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Autonomous processing in the brain

Brain Cortical Neuronal Circuits

Ann M. Graybiel and Scott L. Rauch, "Toward a Neurobiology of Obsessive-Compulsive Disorder" (2000), suggest that "parallel processing" may occur in the brain to allow emergence of OCD symptoms. They propose that while one circuit supports conscious information processing, another separate circuit might support automatic information processing. To avoid confusion with functional parallel cortical-subcortical circuits, however, this kind of dysfunction is called"autonomous processing." In other words, parallel circuits that normally share information across pathways to shape behavior, for some reason, begin to function autonomously. This idea is key to understanding many troublesome behavioral symptoms. For example, while one circuit focuses on cognition including problem solving and processing of whatever daily stimuli one encounters, another independent circuit might inappropriately prompt motor routines, especially routines generated from bioprograms that have, over evolutionary time, developed to discharge energy in the face of frustration or to maintain relationships (e.g., grooming). As we discuss in Part 2 of CorticalBrain.com, when they occur out of context, such behaviors are called displacement activities and often include fixed-action patterns that can, under chronic stress, including isolation, turn into dangerous stereotypies. (See Fixed-action patterns and OCD and Displacement, stereotypies, frustration, and perseveration—understanding ADHD, OCD, PTSD, and Tourette Syndrome.)




































To see a diagram of how the cortical-subcortical circuits are organized, including the direct pathway (labeled A - RELEASE) and the indirect pathway (labeled B - INHIBIT) mentioned above, link here to the American Journal of Psychiatry. We will discuss the commentary provided with the graphic and photograph in the paragraphs below. Source: Images in Neuroscience, Carol A. Tamminga, M.D., Editor, Am J Psychiatry 158:1, January 2001.

Although the science is high-level and difficult for me to interpret, Charles R. Gerfen, in a 1984 article titled "The Neostriatal Mosaic: Compartmentalization of Corticostriatal Input and Striatonigral Output Systems," elucidates the mechanism that, when functional and integrated, coordinates thinking-feeling behavior with motor behavior. When dysfunctional, however, the same system could result in autonomous processing, wherein emotional-cognitive signals are separately processed from motor signals in the corpus striatal complex. In other words, during such autonomous processing, you would be thinking about one thing and doing another thing.

The striatum (caudate-putamen) of the basal ganglia in the mammalian forebrain is a mosaic of two interdigitating, neurochemically distinct compartments. One type, the "patch" compartment, is identified by patches of dense opiate receptor binding and is enriched in enkephalin- and substance P-like immunoreactivity. The other compartment, the "matrix", has a high acetyl-cholinesterase activity and is shown here to have a dense plexus of fibres displaying somatostatin-like immunoreactivity. The present study demonstrates the two compartments have distinct connections, using a method that concurrently reveals striatal input, output and neurochemical systems in the rat.

Patches receive inputs from the prelimbic cortex (a medial frontal cortical area with direct "limbic" inputs from the amygdala and hippocampus); they also project to the substantia nigra pars compacta (the source of the nigrostriatal dopaminergic system). Conversely, the matrix receives inputs from sensory and motor cortical areas; here it is shown to project to the substantia nigra pars reticulata (the source of the non-dopaminergic nigrothalamic and nigrotectal system). Also, an intrinsic striatal somatostatin-immunoreactive system is described that may provide a link between the two compartments. The striatal patch and matrix compartments thus appear to be functionally distinct and interactive parallel input-output processing channels.

In a short essay accompanying visuals in the 2009 American Journal of Psychiatry mentioned above, Ann M. Graybiel refers to striosomes and matrix components of the striatum. So what Graybiel calls striosomes in 2009, Gerfen called patches in 1984. Graybiel writes: "Already it is known that the matrix receives the striatal afferents most directly related to sensorimotor processing. In contrast, striosomes (including the entire ventral striatum) tend to receive inputs from neural structures affiliated with the limbic system, particularly the amygdala. Their segregated projections, intimately associated within the striatum, could subserve communication between these functionally distinct pathways.

brain striatum graybiel brain striatum graybiel

The following paragraphs accompany the image to the right (links to source) in an award nomination called "Neurochemical Compartmentalizatin of the Striatum." the bold emphasis is added .

Our brain can construct language, music and mathematics, but the same brain also lets us develop habits of thought and action. These semi-automatic routines free us to think and to attend to the world. Getting the right balance of what we do with conscious effort and what we do seemingly effortlessly by habit is part of the role of the basal ganglia, deep structures in the forebrain that interact with the neocortex above. The striatum, the main input structure of the basal ganglia, is responsible for much of what we call habit learning. Moreover, the striatum is centrally implicated in human neurologic and neuropsychiatric disorders. These range from problems that affect the motor system, as in Parkinson's disease, to problems that affect cognition and emotion and action control, as in obsessive-compulsive disorder, Tourette syndrome, depression and states of addiction. Imbalances in neurotransmitters in the striatum are now known to be important both for the normal functions of cortico-basal ganglia circuits and for the development of disordered functions in basal ganglia-based disorders.

