Traditional Neuroscience Research Methods Research Paper

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Brain science is difficult and tricky, for some reason; consequently one should not believe a result (one’s own or anyone else’s) until it is proven backwards and forwards or fits into a framework so highly evolved and systematic that it couldn’t be wrong. —DavidHubel, personal communication, 1992

It might be an interesting exercise, for someone who has nothing better to do, to compile a list of previously held beliefs about the brain that turned out to be false. Neuroscientists have learned to be cautious. Findings need to be replicated under several conditions with several populations or species, and checked with more than one research method. A conclusion that survives a variety of tests is presumably not an artifact of the limitations of any one method or population.

Today, much of the excitement in research comes from studies using functional magnetic resonance imaging (fMRI) and other brain-scan techniques, as discussed in another chapter of this volume. However, these newer procedures supplement the older techniques without replacing them. This research-paper surveys a variety of approaches to understanding brain-behavior relations. It will not deal with purely anatomical, chemical, or physiological brain research unrelated to behavior. It also will not provide a how-to-do-it laboratory manual for any of the techniques. The goal is to consider the research strategies, with emphasis on their potentials and limitations.

Research methods for studying brain-behavior relationships fall into four logical categories:

Damage part of the brain or decrease its activity and see what deficits occur in behavior.
Stimulate increased activity in some brain area and record what behavior increases, or what experience people report.
Record brain activity and examine its correlation with simultaneous behaviors.
Compare individuals who show unusual features in either their behavior or their brain anatomy, and seek a possible correlation between behavior and anatomy.

Each of these approaches has a variety of subcategories. Some are suitable for laboratory animals but not humans; some provide good temporal resolution but poor spatial resolution, or vice versa. Different methods answer different questions.

Effects Of Brain Damage

The earliest discoveries about the functions of various brain areas came from studies of damage. The first clear demonstration that different parts of the nervous system have different functions came in 1822, when François Magendie found that cutting the dorsal nerves of the spinal cord blocked sensory information and cutting the ventral nerves blocked motor output (Gallistel, 1981). In 1861 Paul Broca reported a link between damage to part of the left frontal cortex and a loss of the ability to speak.

Since then, researchers have made countless reports of behavioral impairments after brain damage from stroke, disease, and other causes. The famous studies of patient H. M. provided the first clue linking the hippocampus to memory (Scoville & Milner, 1957). Patients with prosopagnosia demonstrated the importance of the fusiform gyrus for facial recognition (McCarthy, Puce, Gore, & Allison, 1997; Tarr & Gauthier, 2000). We learned about the functions of the corpus callosum from studies of split-brain patients (Gazzaniga, 1970). The list goes on and on.

Many reports of brain damage prompt the reaction, “Isn’t it amazing that brain damage can produce such a specific deficit!” For example, people with damage to the parietal lobe can still see objects, but cannot determine their locations. Those with damage to the middle temporal cortex can see in most regards, except that they lose the ability to detect the speed and direction of a moving object (Zihl, von Cramon, & Mai, 1983). Someone with a loss of input to the somatosensory cortex has no conscious sensation of touch, but still reports a “pleasant” experience after a gentle stroke along the skin, showing the possibility of losing the sensation itself but keeping the emotional reaction to it (Olausson et al., 2002).

However, studies of humans face inherent limitations. One is that most brain structures are bilateral, whereas strokes and other spontaneous injuries almost never produce symmetrical, bilateral lesions. Essentially, never do they produce discrete lesions of some of the tiny nuclei of the hypothalamus or amygdala that researchers find so theoretically interesting. Another limitation is that no two people have the same damage, or the same brain functioning before the damage. Thus, neurologists sometimes report patients with similar brain damage but significantly different behavioral symptoms, and the reasons for the differences are difficult to establish. Indeed, even in the classic case of aphasia after damage to Broca’s area, neurologists in the century and a half since Broca have made only limited progress in understanding the brain mechanisms of language. The pattern of language abilities and disabilities varies from one patient to another, as does the pattern of brain damage, and only within broad limits can anyone infer the location of brain damage from a patient’s behavior, or predict the behavior from the brain damage.

