Startle response

Last updated

In animals, including humans, the startle response is a largely unconscious defensive response to sudden or threatening stimuli, such as sudden noise or sharp movement, and is associated with negative affect. [1] Usually the onset of the startle response is a startle reflex reaction. The startle reflex is a brainstem reflectory reaction (reflex) that serves to protect vulnerable parts, such as the back of the neck (whole-body startle) and the eyes (eyeblink) and facilitates escape from sudden stimuli. It is found across many different species, throughout all stages of life. A variety of responses may occur depending on the affected individual's emotional state, [2] body posture, [3] preparation for execution of a motor task, [4] or other activities. [5] The startle response is implicated in the formation of specific phobias.[ citation needed ]

Contents

Startle reflex

Neurophysiology

Layout of the brain Brain headBorder.jpg
Layout of the brain

A startle reflex can occur in the body through a combination of actions. A reflex from hearing a sudden loud noise will happen in the primary acoustic startle reflex pathway consisting of three main central synapses, or signals that travel through the brain.

First, there is a synapse from the auditory nerve fibers in the ear to the cochlear root neurons (CRN). These are the first acoustic neurons of the central nervous system. Studies have shown a direct correlation to the amount of decrease of the startle to the number of CRNs that were killed. Second, there is a synapse from the CRN axons to the cells in the nucleus reticularis pontis caudalis (PnC) of the brain. These are neurons that are located in the pons of the brainstem. A study done to disrupt this portion of the pathway by the injection of PnC inhibitory chemicals has shown a dramatic decrease in the amount of startle by about 80 to 90 percent. Third, a synapse occurs from the PnC axons to the motor neurons in the facial motor nucleus or the spinal cord that will directly or indirectly control the movement of muscles. The activation of the facial motor nucleus causes a jerk of the head while an activation in the spinal cord causes the whole body to startle. [6]

During neuromotor examinations of newborns, it is noted that, for a number of techniques, the patterns of the startle reaction and the Moro reflex may significantly overlap, the notable distinction being the absence of arm abduction (spreading) during startle responses. [7]

Reflexes

There are many various reflexes that can occur simultaneously during a startle response. The fastest reflex recorded in humans happens within the masseter muscle or jaw muscle. The reflex was measured by electromyography which records the electrical activity during movement of the muscles. This also showed the response latency, or the delay between the stimulus and the response recorded, was found to be about 14 milliseconds. The blink of the eye which is the reflex of the orbicularis oculi muscle was found to have a latency of about 20 to 40 milliseconds. Out of larger body parts, the head is quickest in a movement latency in a range from 60 to 120 milliseconds. The neck then moves almost simultaneously with a latency of 75 to 121 milliseconds. Next, the shoulder jerks at 100 to 121 milliseconds along with the arms at 125 to 195 milliseconds. Lastly the legs respond with a latency of 145 to 395 milliseconds. This type of cascading response correlates to how the synapses travel from the brain and down the spinal cord to activate each motor neuron. [8]

Acoustic startle reflex

The acoustic startle reflex is thought to be caused by an auditory stimulus greater than 80 decibels. [1] The reflex is typically measured by electromyography, brain imaging or sometimes positron emission tomography. [9] [10] There are many brain structures and pathways thought to be involved in the reflex. The amygdala, hippocampus, bed nucleus of the stria terminalis (BNST) and anterior cingulate cortex are all thought to play a role in modulating the reflex. [11] [12] The anterior cingulate cortex in the brain is largely thought to be the main area associated with emotional response and awareness, which can contribute to the way an individual reacts to startle-inducing stimuli. [11] Along with the anterior cingulate cortex, the amygdala and the hippocampus are known to have implications in this reflex.

The amygdala is known to have a role in the "fight-or-flight response", and the hippocampus functions to form memories of the stimulus and the emotions associated with it. [13] The role of the BNST in the acoustic startle reflex may be attributed to specific areas within the nucleus responsible for stress and anxiety responses. [12] Activation of the BNST by certain hormones is thought to promote a startle response [12] The auditory pathway for this response was largely elucidated in rats in the 1980s. [14] The basic pathway follows the auditory pathway from the ear up to the nucleus of the lateral lemniscus (LLN) from where it activates a motor centre in the reticular formation. This centre sends descending projections to lower motor neurones of the limbs[ clarification needed ].