This image [above right] illustrates a thin slice through the striatum of the human brain stained with a molecular stain that shows in white the distribution of one of the most important neurotransmitter systems in the basal ganglia, acetylcholine. Within the large white zones there are small gray zones of lower cholinergic staining. These are the striosomes (striatal bodies) that are thought to function in integrating emotional and cognitive signals with sensorimotor signals in the striatum. It is now thought that a balance between the striosomes and the extrastriosomal matrix is critically important in the balance between repeating the same action or choosing another action, and that disruption of this balance may contribute to dysfunction in basal-ganglia based neurologic and neuropsychiatric disorders. The jet black zone that cuts into the white-stained striatum is not the striatum, but the large bundle of fibers that interconnect the neocortex with the striatum and other sites. Striosomes were first identified in the human brain in 1978 by the Graybiel Laboratory at MIT.

Dopamine-driven bioprograms in the brain:

In "The Role of Nucleus Accumbens Dopamine in Motivated Behavior: A Unifying Interpretation with Special Reference to Reward-Seeking," Satoshi Ikemoto and Jaak Panksepp emphasize that "all brain DA systems promote widespread sensory-motor arousal and competence within the brain." It is my contention that chronic stress can kindle changes in neurocircuitry, including excessive transmission of dopamine and that this can result in OCD, compulsive grooming, PTSD, and hypersensitivity that may look like ADHD symptoms. Or, looking at things another way, this kind of chronic stress might activate genetic vulnerabilities or exacerbate mild symptoms that otherwise would go undetected.

Ikemoto and Panksepp point out that aversive, stressful stimuli, including social isolation, appears to facilitate dopamine release in the nucleus accumbens. The authors note that experiments in rats involving foot shock and tail pinch indicate that both unconditioned and conditioned stimuli prompts this increased dopamine release. For nonscientists, Ikemoto and Panksepp offer the following primer on the differences between types of stimuli.

In the Pavlovian (or classical) conditioning procedure, biologically important stimuli are defined as unconditioned stimuli because they can trigger unconditioned responses, that are 'inborn' or 'species-typical' reflexes. Examples of unconditioned stimuli are food, water, and various noxious stimuli. When other comparatively neutral sensory stimuli precede the presentation of such unconditional stimuli, and this pairing is repeated, conditioning occurs. Conditioned responses that were not present prior to such pairings can be now observed when the previously neutral sensory stimuli are presented alone. The sensory stimuli are now referred to as conditioned stimuli.

In the next paragraphs, we will discuss several experiments more specifically to show how stress affects release of dopamine in the nucleus accumbens. If Ikemoto and Panksepp are interpreted correctly, evolution is responsible for the increased dopamine release in these kinds of aversive-stimuli experiments. The increased dopamine enables animals within a natural habitat to aggressively seek safety. For humans in the modern world who encounter complex and conflict-laden stressful stimuli, however, such safety-seeking behaviors might not be so easy to put into action. It is contended that it is in situations of chronic stress that increased dopamine release, via possible actuator action of the nucleus accumbens, can prompt automatic behavioral responses—either motor, cognitive, or both—from a repertoire of atavistic or kindled bioprograms.

brain dopamine anticipation

In anticipation of receiving cocaine, dopamine transmission in the nucleus accumbens of rats rises rapidly. In drug-addicted humans, scientists hypothesize that this surge of dopamine erodes their resolve to abstain. In other words, the dopamine surge activates learned behavior that is not easily controlled. The caption for the image to the right (links to source) reads: "Rats trained to self-administer cocaine exhibited elevations in dopamine concentrations when they anticipated cocaine and again when they began to seek the drug." Arrows mark these increases in the illustration. Once a rat pressed the lever, anticipation and dopamine peaks, and with a cocaine infusion, dopamine plummets.

Perhaps excessive dopamine production due to stress may function in a similar way as the increased dopamine production seen in the anticipation of cocaine in rat experiments. Perhaps excessive or repeated dopamine production somehow overwhelms inhibitory GABA activity, and in effect begins to automate and differentiate a learned behavior, without regard for whether the behavior is appropriate. In Toward a Neurobiology of Obsessive-Compulsive Disorder," Graybiel eloquently explains the somatic marker hypothesis. "In what has come to be called the somatic marker hypothesis, Damasio and his colleagues suggest that exposure to particular stimuli or contexts reactivate somatic states (autonomic responses, as indicated in their experiments by galvanic skin responses) that, through experience, have become associated with the stimuli. They propose that in OCD, this reactivation of somatic markers in response to expected outcomes becomes excessive, driving the behavioral repetition."