Lesion Studies With Laboratory Animals

Researchers who turn to laboratory animals gain control of the location and the extent of the damage, as well as the animal’s history and environment, at the cost of being unable to study language or other distinctively human behaviors. To study the function of a structure on the surface of the brain, researchers can ablate (remove) it with a knife or by suction. To study a structure in the interior of the brain, one procedure is to create a lesion by means of a stereotaxic instrument, which enables precise placement of electrodes in the brain. Stereotaxic atlases, which are available for the brains of many common laboratory animals, specify the position of each brain area in terms of the dorsal-ventral, anterior-posterior, and left-right coordinates, relative to landmarks on the skull of the animal. For example, the ventromedial hypothalamus of a rat is 0.2 mm anterior to bregma (a point on the skull where four major bones join), 10 mm ventral to the dura mater that covers the brain, and 0.8 mm left and right of the midline (Pellegrino & Cushman, 1967). An investigator anesthetizes the animal, shaves part of the scalp and cuts back a flap of skin, drills a small hole in the skull, inserts an electrode insulated except at the tip, and lowers it to the target as determined from the atlas. The experimenter then causes a lesion by passing an electrical current through the tip of the electrode, using a second electrode on the tail or elsewhere as the reference electrode. The experimenter might apply 2 milliamps of direct current for 15 seconds, or a weaker current for a longer duration. An alternative method is to use a radio frequency instead of electricity. In either case, the procedure kills neurons by overheating them. To make bilateral lesions, the researcher repeats the procedure on the other side of the brain. At the end of the experiment, the brain is removed for histological analysis to determine the actual, as opposed to intended, location of the damage. Slices of the brain are subjected to chemicals that stain cell bodies or axons, so that researchers can see the areas of damage. Animals in a control group go through the same procedure except that the experimenter passes no current through the electrode. Once the mainstay of behavioral neuroscience, stereotaxic surgery has become less common as alternative methods have arisen.

An alternative procedure for producing lesions is to inject certain chemicals. For example, an injection of kainic acid, ibotenic acid, or monosodium glutamate into a brain area overstimulates glutamate synapses, leading to a surge of sodium and other positive ions within neurons near the site of injection, thereby poisoning their mitochondria and killing the neurons. The advantage of this procedure over electrolytic surgery is that it spares axons passing through the area. An investigator interested in the lateral hypothalamus, for example, might want to distinguish between the functions of cells there and the many axons passing by (Stricker, Swerdloff, & Zigmond, 1978). Another approach is to inject, either systemically or locally, a chemical that selectively damages particular kinds of neurons or their synapses. For example, 6-hydroxy-dopamine (6-OH-DA), which is absorbed selectively by neurons that release dopamine as their neurotransmitter, attacks the whole network of dopamine neurons while sparing other nearby cells. Similarly, a chemical known as AF64A attacks synapses that use acetylcholine (Sandberg, Sanberg, & Coyle, 1984). Selective damage helps researchers determine how different neurotransmitters contribute to behavior.

In still another approach, known as gene knockout, researchers use biochemical methods to direct a mutation to a particular gene (Joyner & Guillemot, 1994). This procedure can eliminate a particular type of cell, a neurotransmitter, or a receptor. It is well suited to studying a system that is spread out in the brain, instead of destroying a mixture of cell types that happen to be in the same place. However, eliminating a gene sometimes produces widespread and unknown effects that go beyond eliminating one kind of cell or receptor, as the remaining cells reorganize in complex ways that one might not have predicted.

