets into the other. After one year, they found preferential neurodegeneration (cell layer irregularity, soma shrinkage, dendritic atrophy, and condensation) in the cortisol-exposed side, specifically restricted to the vulnerable CA3/CA2 cellfield . This finding suggested that sustained high levels of stress hormones, which often occur during chronic stress, can be the proximal damaging agent to hippocampal neurons in primates, mirroring previous findings in rodents and aligning with observations in monkeys that died from sustained social stress

selective breeding

is a technique used in animal modeling to investigate the influence of genetics on behavior by systematically mating animals that exhibit a specific, desired trait.

The goal is to determine if a behavior is heritable, meaning it is passed down through genes. For example, when studying aggression, researchers identify animals, such as mice, with either short attack latency (highly aggressive, attacking quickly) or long attack latency (less aggressive, slow to attack or non-aggressive). By repeatedly breeding the most aggressive individuals together over several generations, scientists can produce distinct strains of animals—one highly aggressive and one non-aggressive. If the behavior in question, like aggression, becomes clearly exaggerated or diminished across generations, it strongly suggests that the behavior is linked to a genetic base.

Van Oortmerssen and Bakker (1981),

The key study detailing selective breeding for aggression, which used the resident-intruder paradigm on wild mice. The researchers initially selected mice based on their attack latency scores: those with the shortest latency (most aggressive) were bred together, and those with the longest latency (least aggressive) were bred together over 11 generations. The results demonstrated that the short-latency mice became increasingly aggressive and the long-latency mice became less aggressive across generations, providing evidence that aggression is subject to genetic inheritance. Furthermore, the study calculated a heritability of 0.30 for aggression, meaning that 30% of the variation in the behavior could be explained by genetic factors.

Gene Knockout

Gene Knockouts and Behavior

• Definition: A gene knockout is a procedure where researchers inactivate or "turn off" a specific gene in an animal, typically a mouse, creating a "knockout mouse". This process is functionally similar to lesioning or ablation, but focuses on genetic rather than physical removal.

• Purpose: By comparing the behavior of the knockout mouse (where the gene is absent) with a control mouse (where the gene is present), scientists can establish a clear link between that particular gene and the behavior in question.

• Application (Serotonin and Aggression): Gene knockouts have been used to research the link between the neurotransmitter serotonin and aggression.

  • Research has shown that low levels of serotonin lead to increased aggression.

  • One gene targeted in this research is TPH2 (Tryptophan Hydroxylase 2), an enzyme responsible for converting tryptophan into serotonin.

• TPH2 Knockout Findings (Rats): Studies on TPH2 knockout rats showed that removing the gene led to lower levels of serotonin in the brain, which in turn led to increased aggression. This supports the hypothesis that the TPH2 gene plays a crucial role in regulating serotonin and, consequently, aggressive behavior.

Mosienko et al. (2012) – TPH2 Knockout Mice

This study investigated the specific role of the TPH2 gene—which is responsible for serotonin production—by creating genetically modified mice with this gene knocked out and comparing them to a control group. The TPH2 knockout mice had significantly lower levels of serotonin in the brain. When tested for aggression, the knockout mice displayed aggressive behavior (attacks) six times faster and performed a larger total number of attacks than the control group. Crucially, during the resident-intruder test, 100% of the knockout mice attacked within five minutes, whereas only 20% of the control group attacked, and their attacks were less frequent. The findings conclude that knocking out the TPH2 gene causes a significant increase in aggressive behavior, directly linking this gene and its subsequent effect on low serotonin levels to increased aggression.

What is a Gene Knockout and why is it used in behavioral genetics research?

Gene Knockout is a procedure where a specific gene (e.g., TPH2) is inactivated or "turned off" in an animal, creating a "knockout mouse". It is used to establish a causal link between a particular gene and a specific behavior (e.g., aggression) by comparing the knockout animal to a control animal.

Key Study: What did Mosienko et al. (2012) find when knocking out the TPH2 gene?

Study: TPH2 knockout mice (lacking the serotonin production gene) had lower serotonin and showed a significant increase in aggressive behavior. Results: Knockout mice were 6 times faster to attack and showed a higher total number of attacks than the control group.