scholarly journals Generalization of conditioned fear-potentiated startle in humans: Experimental validation and clinical relevance

2008 ◽  
Vol 46 (5) ◽  
pp. 678-687 ◽  
Author(s):  
Shmuel Lissek ◽  
Arter L. Biggs ◽  
Stephanie J. Rabin ◽  
Brian R. Cornwell ◽  
Ruben P. Alvarez ◽  
...  
2009 ◽  
Vol 101 (3) ◽  
pp. 1201-1210 ◽  
Author(s):  
Chung-Chih Kuo ◽  
Ruei-Jen Chiou ◽  
Keng-Chen Liang ◽  
Chen-Tung Yen

The present study examined the role of neurons in different pain-related functions of the anterior cingulate cortex (ACC) and primary sensorimotor cortex (SmI) by assessing their abilities to code different levels of noxious heat and activity changes evoked by classical fear conditioning involving electric shocks. Multiple single-unit activity was recorded with microwires implanted in the SmI and ACC of each rat. In the first set of experiments, the middle segment of the tail in each rat was irradiated with laser-heat pulses of various intensities. Neuronal responses in both the SmI and ACC increased with the intensity of the laser heat, although there was a significantly higher percentage of intensity-related units in the SmI. Furthermore, the stimulus–response curve of SmI ensemble activity had a steeper slope than that of the ACC. In the second set of experiments, rats were trained and tested on a conditioned fear-potentiated startle task in which a light was paired with an electric shock and, later, the startle response was elicited by a burst of noise in the presence or absence of light. A higher percentage of ACC units changed their neuronal responses to the conditioned stimulus after the light–shock pairing and the average activity change was also significantly stronger. Our results suggest that SmI neurons are better at coding laser-heat intensity than ACC neurons, whereas more ACC neurons are involved in conditioned fear associated with an electric shock than SmI neurons. These data provide evidence for differential contributions of the SmI and ACC to sensory and affective dimensions of pain.


2004 ◽  
Vol 92 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Denis Paré ◽  
Gregory J. Quirk ◽  
Joseph E. Ledoux

It is currently believed that the acquisition of classically conditioned fear involves potentiation of conditioned thalamic inputs in the lateral amygdala (LA). In turn, LA cells would excite more neurons in the central nucleus (CE) that, via their projections to the brain stem and hypothalamus, evoke fear responses. However, LA neurons do not directly contact brain stem-projecting CE neurons. This is problematic because CE projections to the periaqueductal gray and pontine reticular formation are believed to generate conditioned freezing and fear-potentiated startle, respectively. Moreover, like LA, CE may receive direct thalamic inputs communicating information about the conditioned and unconditioned stimuli. Finally, recent evidence suggests that the CE itself may be a critical site of plasticity. This review attempts to reconcile the current model with these observations. We suggest that potentiated LA outputs disinhibit CE projection neurons via GABAergic intercalated neurons, thereby permitting associative plasticity in CE. Thus plasticity in both LA and CE would be necessary for acquisition of conditioned fear. This revised model also accounts for inhibition of conditioned fear after extinction.


2006 ◽  
Vol 32 (2) ◽  
pp. 332-342 ◽  
Author(s):  
Yi-Ling Yang ◽  
Ya-Wen Su ◽  
Ming-Chong Ng ◽  
Po-Kuan Chao ◽  
Li-Chu Tung ◽  
...  

2021 ◽  
Author(s):  
Anna Gerlicher ◽  
Vivian Nicole Metselaar ◽  
Merel Kindt

Conditioned fear can substantially reduce the likelihood that an individual will engage in reward- related behaviour - a phenomenon coined conditioned suppression. Despite the unmistakable relevance of conditioned suppression for excessive fears and their adverse consequences, the phenomenon has primarily been observed in animal models and is not yet well understood. Here, we aimed to develop a conditioned suppression paradigm that enables a robust quantification of the effect of Pavlovian aversive stimuli on subsequent reward-related behaviour in humans and assess its potential relation to physiological measures of fear. In phase 1, an instrumental response was incentivized with monetary rewards. In phase 2, one of two conditioned stimuli (CS+) was reinforced with an aversive unconditioned stimulus (US, i.e., electric stimulus). During aversive Pavlovian learning we assessed differential skin conductance (SCR) and fear potentiated startle responses (FPS). Lastly, we tested the effect of the aversively conditioned CS+ on the response rate of the instrumental response in a transfer phase. Despite strong aversive Pavlovian conditioning, as indicated by large effect sizes in differential SCR and FPS, we did not find any evidence for conditioned suppression: i.e., there was no significant reduction of instrumental responding in the presence of the CS+ compared to a new control stimulus. This lack of conditioned suppression is in line with previous studies that reported difficulties inducing conditioned suppression and points towards a general challenge in investigating conditioned suppression in humans. Implications and directions for future research on the highly relevant behavioural effects of fear and anxiety are discussed.


Nature ◽  
1990 ◽  
Vol 345 (6277) ◽  
pp. 716-718 ◽  
Author(s):  
Mindy J. D. Miserendino ◽  
Catherine B. Sananes ◽  
Kathleen R. Melia ◽  
Michael Davis

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