Physiological components

Physiological components

    While emotional behavior is largely regulated by relatively ancient and deeper brain structures, the frontal lobe of the cortex is involved in human anxiety. It is no coincidence that destructive surgery of parts of it reduces anxiety in patients suffering from these disorders. The most important 'building blocks' of the brain are the neurons or nerve cells. Connected in highly complex networks, they transmit information through chemical substances that act as messengers: neurotransmitters (v.). At least fifty types have been identified, which differ considerably depending on the location: some of them are linked to a particular anatomical structure, and others are scattered throughout the brain. When we talk about anxiety, the three most important neurotransmitters are norepinephrine (also called 'norepinephrine'), serotonin, and GABA. The latter is an inhibitory neurotransmitter that reduces the likelihood of activating nerve cells; unlike norepinephrine and serotonin, it is located throughout the brain. The strongest evidence of a GABA connection to anxiety comes from pharmacological studies, especially those of benzodiazepines, anti-anxiety drugs that enhance the effects of GABA by causing reduced anxiety, relaxation of muscles, and drowsiness; they also exert an anti-convulsant action. Norepinephrine is used by so-called adrenergic neurons; it forms in both the central and peripheral nervous systems. The strongest evidence of a GABA connection to anxiety comes from pharmacological studies, especially those of benzodiazepines, anti-anxiety drugs that enhance the effects of GABA by causing reduced anxiety, relaxation of muscles, and drowsiness; they also exert an anti-convulsant action. Norepinephrine is used by so-called adrenergic neurons; it forms in both the central and peripheral nervous systems. anti-convulsant action. Norepinephrine is used by so-called adrenergic neurons; it forms in both the central and peripheral nervous systems. anti-convulsant action. Norepinephrine is used by so-called adrenergic neurons; it forms in both the central and peripheral nervous systems.

    As for the norepinephrine of the brain, 70% of it is found in a small blue area (locus coeruleus) located in an ancient and deep part of the brain that has evolved over time. There are also relatively few adrenergic cells in the locus coeruleus, but each of them then spreads widely by making contact with at least 100,000 other neurons. Since noradrenergic pathways cover large areas of the brain, it is not surprising that norepinephrine is implicated in so many activities, such as sleep and wakefulness, attention, learning, arousal, mood, and anxiety. Electrical stimulation of the locus coeruleus produces fear-like reactions in animals, while pharmacological stimulation of the same area, e.g. through high doses of yohimbine, creates subjective anxiety in men. A little higher than the locus coeruleus are the raphe nuclei, where we find the neurotransmitter serotonin. Like norepinephrine, it spreads to many other areas of the brain and the spine.

    Low serotonin levels have long been thought to be associated with low mood and depression, but more recent pharmacological research indicates that how serotonin works may be important in understanding anxiety and its disorders. Drugs that increase the availability of serotonin not only improve mood but also reduce the incidence and intensity of panic attacks, are effective in the treatment of aggression, while, as a side effect, they cause a lowering of libido. This suggests that serotonin has something to do with the organization of instinctual behavior, whether it is expressed in the form of aggression directed towards others, or instead manifested in the form of aggression towards oneself, such as, for example, in the case of depression, sudden and intense anxiety, the urge to overeat and sexual urges. Serotonin and norepinephrine certainly interact, but the mechanisms of the interaction are not fully known. Physiological changes in states of anxiety are not limited to the brain. The brain and spinal cord, which make up the central nervous system, are connected to all other organs through the autonomic nervous system. This, in turn, is divided into the sympathetic nervous system and the parasympathetic nervous system. The sympathetic nervous system has adrenaline and norepinephrine as transmitters. Once the brain activates the sympathetic parts of the autonomic nervous system, (nor)adrenaline is released into the blood resulting in an increased heart rate, with the dilation of the pupils, the inhibition of the lacrimal glands, and the opening of the respiratory tract. All of these responses, mediated by (nor)adrenaline, constitute that 'emergency reaction' of a physiological type that we experience as fear. The parasympathetic nervous system opposes its sympathetic counterpart in various ways. If this system is activated, the neurotransmitter acetylcholine is released into the blood and a decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. While the sympathetic nervous system is activated in emergencies, when a reaction is needed, the parasympathetic system produces a relaxation response. inhibition of the lacrimal glands, the opening of the respiratory tract. All of these responses, mediated by (nor)adrenaline, constitute that 'emergency reaction' of a physiological type that we experience as fear. The parasympathetic nervous system opposes its sympathetic counterpart in various ways. If this system is activated, the neurotransmitter acetylcholine is released into the blood, and a decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. While the sympathetic nervous system is activated in emergencies, when a reaction is needed, the parasympathetic system produces a relaxation response. inhibition of the lacrimal glands, the opening of the respiratory tract. All of these responses, mediated by (nor)adrenaline, constitute that 'emergency reaction' of a physiological type that we experience as fear. The parasympathetic nervous system opposes its sympathetic counterpart in various ways. If this system is activated, the neurotransmitter acetylcholine is released into the blood and a decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. 

If this system is activated, the neurotransmitter acetylcholine is released into the blood, and a decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. While the sympathetic nervous system is activated in emergencies, when a reaction is needed, the parasympathetic system produces a relaxation response. The parasympathetic nervous system opposes its sympathetic counterpart in various ways. If this system is activated, the neurotransmitter acetylcholine is released into the blood and a decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. While the sympathetic nervous system is activated in emergencies, when a reaction is needed, the parasympathetic system produces a relaxation response. The parasympathetic nervous system opposes its sympathetic counterpart in various ways. If this system is activated, the neurotransmitter acetylcholine is released into the blood, and decrease in heart rate, narrowing of the pupils, secretion of the lacrimal glands, and constriction of the airways can be observed. While the sympathetic nervous system is activated in emergencies, when a reaction is needed, the parasympathetic system produces a relaxation response.

    The emergency reaction prepares the organism perfectly to respond to danger. As soon as the danger subsides, the parasympathetic nervous system takes over and mounts a relaxation response such as for example, a slowing heart rate and a lowering of blood pressure.

    The biological implant is highly adaptive in the sense that it allows us to react appropriately to danger, but the neural pathways implicated in anxiety often activate in the absence of real danger (false alarms) and this can be disabling for the individual. False alarms generally occur in the event that the emergency system is hypersensitive (e.g. the locus coeruleus can, through hyperactive and noradrenergic activity, expand even in the presence of very slight voltages), or in the case in which, through learning processes, subjects associate harmless stimuli with some catastrophe. Even if the origin of false alarms is psychological, this does not mean that the process excludes physiological factors. As we have seen, the association of events is done in cortical areas. The subject's memory may contain a misrepresentation of which events are dangerous (eg, spiders), but this is not a brain problem; conversely, if the individual is constantly anxious due to the relative unavailability of GABA, this in fact represents a real brain problem.