Michael Myers made his way back onto movie screens this past weekend—donning that infamous creepy white mask and clutching a shiny kitchen knife. People like me will get a thrill from all the suspense and gore the new Halloween serves up, while others will be severely stressed, horrified, and probably sleepless, as thoughts of this maniac killer stay with them for nights. They may even pass out watching it, if it’s anything like Netflix’s new horror series The Haunting of Hill House.

Heights have that same dividing effect. I convinced myself that being strapped into a harness would be enough to make me feel safe while parasailing. I was wrong. Around 800 feet in the air, I panicked. There was convulsing, vomiting, and head slouching. Until that point, my parasailing partner stayed perfectly calm, basking in the excitement of floating above the ocean. I feared for my life. But for him, it was a rush.

Why are some people’s nightmares other people’s joyrides?

It’s because our brains react to and process fearful situations differently. In a way, when it comes to these moments, we all start out the same, but depending on which part of our brain “wins” out, we can end up in different places. It’s also important to know that a lot of the same neural circuitry associated with our “fight or flight” response is also involved in how we experience pleasure and positive emotional states.

The process of fear

When faced with a perceived threat or a scary situation, the fight or flight response kicks in, sending signals from the part of the brain known as the amygdala to the rest of our body to react. Our sympathetic nervous system is activated. We become more alert. Blood pressure and heart rate go up. We feel faint. Stress hormones, like adrenaline and cortisol, are released.

The brain’s hippocampus and the prefrontal cortex regions then help us decide our next move: Is this something that I should be genuinely fearful of or not? The “emotional” part of our brain—the amygdala—communicates with the higher-level “thinking” part of our brain to make the final call.

“Riding a roller coaster, for example, can be debilitating to one person but not to another,” said Thea Gallagher, PsyD, the clinic director at Penn’s Center for the Treatment and Study of Anxiety. “So, it’s the same symptoms and experiences, but for some people it’s just not pleasurable. And that comes down to attribution.”

The hippocampus and prefrontal cortex are tasked with giving the situation context, to reason with the “emotional” part of our brain. “You’ve seen this before and nothing happened,” or “You’ve ridden this roller coaster 10 times already and everything turned out OK.”

Up in my seat and harness high above the water, my brain seemed to convince the rest of me that the harness wasn’t enough and I may fall, while my parasailing partner’s brain did a better job of keeping the peace. He overcame the fight or flight response. In fact, with all that adrenaline pumping through him, he was able enjoy the ride.

It’s the same reason people are attracted to the thrill experienced during and after going through a haunted house or watching scary movies, Gallagher said. There’s fear, but deep down they know there’s no real threat.

Learning the difference

Everyone is born with two innate fears: falling and loud sounds. The rest are learned. Our environment—parents, siblings, friends, TV—teaches us at a young age to be scared of things, like the dark or monsters.

Experience shapes our fears as we get older. An early encounter with an aggressive dog could dictate how we view other dogs, or worse, a violent experience with a person or place can leave a lasting fear. But the more we experience something, the less likely we will be scared of it, like watching a movie that keeps you up at night over and over again. I had never parasailed; he had been many times.

There’s also a process called fear extinction, defined in the scientific literature as a decline in fear responses due to multiple “non-reinforced” exposures.

“Extinction is not forgetting a memory; it’s actually forming a new memory,” said David Connor, PhD, a postdoctoral researcher in the lab of John A. Dani, PhD, chair of the department of neuroscience. “It’s learning a new safe association between the context or whatever cues were initially associated with danger. During extinction, you have a second form of learning happening that is competing with the original fear memory.”

For example, if someone is in an accident while driving through an intersection, they may feel afraid of getting hit when going through that same intersection later. It may be that the feelings of fear can only be put behind them by driving through that same intersection several—or many—times.

Fear is necessary—it keeps us safe from real danger. But people with fear disorders, like PTSD or panic attacks, don’t manage fear extinction as well. They are incapable of extinguishing fear because of misplaced attribution or generalizations.

Panic attacks come unexpectedly. An object or a sound associated with a past traumatic event triggers PTSD.

“The problem is, there is no threat, but your brain is telling you there is one,” Gallagher said. “In treatment, we have to re-associate these networks.”

Cognitive behavior therapy (CBT) is one way people learn to cope with a fear by changing the way they think, feel, or behave around it. It’s facing the fear and assigning it a new context.

The therapy, along with prescriptions drugs, like benzodiazepines and SSRIs (selective serotonin reuptake inhibitors), are also used to treat patients with anxiety and stress disorders.

Fear research

Connor studies fear extinction and nicotine, with an eye towards improved treatments for these disorders.

“A lot of the circuits and brain regions that are involved with addiction also are also highly associated with fear and anxiety-related behaviors,” he said. “People with anxiety have higher rates of addiction because drugs, such as nicotine and alcohol, are perceived to provide short-term relief from their anxiety.”

But that may not be the case. According to a study he co-authored and published this month in Neuropharmacology, nicotine may actually be making it worse.

In the preclinical study, Connor and his colleagues studied the role nicotine plays during fear extinction. Mice were given two, mild-foot shock stimuli in a cage and returned repeatedly to the same cage, minus the stimulus, to measure their fear extinction. Each time, they became less scared, measured by how long they “froze” after returning to the cage. However, they discovered that mice given nicotine took longer for their freezing levels to decrease. In other words, they stayed scared longer.

“This suggest that nicotine can actually cause deficits in some forms of learning,” Connor said. “In this case, it’s in fear extinction learning.”

The researchers also found that nicotine increased neural activity in the ventral hippocampus and amygdala. Further, when the ventral hippocampus, which directly signals to the amygdala, was infused with nicotine, mice showed deficits in fear extinction, further suggesting a hippocampal link between nicotine and extinction deficits.

“That’s important because it reveals nicotinic receptors in the brain as a potential target to alter fear extinction signaling,” Connor said. “It may be new avenue to target the disorders.”