So whereas incentive salience involves amygdala processing and labeling of stimuli, the somatic marker hypothesis relates to the whole-body (somatic) response to specific stimuli. Perhaps these two theories are more alike than different.

In a 1995 study of conditioned dopamine release designed in part to measure the effects of stress on dopamine release in the rat nucleus accumbens, N. Saulskaya and C.A. Marsden write: "The extracellular level of dopamine in the medial nucleus accumbens markedly increased for up to 40 min when rats were given mild footshock in the testing. When the rats were returned to the testing, but not given footshock (conditioned emotional response), there was an immediate and long-lasting (80 min) increase in extracellular dopamine." The authors conclude that their study's results "indicate that the acquisition of conditioned emotional response causes long-lasting changes in the mechanisms involved in the glutamatergic control of dopamine release in the nucleus accumbens."

Getting specific about dopamine fluctuations in certain regions of the nucleus accumbens, Peter W. Kalivas and Patricia Duffy, in "Selective Activation of Dopamine Transmission in the Shell of the Nucleus Accumbens By Stress" (1995) write: "A microdialysis probe was placed in either the shell or core compartment of the nucleus accumbens and rats were exposed to mild footshock. Extracellular dopamine levels in the shell of the nucleus accumbens were elevated during the 20-min collection period immediately after discontinuing footshock. In contrast, the levels of dopamine remained unaltered in the core of the nucleus accumbens."

Explaining obsessions and compulsions:

Differentiated processing takes place in cortical-subcortical loops. Within each loop there are neurochemical RELEASE mechanisms that prompt behavior and INHIBITORY mechanisms that restrict behavior. Symptoms might arise when the processing in these loops is not integrated or when the release and inhibitory mechanisms are out of balance.

In "A Psychological and Neuroanatomical Model of Obsessive-Compulsive Disorder" (2008), Huey et al. write: "The most accepted neuroanatomic model of OCD is based on the finding that there are separate cortico-basal ganglia-thalamic-cortical loops." We discuss these loops above in The brain's cortical-subcortical circuits.

Regarding cortico-basal ganglia-thalamic-cortical loops, Huey et al. discuss how the model explaining obsessions and compulsions has been refined "by specifying that overactivation of the direct pathway in the basal ganglia relative to the indirect pathway results in an orbitofrontal-subcortical hyperactivity." In the graphic provided in the 2009 American Journal of Psychiatry, the direct pathway is labeled "A-Release" and the indirect pathway is labeled "B-Inhibit." Note that this illustration implies that the direct and indirect pathways involve different dopamine receptors.

In Autonomous processing in the brain, above, we discuss how emotive-cognitive neurosignaling and motor neurosignaling are processed—not only within differentiated circuits—but within different compartments within the corpus striata complex. Symptoms might arise when the processing in these compartments is not functionally integrated due to injury, disease or an overload of dopamine from either of two sources—the VTA or the substantia nigrae.

Regarding dopamine output to the striatum, in Dopamine action, synthesis, and pathways, we discuss how dopamine-producing neurons in the VTA project to the nucleus accumbens or the ventral striatum while dopamine-producing neurons in the substantia nigra project to the caudate-putamen or dorsal striatum. In "Learning and Memory Functions of the Basal Ganglia," M.G. Packard and B.J. Knowlton clarify further these projections in terms of patches (or "striosomes" including the entire ventral striatum / nucleus accumbens) and matrix compartments. They write: "Both striatal compartments receive dopaminergic input, although dopamine pathways originating in the ventral tegmental area and substantia nigra appear to primarily innervate the patch and matrix, respectively." In other words, SEEKING system, motivating dopamine produced in the VTA transmits directly to the nucleus accumbens (a patch/striosome area).

In "Obsessive-Compulsive and other Behavioural Changes with Bilateral Basal Ganglia Lesions: A Neuropsychological, Magnetic Resonance Imaging and Positron Tomography Study" (1989), D. Laplane et al. report: "The existence of distinct nonoverlapping circuits in the motor field or in the associative field can explain the fact that basal ganglia lesions may give rise to a clinical picture that is either purely motor, purely behavioural (as in some of our patients), or both." Also, Huey et al. point out that "patients with excessive nigrostriatal dopaminergic input (such as patients with Huntington's disease) have excessive motor output." We discuss Huntington's Disease in The corpus striata (basal ganglia) complex.

Excessive dopamine may kindle neural patterns. Such an overproduction of dopamine may occur when one is overly motivated to solve problems–that is, in cases of chronic stress including emotional stress.