Temporary Inactivation

For many research questions, one might want to study the effect of inactivating a particular brain area at a particular time. For example, is the amygdala more important during acquisition of a learned response, or during its retrieval? To answer such questions, one might insert a thin cannula into a brain area, again using a stereotaxic atlas, and then deliver a compound such as muscimol. Muscimol, a psychoactive chemical found in certain mushrooms, selectively stimulates receptors sensitive to GABA, the brain’s main inhibitory neurotransmitter. As a result, muscimol suppresses activity in nearly all neurons in the affected area. A researcher can also inactivate neurons in a particular brain area by cooling them with a metal probe that is cold at the tip but insulated along the rest of its surface (e.g., Chambers & Wang, 2004). Either muscimol or cooling can temporarily suppress activity in a brain area. However, these procedures do not enable someone to turn a brain area off and on quickly. For an example of a study using temporary inactivation, Richard Thompson and his associates inactivated the red nucleus of rabbits during the training phase of a classical conditioning experiment. During this phase, the rabbits showed no conditioned responses. However, when the red nucleus recovered its activity, the rabbits showed the full response, indicating that the red nucleus was necessary for the response but not for learning. In contrast, when the researchers inactivated the lateral interpositus nucleus of the cerebellum, rabbits showed no responses during training and no retention at a later test. Evidently the lateral interpositus nucleus was necessary for learning and not just for the motor response (Krupa, J. K. Thompson, & R. Thompson, 1993).

Researchers would not subject a human brain to either muscimol or a cold metal probe. However, the technique of transcranial magnetic stimulation is available for temporarily inactivating part of the human brain. An investigator applies an intense magnetic field over a portion of the scalp, temporarily inactivating the neurons nearest the magnet (Walsh & Cowey, 2000). Again, this procedure makes it possible to turn a brain area on and off during different phases of a task. A scientific limitation is that it can be applied only to brain areas on the surface, as opposed to the interior of the brain. An ethical limitation is that repetitive pulses can induce seizures and possibly other health problems (Wasserman, 1998).

Difficulties Interpreting Lesion Studies

The results of a lesion study provide, at best, a start toward understanding the function of some brain area or system. They tell us where something happens, but not how. If you remove a chip from inside your computer and find a loss of sound, you know that this chip contributes in some way to producing sound, but you do not know in what way. Similarly, if you damage a brain area and see that an animal learns less readily, you could imagine many possible explanations. The damaged animal might be impaired in perception, attention, motivation, or other processes that affect learning, or in the learning process itself. If learning is impaired, the problem might relate to storing information, retaining it, retrieving it, or avoiding interference that increases forgetting. In some cases, damaging an area impairs some aspect of behavior only because the lesion interrupted axons passing nearby the area (e.g., Almli, Fisher, & Hill, 1979; Berridge, Venier, & Robinson, 1989).

Ideally, researchers like to demonstrate a double dissociation of function—that is, a demonstration that one lesion impairs behavior A more than behavior B, whereas a second lesion impairs B more than A. If some kind of brain damage impairs explicit memory more than implicit memory, we don’t know that it is specifically important for explicit memory, because an alternative explanation is that explicit memory is more difficult than implicit memory. In that case, any lesion that impaired attention, arousal, motivation, or other processes would impair explicit more than implicit memory. However, if other kinds of brain damage impair implicit more than explicit memory, we gain confidence that the two kinds of lesions are really affecting memory in different ways.

A further difficulty with lesion studies is that the brain’s plasticity can mask the effect of a deficit. For example, many neurotransmitters contribute to the regulation of feeding, but a targeted disruption of one of them may have little effect because the others compensate. In some cases, disrupting one pathway sets in motion a reorganization of others with far-reaching, unpredicted effects. In one study, researchers knocked out the gene for one type of potassium channel in the neuronal membrane in mice. Although one would expect to find deficits, the first effect they noticed was that the mice had a thousand fold increase in their olfactory sensitivity (Fadool et al., 2004).

Effects Of Brain Stimulation

If brain damage impairs some behavior, stimulation should increase it. Thus, one way to confirm the results from a lesion study is to follow up with a stimulation study. One method suitable for use with healthy humans is to apply a magnetic field to the scalp, using much briefer and milder amounts than with the transcranial magnetic stimulation mentioned earlier. The result is increased activity of neurons in the brain areas nearest the magnet (Fitzgerald, T. L. Brown, & Daskalakis, 2002). Occasionally, neurologists have electrically stimulated spots in the brain of a person who is undergoing brain surgery under local anesthesia. For example, that kind of research was responsible for the first mapping of the human motor cortex and somatosensory cortex (Penfield & Rasmussen, 1950).

