Health Psychology. Michael Murray
2.7.
Figure 2.7 Schematic diagram of the autonomic nervous system
Source: Adapted from Geo-Science-International
Emotion, Reward, Punishment and Inhibition
The earliest scientific studies of human emotion were by Cannon (1915). Both in language and behavioural terms, we differentiate distinctive emotional responses. For example, in fear, humans go through basically the same steps: we stop what we are doing, turn towards the source of the threat, and initially show behavioural inhibition while trying to assess the threat. If this assessment confirms a threat, typically we try to flee or hide rather than engage in confrontation. If confrontation is unavoidable, fighting the threat becomes the last remaining option.
Attempts have been made to identify NS activity components associated with different emotions. The amygdala triggers bodily responses to emotional events, including the release of adrenalin by the adrenal glands. Adrenalin helps memories to be encoded more effectively in the hippocampus and the temporal lobe. We are better at remembering things that trigger our emotions. A review by Kreibig (2010) concerning emotion in healthy individuals suggested some level of response specificity in the ANS to different emotions, with some overlaps. See Box 2.1 for a few examples.
BOX 2.1 Differentiation of human emotions in the autonomic nervous system
Anger: reciprocal sympathetic activation and increased respiratory activity, particularly faster breathing.
Anxiety: sympathetic activation and vagal deactivation, a pattern of reciprocal inhibition, together with faster and shallower breathing (overlaps with anger).
Disgust (A) in relation to contamination and pollution: sympathetic–parasympathetic co-activation and faster breathing, particularly decreased inspiration.
Disgust (B) in relation to mutilation, injury and blood: sympathetic cardiac deactivation, increased electrodermal activity, unchanged vagal activation and faster breathing.
Embarrassment: largely overlaps with anger and anxiety but includes facial blushing.
Fear: broad sympathetic activation, including cardiac acceleration, increased myocardial contractility, vasoconstriction and increased electrodermal activity.
Sadness: a heterogeneous pattern of sympathetic–parasympathetic coactivation.
Affection, love, tenderness or sympathy: decreased heart rate (similar to sadness), unspecific increase in skin conductance.
Amusement: increased cardiac vagal control, vascular-adrenergic, respiratory and electrodermal activity, together with sympathetic cardiac-adrenergic deactivation.
Contentment: a strong sympathetically deactivating component.
Happiness: increased cardiac activity due to vagal withdrawal, vasodilation, increased electrodermal activity and increased respiratory activity.
Joy: increased cardiac vagal control, decreased-adrenergic, increased-adrenergic and increased cholinergically mediated sympathetic influence as well as increased respiratory activity.
Source: Kreibig (2010)
Another approach has been to identify the brain areas and circuits responsible for reward and punishment (Figure 2.8).
Figure 2.8 The reward and punishment circuits
The main centres of the brain’s reward circuit are located along the medial forebrain bundle (MFB). The ventral tegmental area (VTA) and the nucleus accumbens are the two major centres in this circuit, but it also includes several others, such as the septum, the amygdala, the prefrontal cortex and parts of the thalamus. All of these centres are interconnected and innervate the hypothalamus, informing it of the presence of rewards. The lateral and ventromedial nuclei of the hypothalamus are especially involved in this reward circuit. The hypothalamus then acts in return not only on the ventral tegmental area, but also on the autonomic and endocrine functions of the entire body, through the pituitary gland.
Turning from rewarding to aversive stimuli, fight-or-flight responses activate the brain’s punishment circuit (the periventricular system, or PVS), which enables us to cope with unpleasant situations. The PVS was identified by De Molina and Hunsperger (1962). It includes the hypothalamus, the thalamus and the central grey substance surrounding the aqueduct of Sylvius. Some secondary centres of this circuit are found in the amygdala and the hippocampus. The punishment circuit functions by means of acetylcholine, which stimulates the secretion of adrenal cortico-trophic hormone (ACTH). ACTH in turn stimulates the adrenal glands to release adrenalin to prepare the body’s organs for fight-or-flight actions.
The MFB and the PVS provide two motivational systems that enable people to suppress their instinctive impulses and avoid painful experiences. A third circuit is known as the ‘behavioural inhibition system’ (BIS). The BIS is associated with the septo-hippocampal system, the amygdala and the basal nuclei. It receives inputs from the prefrontal cortex and transmits its outputs via the noradrenergic fibres of the locus coeruleus and the serotininergic fibres of the medial Raphe nuclei. The BIS is activated when both fight and flight seem impossible and the only remaining option is to passively submit by doing nothing. Long-term behavioural inhibition can be stressful, with an increased probability of long-term illness (Pennebaker, 1985). Large individual differences are observed in behavioural inhibition which, in adolescents, can be associated with anxiety and depression (Muris et al., 2001).
Neuroplasticity, learning and memory
The hippocampus has been a focus for research on synaptic plasticity, the ability to potentiate transmission at the synapse by repeated stimulation, providing a neural foundation for learning and memory in terms of ‘long-term potentiation’ (LTP) (Bliss and Lømo, 1973). When we learn something, the efficiency of hippocampal synapses increases, facilitating the passage of nerve impulses along a particular circuit. For example, when exposed to a new word, we have to make new connections among certain neurones to deal with it: some neurones in the visual cortex to recognize the spelling, others in the auditory cortex to hear the pronunciation, and still others in the associative regions of the cortex to relate the word to our existing knowledge. All memories of events, words and images correspond to particular activities of neuronal networks that have strengthened interconnections with one another.
As noted, at least half of the synapses in the CNS are glutamatergic. Glutamate is the major excitatory neurotransmitter in the NS. Glutamatergic pathways are linked to many other neurotransmitter pathways, and receptors are found throughout the brain and spinal cord in neurons and glia. As an amino acid and neurotransmitter, glutamate has multiple normal physiological functions and any dysfunction can have profound effects both in disease and injury. At least 30 proteins at, or near, the glutamate synapse control or modulate neuronal excitability. The N-methyl-D-aspartate receptor (NMDA receptor) is a glutamate receptor found in nerve cells. It is activated when glutamate and glycine (or D-serine) bind to it, and when activated it allows positively charged ions to flow through the cell membrane. These are especially important in synaptic plasticity and the encoding and intermediate storage of memory traces, while AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors mediate fast synaptic transmission necessary for memory retrieval (Tsien et al., 1996).
Collingridge and Singer (1990) discovered that excitatory amino acid receptors mediate synaptic transmission at many synapses that display LTP-type synaptic efficiency. These amino acids are one mechanism of synaptic plasticity in health and disease, and alterations in these processes may lead to brain disorders, such as Alzheimer’s disease.
The Endocrine System
The endocrine system