Scientific Understanding of Consciousness
Consciousness as an Emergent Property of Thalamocortical Activity

Reward and Punishment

 

Having reward and punishment systems is the solution that evolution has developed to produce appropriate behavior. (Rolls; Emotion Explained, 7)

Computing the reward and punisher value of sensory stimuli, and then using selection between different rewards and avoidance of punishers in a common reward-based currency appears to be the fundamental design that brains use in order to produce appropriate behavior. (Rolls; Emotion Explained, 7)

Emotion and motivation are linked by the property that both involve rewards and punishers. (Rolls; Emotion Explained, 1)

Rewards and Punishers as primary at reinforcers

 

 

Science 13 February 2009: Vol. 323. no. 5916, pp. 890 - 891

Pains and Pleasures of Social Life

Matthew D. Lieberman and Naomi I. Eisenberger

Department of Psychology, 1285 Franz Hall, University of California at Los Angeles, Los Angeles, CA 90095-1563, USA.

Neuroscientists have identified neural systems responsible for experiences of pain and pleasure.

The cortical pain network consists primarily of the dorsal anterior cingulate cortex (dACC), insula, and somatosensory cortex, with subcortical contributions from the periaqueductal gray and thalamus. Whereas the somatosensory cortex is associated with sensory aspects of cutaneous physical pain (e.g., its location on the body), the dACC is associated with the distressing aspect of pain.

The brain's reward circuitry consists of neural structures receiving the neurotransmitter dopamine from the ventral tegmental area, and responds to physically rewarding stimuli such as food, drugs, and sexual activity. The nucleus accumbens in ventral striatum plays a critical role in reward learning and pleasurable states, while the ventromedial prefrontal cortex and amygdala are also major dopaminergic targets that have been implicated in reward processes

 

 

Pleasure is a key factor in controlling the motivated behavior of humans. (Kandel; Principles of Neural Science, 1007)

Stimulation of the nucleus accumbens in humans elicits smiling, laughter, pleasurable feelings, happiness, even euphoria. (Cardoso; Hardwired for Happiness, 173)

Amygdala and its connections to the prefrontal cortex and basal ganglia are likely to influence the selection and initiation of behaviors aimed at obtaining rewards and avoiding punishments. (Purves; Neuroscience, 701)

Orbital cortex may be especially involved in working memories about rewards and punishments. (LeDoux; Emotional Brain, 285)

Nucleus accumbens -- part of a network of structures involved in feelings of pleasure and reward, whether it is through eating, having sex, or listening to pleasurable music. (Levitin; Your Brain on Music, 89)

 

Pain and pleasure systems

All feelings contain some aspect of pain or pleasure as a necessary ingredient. (Damasio; Looking for Spinoza, 123)

Pain is the perception of a sensory representation of local living tissue dysfunction. (Damasio; Feeling of What Happens, 76)

Pleasures associated with eating or drinking. (Damasio; Feeling of What Happens, 77)

Thwarting of the consummation may actually cause anger. (Damasio; Feeling of What Happens, 77)

Alleviation or suspension of the state of pain may cause the emergence of pleasure and positive emotions. (Damasio; Feeling of What Happens, 77)

More than two emotions, some aligned with pain, some aligned with pleasure, mostly with pain. (Damasio; Feeling of What Happens, 77)

Pleasure leads an organism to attitudes and behavior that are conducive to the maintenance of its homeostasis. (Damasio; Feeling of What Happens, 77)

 

 

Nature 454, 600-606 (31 July 2008)

Switching on and off fear by distinct neuronal circuits

Cyril Herry, Stephane Ciocchi, Verena Senn, Lynda Demmou, Christian Müller, Andreas Lüthi

Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland

Switching between exploratory and defensive behaviour is fundamental to survival of many animals. The amygdala is a key brain structure mediating defensive behaviour in states of fear and anxiety. Such states can be induced by classical auditory fear conditioning, in which an initially neutral auditory stimulus (the conditioned stimulus, CS) comes to elicit a fear response after pairing with an aversive foot shock (the unconditioned stimulus, US). Subsequent repetitive presentations of the CS alone induce a progressive decrease in the fear response, a phenomenon called extinction. Whereas firing of amygdala neurons is critical for the retrieval of conditioned fear memories, their firing after the extinction of conditioned fear is thought to be constrained by local inhibitory circuits activated by the medial prefrontal cortex (mPFC), Converging evidence from animal studies indicates, however, that the basolateral complex of the amygdala (BLA), comprising the lateral (LA) and the basal (BA) nuclei, actively participates in fear extinction. Although fear extinction is an active learning process eventually leading to the formation of a consolidated extinction memory, it is a fragile behavioural state that is readily influenced by context. Changing context results in the immediate recovery of the previously conditioned fear response, a process known as fear renewal. In vivo pharmacological studies indicate that the hippocampus, which is reciprocally connected to the BLA, processes contextual information during fear conditioning, extinction and renewal. Thus, bi-directional changes in fear behaviour during extinction and context-dependent renewal are likely to be encoded within a distributed network containing the BLA, the mPFC and the hippocampus.