With laboratory animals, researchers can use a stereotaxic instrument to insert an electrode to stimulate a small area anywhere in the brain, such as the hypothalamus. Alternatively, they inject chemicals either into the bloodstream or directly into the brain. Examples include drugs that stimulate or block particular neurotransmitter receptors. Other examples include hormones, which modulate activity of whatever neurons respond to them. If injected systemically, the chemicals exert their effects wherever the corresponding receptors occur in the brain. If injected in small amounts into a specific brain area, they have much more localized effects. This type of research has become common in behavioral neuroscience.

An alternative to injecting chemicals is to use a virus vector to increase the expression of a particular gene. For example, male prairie voles form pair bonds with females and help them rear their young, whereas males of the closely related meadow voles do not. They differ in their secretion of the pituitary hormone vasopressin, with prairie voles secreting much more. When researchers used a viral vector to transfer a gene into the hypo-thalamus and pituitary of meadow voles, increasing their production and release of vasopressin, the males became monogamous and began helping with infant care (Lim et al., 2004).

Directly stimulating the brain is, of course, unlike normal brain activity. When you see a face or hear a melody, you have a distinct pattern of activity distributed over a huge number of cells, modulated in a specific way over time. Electrical or magnetic stimulation of a small brain area can produce meaningful results in certain areas where precise timing is less important—for example, the areas controlling hunger or thirst. However, stimulation of any one spot in the primary visual cortex produces reports of flashes of light, not of meaningful objects.

For decades, the same appeared to be true of the motor cortex as well. Brief electrical stimulation of monkeys’ motor cortex produced only uncoordinated muscle twitches. However, later researchers found that a half-second pulse of stimulation elicited complex sequences of actions. In one case, stimulation of a certain spot led a monkey to move its hand from wherever it was to its mouth, even though the monkey had to use different muscles depending on the starting position of the hand (Graziano, Taylor, & Moore, 2002). In this case, stimulation research led us to a new conclusion: Cells of the motor cortex have their output organized according to the outcome of the movement, not the muscle contractions themselves (Scott, 2004).

Recording Brain Activity

We generally think of biological psychology or behavioral neuroscience as a field that uses experimental methods. However, a significant amount of research also uses correlational methods. For example, researchers correlate observed behavior with measurements of brain activity.

Electroencephalography and Related Procedures

In contrast to research that requires inserting electrodes into the brain, subjecting it to hazardous chemicals, or applying strong magnetic fields, one of the least intrusive research methods is an electroencephalograph (EEG). To set up an EEG, a researcher glues some electrodes to a person’s scalp—ranging from just a few electrodes to a hundred or more. Each electrode provides an average for the instantaneous activity of the population of cells under it. That output is amplified and recorded. A classic use of EEG is to monitor stages of sleep, with slow waves indicating stages 3 and 4 of sleep.

Researchers can use the same equipment to record brain activity in response to sensory stimuli, in which case the procedure is called evoked potentials or evoked responses. Researchers attend particularly to the responses evoked at particular latencies after a stimulus. For example, a typical person shows a strong positive response, known as the P300 wave, about 300 ms after an especially meaningful stimulus, such as a rare target to which the person is supposed to respond. The P300 wave is weaker than average among people with schizophrenia, attention deficit disorder, and other conditions that impair attention (Du et al., 2006; Price et al., 2006).

A magnetoencephalograph (MEG) is similar to an EEG, but it measures the faint magnetic fields generated by brain activity instead of electrical activity (Hari, 1994). MEG has superb resolution over time, sensitive to changes occurring in as little as a millisecond. This fine resolution enables researchers to follow a wave of brain activity from its point of origin to all the other areas that it affects (Salmelin, Hari, Lounasmaa, & Sams, 1994). However, both EEG and MEG have mediocre resolution over space, as they average the activity occurring over a surface of at least a square centimeter.