In slightly more detail this corresponds to ear (cochlea) → cranial nerve VIII (auditory) → cochlear nucleus (ventral/inferior) → LLN → caudal pontine reticular nucleus (PnC). The whole process has a less than 10ms[ clarification needed ] latency. There is no involvement of the superior/rostral or inferior/caudal colliculus in the reaction that "twitches" the hindlimbs, but these may be important for adjustment of pinnae and gaze towards the direction of the sound, or for the associated blink. [15]

Application in occupational settings

A study undertaken in 2005 by researchers at the Department of Aviation and Logistics, University of Southern Queensland, looked at the performance of aircraft pilots following unexpected critical events. Analysing a number of recent aircraft accidents, the authors identified the negative impact of the startle response as causal or contributory in these accidents. The authors argued that fear resulting from threat, especially if life-threatening, [16] [17] prompted startle effects which had a serious negative impact on pilots' performances. The study considered training strategies to address this, including exposing pilots to unexpected critical events more often, enabling them to improve their responses. [18]

See also

Related Research Articles

Articles related to anatomy include:

<span class="mw-page-title-main">Olfactory bulb</span> Neural structure

The olfactory bulb is a neural structure of the vertebrate forebrain involved in olfaction, the sense of smell. It sends olfactory information to be further processed in the amygdala, the orbitofrontal cortex (OFC) and the hippocampus where it plays a role in emotion, memory and learning. The bulb is divided into two distinct structures: the main olfactory bulb and the accessory olfactory bulb. The main olfactory bulb connects to the amygdala via the piriform cortex of the primary olfactory cortex and directly projects from the main olfactory bulb to specific amygdala areas. The accessory olfactory bulb resides on the dorsal-posterior region of the main olfactory bulb and forms a parallel pathway. Destruction of the olfactory bulb results in ipsilateral anosmia, while irritative lesions of the uncus can result in olfactory and gustatory hallucinations.

In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.

<span class="mw-page-title-main">Fear conditioning</span> Behavioral paradigm in which organisms learn to predict aversive events

Pavlovian fear conditioning is a behavioral paradigm in which organisms learn to predict aversive events. It is a form of learning in which an aversive stimulus is associated with a particular neutral context or neutral stimulus, resulting in the expression of fear responses to the originally neutral stimulus or context. This can be done by pairing the neutral stimulus with an aversive stimulus. Eventually, the neutral stimulus alone can elicit the state of fear. In the vocabulary of classical conditioning, the neutral stimulus or context is the "conditional stimulus" (CS), the aversive stimulus is the "unconditional stimulus" (US), and the fear is the "conditional response" (CR).

<span class="mw-page-title-main">Neural pathway</span> Connection formed between neurons that allows neurotransmission

In neuroanatomy, a neural pathway is the connection formed by axons that project from neurons to make synapses onto neurons in another location, to enable neurotransmission. Neurons are connected by a single axon, or by a bundle of axons known as a nerve tract, or fasciculus. Shorter neural pathways are found within grey matter in the brain, whereas longer projections, made up of myelinated axons, constitute white matter.

<span class="mw-page-title-main">Dopaminergic pathways</span> Projection neurons in the brain that synthesize and release dopamine

Dopaminergic pathways in the human brain are involved in both physiological and behavioral processes including movement, cognition, executive functions, reward, motivation, and neuroendocrine control. Each pathway is a set of projection neurons, consisting of individual dopaminergic neurons.

<span class="mw-page-title-main">Ventral tegmental area</span> Group of neurons on the floor of the midbrain

The ventral tegmental area (VTA), also known as the ventral tegmental area of Tsai, or simply ventral tegmentum, is a group of neurons located close to the midline on the floor of the midbrain. The VTA is the origin of the dopaminergic cell bodies of the mesocorticolimbic dopamine system and other dopamine pathways; it is widely implicated in the drug and natural reward circuitry of the brain. The VTA plays an important role in a number of processes, including reward cognition and orgasm, among others, as well as several psychiatric disorders. Neurons in the VTA project to numerous areas of the brain, ranging from the prefrontal cortex to the caudal brainstem and several regions in between.

<span class="mw-page-title-main">Reticular formation</span> Spinal trigeminal nucleus

The reticular formation is a set of interconnected nuclei that are located in the brainstem, hypothalamus, and other regions. It is not anatomically well defined, because it includes neurons located in different parts of the brain. The neurons of the reticular formation make up a complex set of networks in the core of the brainstem that extend from the upper part of the midbrain to the lower part of the medulla oblongata. The reticular formation includes ascending pathways to the cortex in the ascending reticular activating system (ARAS) and descending pathways to the spinal cord via the reticulospinal tracts.