 

Release of dopamine onto the nucleus accumbens appears to underlie all reward feelings. (Johnston; Why We Feel, 116)

EEG recordings from various parts of the brain during orgasm. Slow, high-amplitude waves similar to those in epilepsy appear, principally in the septum. Orgasm for man and for woman is the supreme ecstasy, intense waves of pleasure and emotion. Acetylcholine in the septum of a female provoked intense sexual pleasure, culminating in repeated orgasm. (Changeux; Neuronal Man, 111-113)

 

Interactions between the amygdala and nucleus accumbens contribute to motivation. (LeDoux; Synaptic Self, 250)

 

Amygdala

Lateral nucleus of amygdala is a key site of plasticity during fear learning. (LeDoux; Synaptic Self, 124)

 

Addiction

Nature 458, 534-537 (26 March 2009)

Nicotine binding to brain receptors requires a strong cation– interaction

Xinan Xiu, Nyssa L. Puskar, Jai A. P. Shanata, Henry A. Lester & Dennis A. Dougherty

Divisions of Chemistry and Chemical Engineering and Biology

California Institute of Technology, 1200 East California Boulevard, Pasadena, California 91125, USA

Nicotine addiction begins with high-affinity binding of nicotine to acetylcholine (ACh) receptors in the brain. The end result is over 4,000,000 smoking-related deaths annually worldwide and the largest source of preventable mortality in developed countries. Stress reduction, pleasure, improved cognition and other central nervous system effects are strongly associated with smoking. However, if nicotine activated ACh receptors found in muscle as potently as it does brain ACh receptors, smoking would cause intolerable and perhaps fatal muscle contractions. Despite extensive pharmacological, functional and structural studies of ACh receptors, the basis for the differential action of nicotine on brain compared with muscle ACh receptors has not been determined. Here we show that at the 42 brain receptors thought to underlie nicotine addiction, the high affinity for nicotine is the result of a strong cation– interaction to a specific aromatic amino acid of the receptor, TrpB. In contrast, the low affinity for nicotine at the muscle-type ACh receptor is largely due to the fact that this key interaction is absent, even though the immediate binding site residues, including the key amino acid TrpB, are identical in the brain and muscle receptors. At the same time a hydrogen bond from nicotine to the backbone carbonyl of TrpB is enhanced in the neuronal receptor relative to the muscle type. A point mutation near TrpB that differentiates 42 and muscle-type receptors seems to influence the shape of the binding site, allowing nicotine to interact more strongly with TrpB in the neuronal receptor. ACh receptors are established therapeutic targets for Alzheimer's disease, schizophrenia, Parkinson's disease, smoking cessation, pain, attention-deficit hyperactivity disorder, epilepsy, autism and depression. Along with solving a chemical mystery in nicotine addiction, our results provide guidance for efforts to develop drugs that target specific types of nicotinic receptors.

Nicotinic acetylcholine receptors (nAChRs) comprise a family of 20 homologous subtypes that mediate fast synaptic transmission throughout the central and peripheral nervous systems. The neuronal receptors are found in the central nervous system (CNS) and autonomic ganglia. Of these, the subtype most strongly associated with nicotine addiction and the target of recently developed smoking cessation drugs is termed 42. The high nicotine affinity of 42 receptors, when combined with the ability of nicotine to cross the blood–brain barrier and its favourable pharmacokinetics, allows nicotine at the submicromolar concentrations in tobacco smoke to activate acutely these receptors, providing reward, cognitive sensitization and perhaps other effects. In addition, the high-affinity interaction allows smoked nicotine to act as an intracellular pharmacological chaperone of 42 receptors, leading to the upregulation of receptors thought to underlie effects of chronic exposure.

 

Science 22 May 2009: Vol. 324. no. 5930, pp. 1080 - 1084

Phasic Firing in Dopaminergic Neurons Is Sufficient for Behavioral Conditioning

Hsing-Chen Tsai,^1,2, Feng Zhang,^2, Antoine Adamantidis,³ Garret D. Stuber,⁴ Antonello Bonci,⁴ Luis de Lecea,³ Karl Deisseroth^2,3,

¹ Neuroscience Program, W080 Clark Center, 318 Campus Drive West, Stanford University, Stanford, CA 94305, USA.
² Department of Bioengineering, W083 Clark Center, 318 Campus Drive West, Stanford University, Stanford, CA 94305, USA.
³ Department of Psychiatry and Behavioral Sciences, W083 Clark Center, 318 Campus Drive West, Stanford University, Stanford, CA 94305, USA.
⁴ Ernest Gallo Clinic and Research Center, Department of Neurology, Wheeler Center for the Neurobiology of Drug Addiction, University of California San Francisco, San Francisco, CA 94158, USA.

Natural rewards and drugs of abuse can alter dopamine signaling, and ventral tegmental area (VTA) dopaminergic neurons are known to fire action potentials tonically or phasically under different behavioral conditions. However, without technology to control specific neurons with appropriate temporal precision in freely behaving mammals, the causal role of these action potential patterns in driving behavioral changes has been unclear. We used optogenetic tools to selectively stimulate VTA dopaminergic neuron action potential firing in freely behaving mammals. We found that phasic activation of these neurons was sufficient to drive behavioral conditioning and elicited dopamine transients with magnitudes not achieved by longer, lower-frequency spiking. These results demonstrate that phasic dopaminergic activity is sufficient to mediate mammalian behavioral conditioning.

Dopaminergic (DA) neurons have been suggested to be involved in the cognitive and hedonic underpinnings of motivated behaviors. Changes in the firing pattern of DA neurons between low-frequency tonic activity and phasic bursts of action potentials could encode reward prediction errors and incentive salience. Consistent with the reward prediction-error hypothesis, DA neuron firing activity is depressed by aversive stimuli.

 

 

 

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Link to — Consciousness Subject Outline

Further discussion — Covington Theory of Consciousness