Body Fluid Samples

Because the brain’s metabolites eventually wash out of the brain, researchers can monitor body fluids as an admittedly imperfect but relatively simple gauge of certain kinds of brain activity. For example, when a neuron releases the neurotransmitter serotonin, much of the serotonin returns to the presynaptic neuron, but some of it is metabolized to 5-hydroxyindoleacetic acid (5-HIAA). The neuron synthesizes new serotonin molecules to replace those it loses as 5-HIAA; the overall process is called serotonin turnover. Researchers can assay the 5-HIAA levels of the cerebrospinal fluid, blood, or urine to estimate the amount of serotonin turnover in the brain. Although this method is far from perfect, as platelets and other peripheral tissues produce serotonin also, the measurements do correlate with certain aspects of behavior. For example, decreased levels of serotonin turnover correlate with increased probability of violent behaviors in rats, monkeys, and humans (T. L. Brown et al., 1982; Higley et al., 1996; Valzelli, 1973). This approach is limited to the study of fairly long-lasting trends in behavior. Because the half-life of 5-HIAA in the cerebrospinal fluid is more than an hour (Mignot, Laude, & Elghozi, 1984), researchers cannot apply this measure to moment-by-moment changes in behavior.

Histological Measurements

Another way to monitor activity in various brain areas in laboratory animals is to take slices of the brain and apply stains that react to the protein fos. The fos gene has pervasive effects throughout the body, being activated in the early stages of cell division as well as during neural activity. Within neurons, any pattern of sustained activity, such as might occur during learning, for example, leads to an increase in fos expression that researchers can detect beginning about 15 minutes later. It is apparently a reaction to the increased neuronal activity, rather than a prerequisite for starting it. Although the slow time course precludes measurement of rapid changes, the method does reveal changes over a longer time scale. In one study, researchers found that seizures increased fos expression in the dentate gyrus of the hippocampus 90 minutes later, and still later in surrounding areas of the hippocampus and cerebral cortex (Morgan, Cohen, Hempstead, & Curran, 1987). Staining for fos activity has been useful for such questions as identifying the brain areas responsive to social stress in rodents (Martinez, Calvo-Torrent, & Herbert, 2002) and specifying the nuclei of the hypothalamus that respond to cholecystokinin, a satiety signal (Kobelt et al., 2006).

Correlating Brain Anatomy With Behavior

In addition to correlating behavior with brain activity, researchers sometimes correlate behavior with brain anatomy. That approach has persisted throughout the history of neurology, although the earliest examples are not to be celebrated. Franz Gall and the other phrenologists of the 1800s attempted to relate people’s personalities to their brain anatomy, using bumps and depressions on the skull as an indicator of the brain structures underneath. This effort was ill-fated from the start, as the surface of the skull is a poor indicator of brain anatomy. Furthermore, the phrenologists used their data uncritically, sometimes drawing conclusions about the functions of a particular brain area from their observations of just one or a few people.

Another early goal was to relate intelligence to brain size or structure. Several societies arose in the 1800s and 1900s devoted to preserving the brains of eminent men after death, including the members of those societies themselves, in hope of finding some distinctive aspect of the size or structure of the brain that separated successful from less successful men. (Women were ignored.) These projects led to no conclusion, partly because achieving eminence depends as much on opportunity as intellectual ability, and partly because the correlation of brain anatomy with intelligence is at best a weak one, not obvious with visual inspection of casually selected samples (Burrell, 2004; Schoenemann, Budinger, Sarich, & Wang, 2000).

Although we now regard these early pursuits with either disdain or amusement, let’s admit that we are still subject to a similar temptation today. When the famous scientist Albert Einstein died in 1955, researchers removed his brain, hoping to find some unusual feature responsible for his brilliance. Decades later, the researchers—who were apparently in no hurry about this task—reported that Einstein had a higher than average ratio of glia to neurons in one brain area (Diamond, Scheibel, Murphy, & Harvey, 1985), and that his inferior parietal cortex was noticeably expanded (Witelson, Kigar, & Harvey, 1999). Although the researchers were careful not to draw conclusions, the implication was that these brain features had some relation to Einstein’s scientific achievements. Perhaps so, but we cannot be sure until we compare the brains of many other scientists of Einstein’s stature—and let’s not hold our breath waiting. We also need to determine how often such features occur in the brains of less distinguished people. The problem is not just that Einstein was a single case, but also that the researchers examined many aspects of his brain in search for something noteworthy. Given that we do not know exactly how many total hypotheses researchers considered, we cannot readily interpret a couple of differences between Einstein’s brain and everyone else’s.