Affective neuroscience is the study of how the brain processes emotions. This field combines neuroscience with the psychological study of personality, emotion, and mood. The basis of emotions and what emotions are remains an issue of debate within the field of affective neuroscience.

<span class="mw-page-title-main">Orbitofrontal cortex</span> Region of the prefrontal cortex of the brain

The orbitofrontal cortex (OFC) is a prefrontal cortex region in the frontal lobes of the brain which is involved in the cognitive process of decision-making. In non-human primates it consists of the association cortex areas Brodmann area 11, 12 and 13; in humans it consists of Brodmann area 10, 11 and 47.

<span class="mw-page-title-main">Facial motor nucleus</span>

The facial motor nucleus is a collection of neurons in the brainstem that belong to the facial nerve. These lower motor neurons innervate the muscles of facial expression and the stapedius.

The amygdalofugal pathway is one of the three major efferent pathways of the amygdala, meaning that it is one of the three principal pathways by which fibers leave the amygdala. It leads from the basolateral nucleus and central nucleus of the amygdala. The amygdala is a limbic structure in the medial temporal lobe of the brain. The other main efferent pathways from the amygdala are the stria terminalis and anterior commissure.

<span class="mw-page-title-main">Reward system</span> Group of neural structures responsible for motivation and desire

The reward system is a group of neural structures responsible for incentive salience, associative learning, and positively-valenced emotions, particularly ones involving pleasure as a core component. Reward is the attractive and motivational property of a stimulus that induces appetitive behavior, also known as approach behavior, and consummatory behavior. A rewarding stimulus has been described as "any stimulus, object, event, activity, or situation that has the potential to make us approach and consume it is by definition a reward". In operant conditioning, rewarding stimuli function as positive reinforcers; however, the converse statement also holds true: positive reinforcers are rewarding.

<span class="mw-page-title-main">Medial dorsal nucleus</span>

The medial dorsal nucleus is a large nucleus in the thalamus.

<span class="mw-page-title-main">Synaptic gating</span>

Synaptic gating is the ability of neural circuits to gate inputs by either suppressing or facilitating specific synaptic activity. Selective inhibition of certain synapses has been studied thoroughly, and recent studies have supported the existence of permissively gated synaptic transmission. In general, synaptic gating involves a mechanism of central control over neuronal output. It includes a sort of gatekeeper neuron, which has the ability to influence transmission of information to selected targets independently of the parts of the synapse upon which it exerts its action.

<span class="mw-page-title-main">Basolateral amygdala</span> The lateral, basal, and accessory-basal nuclei of the amygdala

The basolateral amygdala, or basolateral complex, consists of the lateral, basal and accessory-basal nuclei of the amygdala. The lateral nuclei receives the majority of sensory information, which arrives directly from the temporal lobe structures, including the hippocampus and primary auditory cortex. The basolateral amygdala also receives dense neuromodulatory inputs from ventral tegmental area (VTA), locus coeruleus (LC), and basal forebrain, whose integrity are important for associative learning. The information is then processed by the basolateral complex and is sent as output to the central nucleus of the amygdala. This is how most emotional arousal is formed in mammals.

The trisynaptic circuit or trisynaptic loop is a relay of synaptic transmission in the hippocampus. The circuit was initially described by the neuroanatomist Santiago Ramon y Cajal, in the early twentieth century, using the Golgi staining method. After the discovery of the trisynaptic circuit, a series of research has been conducted to determine the mechanisms driving this circuit. Today, research is focused on how this loop interacts with other parts of the brain, and how it influences human physiology and behaviour. For example, it has been shown that disruptions within the trisynaptic circuit lead to behavioural changes in rodent and feline models.

The Mauthner cells are a pair of big and easily identifiable neurons located in the rhombomere 4 of the hindbrain in fish and amphibians that are responsible for a very fast escape reflex. The cells are also notable for their unusual use of both chemical and electrical synapses.

Many experiments have been done to find out how the brain interprets stimuli and how animals develop fear responses. The emotion, fear, has been hard-wired into almost every individual, due to its vital role in the survival of the individual. Researchers have found that fear is established unconsciously and that the amygdala is involved with fear conditioning.