In " Corticostriatal Interactions during Learning, Memory Processing, and Decision Making, Pennartz et al. write, "Components of the neocortical-basal ganglia loops are essential for learned actions to become habitual, and abnormal activity within these loops is implicated in a range of clinical disorders related to action compulsion (as in obsessive-compulsive spectrum disorders and drug addiction) and action disability (as in Parkinson's disease and Huntington's disease) (Graybiel, 2008)." The authors go on to describe highly technical experiments using rats as subjects. The results of these experiments "indicate that habit formation and modification do not involve turning on and off a striatal 'habit system,' but rather a dynamic repatterning of neural activity (Barnes et al., 2005)."

As we discuss throughout Part 2 of CorticalBrain.com regarding ancestral brain systems (See Emotions are Hard-Wired in the Brain: Introduction to Ancestral Brain Systems), emotive neurosignaling is often paired with action-oriented motor behavior although the two are processed in separate compartments of the corpus striata complex. In functional systems, the two modes of behavior are coordinated. As Panksepp explains, emotional systems have "intrinsic response patterning mechanisms, and one of the main functions of higher brain evolution has been to provide ever-greater flexible control over such mechanisms." So what defeats neocortical control, allowing for obsessions and compulsions? It is contended that there are several variables that might disrupt the integration of emotive-cognitive neurosignaling with motor neurosignaling within the corpus striata complex, resulting in symptoms. We discuss these variables in OCD risk factors. In summary, these risks can be genetic, epigenetic, injury-related, viral induced, or involve chronic stress that kindles vulnerable neurocircuits.

Regarding kindling, in the section titled Dopamine-driven bioprograms in the brain, we focused on how chronic stress increases dopamine within the nucleus accumbens, and how such an overload of dopamine might eventually overwhelm the inhibitory action of GABA, turning the nucleus accumbens into a sort of actuator for prompting kindled neural patterns. Although the following information has been included previously, it bears repeating: "The nucleus accumbens, which lies within the basal ganglia, may be a primary ganglion for the organization of action within the brain," writes Jay Schulkin in Effort: A Behavioral Neuroscience Perspective on the Will (2007). "Some time ago, Nauta (1961; Kelley, Domesick, & Nauta, 1982; Nauta & Domesick, 1982) suggested that the nucleus accumbens is an important link between the amygdala and motivation for the organization of action (Mogenson & Huang, 1973). Translation of motivational output from the amygdala to the behavioral outputs of the basal ganglia takes place via the connectivity to the nucleus accumbens (Kelley, 1999; Mogenson, Jones and Yim, 1980; Swanson, 2003)."

Here again is N.M. White's observation: "Evidence at several levels of analysis (including neuroplastic synaptic changes, activity of single neurons, and behavioral changes caused by lesions or neurochemical manipulations) implicate dopamine release from nigro-striatal neurons in the reinforcement, or strengthening, of neural representations in the basal ganglia." So while dopamine from the VTA may prompt the nucleus accumbens to initiate a neural pattern, perhaps it is the dopamine from the substantia nigrae that kindles that neural pattern. To be sure, dopamine is involved.

It is contended here that dopamine promotes the kindling process which can in turn 1) create hard-wired, hypersensitive neural networks or bioprograms or 2) that can sort of hijack and build on atavistic fixed-action patterns.

Our physical existence is organized around pattern generation. Is it any wonder that dysfunctions in our brains might prompt patterned behavior inappropriate to our complex human situations?

Packard and Knowlton write: "With regards to learning and memory functions, one interesting recent hypothesis is that fronto-cortical-striatal loops are used by the basal ganglia to essentially train the cortex to produce learned motor responses in the presence of a particular pattern of sensory information (Wise et al. 1996). However, it is important to note that, although basal ganglia output is clearly looped via the globus pallidus and thalamus back to specific cortical sites, pallidal and nigral outputs also directly project to downstream brain-stem structures that allow for rapid access to spinal control of motor responses."

In trying to understand any kind of behavior, it is important to recognize the importance of pattern generators in the brain. An area of the brain stem known as a central pattern generator, for example, controls the complexities of our breathing. Regarding central pattern generators, Neil Shubin explains in Your Inner Fish: A Journey Into the 3.5-Billion-Year History of the Human Body (2009) that these kinds of mechanisms "produce rhythmic patterns of nerve and, consequently, muscle activation." He adds: "A number of such generators in our brain and spinal cord control other rhythmic behaviors, such as swallowing and walking."

In Toward a Neurobiology of Obsessive-Compulsive Disorder," Graybiel writes: "One hypothesis emerging from these findings is that the basal ganglia may influence both motor pattern generators in the brainstem and spinal cord and “cognitive pattern generators” in the cerebral cortex. By this view, the loops running from the neocortex to the basal ganglia and then to the thalamus and back to the neocortex may help to establish cognitive habits, just as they may influence the development of motor habits (Graybiel, 1997). If so, the cortico-basal ganglia loop dysfunction in OCD could reflect both sides of basal ganglia function, motor and cognitive, to bring about repetitive actions (compulsions) and repetitive thoughts (obsessions)."


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