Nevertheless, much useful research does use the strategy of correlating brain anatomy with behavior. Fascinating studies have reported expansion of the right auditory cortex in professional musicians (Schneider et al., 2002), increased representation of the fingers of the left hand in the somato-sensory cortex of lifelong violin players (Elbert, Pantev, Wienbruch, Rockstroh, & Taub, 1995), and expansion of the hippocampus in London taxi drivers (Maguire et al., 2000). Species comparisons have found that members of the jay family with the greatest spatial memory also have the largest hippocampus (Basil, Kamil, Balda, & Fite, 1996). Each of these differences is consistent enough across individuals to be reliable, and each confirms what other kinds of research indicate about the functions of those brain areas.

If we want to study the physiological basis of an uncommon psychological disorder, the only reasonable starting point is to compare the brains of people affected with the disorder to those of other people. For example, Williams syndrome is a genetically determined condition marked by mental retardation in most regards, yet often remarkably good skills at language, music, and social relationships. The syndrome is consistently associated with reduced gray matter in the occipital cortex and parts of the thalamus, but greater than average volume in parts of the temporal and frontal cortices (Reiss et al., 2004). These differences are reasonably consistent over a large number of people, and they have the potential to inspire further research. For present purposes, the point is that the research is necessarily correlational in nature.

Researchers who study schizophrenia, depression, and a host of other conditions compare the brains of individuals with the condition to control participants. In each case, moderately consistent patterns do emerge, which may provide a clue to understanding the disorder. The most important way in which this approach differs from phrenology is that modern researchers compare large groups of people, reporting only the differences that emerge as statistically reliable. A lingering problem is that anyone who examines all parts of the brain is simultaneously testing a huge number of hypotheses, and therefore has a strong possibility of finding differences by accident.

An additional problem with this kind of research is the choice of a control group. Suppose, for example, we are searching for distinctive brain features associated with schizophrenia. We assemble a group of people with schizophrenia. Who should be in the control group? Any good researcher knows to match people for age and sex, but is that enough? In many cases the ideal comparison is between siblings, of whom one has the condition and one does not. However, in the case of schizophrenia, none of these approaches is fully satisfactory. Many people, especially men with schizophrenia, abuse alcohol or other drugs. Given that alcohol and other drugs can affect brain anatomy, some of the brain abnormalities associated with schizophrenia may in fact be consequences of the drugs themselves, or of drug-related problems, including poor diet and head trauma (Sullivan et al., 2000). If we want to examine the effects of schizophrenia itself, we need a control group matched for use of alcohol and other drugs.

Behavioral Studies

Finally, consider one additional research approach, which does not tell us anything new about brain-behavior relations, but uses what we do know to provide information about individuals. If research has already established that a certain kind of brain damage leads to a particular behavioral deficit, researchers can test that kind of behavior to draw inferences about possible brain impairments. For example, in the Wisconsin General Test Apparatus, one task is to sort a set of cards first by one rule (such as color) and then by a second rule (such as number). Any damage or impairment of the prefrontal cortex impedes a person’s ability to shift to the second rule. Many people with schizophrenia perform poorly on this task, implying possible difficulties in their prefrontal cortex.

Summary

The Nobel laureate biologist Sydney Brenner was quoted as saying that progress in science depends on “new techniques, new discoveries, and new ideas, probably in that order” (McElheny, 2004, p. 71). That is, most scientific discoveries begin with new or improved methods of measuring something. Brain science relies on a huge variety of methods, including the ones described here, which differ enormously in their details but generally fall into four categories: the effects of brain damage, the effects of brain stimulation, measurements of brain activity during behavior, and correlations of brain structure with behavior. Future research will advance as we devise and improve new methods of measurement.

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