References

  1. 1 2 Rammirez-Moreno, David. "A computational model for the modulation of the prepulse inhibition of the acoustic startle reflex". Biological Cybernetics, 2012, p. 169
  2. Lang, Peter J.; Bradley, Margaret M.; Cuthbert, Bruce N. (1990). "Emotion, attention, and the startle reflex". Psychological Review. 97 (3): 377–95. doi:10.1037/0033-295X.97.3.377. ISSN   1939-1471. PMID   2200076.
  3. Castellote et al (2007) cited Brown, P; Day, BL; Rothwell, JC; Thompson, PD; Marsden, CD (1991b). "The effect of posture on the normal and pathological auditory startle reflex". J Neurol Neurosurg Psychiatry. 54 (10): 892–97. doi: 10.1136/jnnp.54.10.892 . PMC   1014574 . PMID   1744643.
  4. Castellote et al (2007) cited Valls-Sole, J; Rothwell, JC; Goulart, F; Cossu, G; Munoz, E (1999). "Patterned ballistic movements triggered by a startle in healthy humans". J Physiol. 516 (3): 931–38. doi:10.1111/j.1469-7793.1999.0931u.x. PMC   2269293 . PMID   10200438.
  5. Castellote et al (2007) cited Nieuwenhuijzen, PH; Schillings, AM; Van Galen, GP; Duysens, J (2000). "Modulation of the startle response during human gait". J Neurophysiol. 84 (1): 65–74. doi:10.1152/jn.2000.84.1.65. PMID   10899184.
  6. Davis, M. (2007). "Neural systems involved in fear and anxiety based on the fear-potentiated startle test." Neurobiology of Learning and Memory (pp. 381–425). Elsevier Incorporated.
  7. Fletcher, Mary Ann (1998). Physical Diagnosis in Neonatology. Lippincott Williams & Wilkins. p. 472. ISBN   978-0397513864.
  8. Davis, M. (1984). "The mammalian startle response". In R. Eaton (Ed.), Neural stop of Startle Behavior (pp. 287–351). Plenum Publishing Corporation.
  9. Pissiota, Anna. "Amygdala and Anterior Cingulate Cortex Activation During Affective Startle Modulation:a PET Study of Fear". The European Journal of Neuroscience , 2003, p. 1325
  10. Phillips, R.G. "Differential Contribution of Amygdala and Hippocampus to Cued and Contextual Fear Conditioning". Behavioral Neuroscience , 1992, p. 274
  11. 1 2 Medford, Nick. "Conjoint Activity of Anterior Insular and Anterior Cingulate Cortex:Awareness and Response". Brain Structure and Function, 2010, p. 535
  12. 1 2 3 Lee, Younglim. "Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex". The Journal of Neuroscience , 1997, p. 6434
  13. Grouen, Wouter. "Amygdala and Hippocampus Enlargement During Adolescence in Autism". Journal of the American Academy of Child & Adolescent Psychiatry , 2010, p. 552
  14. Davis, M; Gendelman, Ds; Tischler, Md; Gendelman, Pm (Jun 1982). "A primary acoustic startle circuit: lesion and stimulation studies". Journal of Neuroscience . 2 (6): 791–805. doi:10.1523/JNEUROSCI.02-06-00791.1982. ISSN   0270-6474. PMC   6564345 . PMID   7086484.
  15. Castellote, Jm; Kumru, H; Queralt, A; Valls-Solé, J (Feb 2007). "A startle speeds up the execution of externally guided saccades". Experimental Brain Research. Experimentelle Hirnforschung. Experimentation Cerebrale. 177 (1): 129–36. doi:10.1007/s00221-006-0659-4. ISSN   0014-4819. PMID   16944110. S2CID   19678962.
  16. Open Access logo PLoS transparent.svg Martin, Wayne; Murray, Patrick; Bates, Paul (2012). The Effects of Startle on Pilots During Critical Events: A Case Study Analysis (PDF). 30th EAAP Conference : Aviation Psychology & Applied Human Factors – working towards zero accidents. Discussion, p. 389. Archived (PDF) from the original on 2019-09-16. Retrieved 2019-09-12.
  17. Field, JN; Boland, EJ; van Rooij, JM; Mohrmann, JFW; Smeltink, JW. Startle Effect Management (Report Number NLR-CR-2018-242) (PDF) (Report). European Aviation Safety Agency. 2.4.3 Fear-potentiated Startle or Surprise, p. 18. Retrieved 2019-09-12. cited Martin, W; Murray, P (2013). Training Interventions for Managing Startle During Unexpected Critical Events. 66th International Air Safety Summit. Flight Safety Foundation.
  18. Martin, Wayne L.; Murray, Patrick S.; Bates, Paul R.; Lee, Paul S. Y. (2015). "Fear-Potentiated Startle: A Review from an Aviation Perspective". The International Journal of Aviation Psychology . 25 (2): 97–107. doi:10.1080/10508414.2015.1128293. S2CID   147250211.