Synaptic Long-Term Memory

Studying the brain has been an affective result in finding out the various neurochemicals that are involved with PTSD. Brain imaging systems nowadays focus on two brain structures, the amygdala and the hippocampus. The amygdala is involved with how we learn about our fear and hippocampus plays a role with our memory formation. Some research focuses on a hormonal system known as hypothalamic-pituitary

When we recall these memories, we re-consolidate them by reactivating the neutrons that compose our memory, which allows us to create new connections. This encourages learning by strengthening these connections and allowing them.

Research has shown that, “people who suffer from PTSD often relive the experience trough nightmares and flashbacks,” (“What”). Survivors’ dreams are most often related to a specific traumatic image or situation the individual was put in, that continues to haunt them years later.

Those diagnosed with PTSD have shown a reduction in the volume of the hippocampus. The hippocampus helps humans remember new memories and then be able to recall them later, and also helps identify between past and present memories. The amygdala is another section of the brain affected by PTSD, and the amygdala is responsible for processing emotions and fear. The ventromedial prefrontal cortex is shown to have a decreased size in cases. The ventromedial prefrontal cortex regulates negative emotions like stress, anxiety, and fear. The strange behaviours of the patients diagnosed with PTSD can be explained by the damage to the brain. “Researchers believe that the brain changes caused by PTSD increase the tendency of a person developing other psychotic and mood disorders” (brainblogger.com). The brain is like a machine made up of small parts, and if one of these parts break, the machine does not function

Traumatic events also produce profound and lasting changes in physiological arousal, emotion, cognition, and memory. Moreover, traumatic events may result in the severance of these normally integrated functions from one another. Traumatized individuals may also suffer from the memories of the tragic or horrifying experiences they have undergone. Frequently, as a result of these many symptoms, it becomes inevitable for the individual to develop certain complications associated with trauma-related disorders, such as posttraumatic stress disorder.

Consolidation is the process by which an acquired memory is stabilized (Mastin, 2010). It begins when information is “bound into a memory trace by the hippocampus and related structures in the medial temporal lobes and diencephalon” (Nadel & Moscovitch, 1997, p. 217). This involves long term

The formation of new memories requires protein synthesis dependent changes in synaptic structure and plasticity in the hippocampus. Studies in humans and animals suggest that these memories are initially stored in hippocampus but later transferred to cortex for permanent storage. This phenomenon is described as systems consolidation of memories. While the specific role for new protein synthesis in hippocampus in early encoding of memories is established, whether protein synthesis in medial prefrontal cortex play a major role in encoding of memories is unclear. To address this question, we used contextual fear conditioning (CFC) of mouse, a behavior training that induce long lasting memories. A single training session produces robust lifelong memory (8) that can be measured using automated procedures (9). Several studies have used CFC training as a model to study hippocampal-cortical communications and mechanisms underlying systems consolidation of memories. Contextual fear memories are initially stored in hippocampus and then moved to medial prefrontal cortex (mPFC) for long-term storage.

Throughout the course of this semester we have examined numerous issues which have all had different implications for the brain = behavior argument. Some who have been skeptical of the validity of this idea have been swayed by observations that processes and behaviors they originally thought to have a cloudy neurobiological basis in fact have a sound biological and physiological underpinning. One such phenomenon which can help elucidate the ongoing brain = behavior debate is Post-Traumatic Stress disorder, or PTSD. Most people are familiar in some sense with the phenomenon of PTSD. This phenomenon has been renamed, reworked, and redefined numerous times over the past

Stout’s description of how the brain reacts under stress shows how traumatic memories can become lost or disorganized. Trauma has a significant impact on stress-responsive neurohormones, which are hormones produced by the nervous system. Trauma causes the areas of the brain involved in

Hippocampus is a small, curved region, which exists in both hemispheres of the brain and plays a vital role in emotions, learning and acquisition of new information. It also contributes majorly to long term memory, which is permanent information stored in the brain. Although long term memory is the last information that can be forgotten, its impairment has become very common nowadays. The dysfunction is exemplified by many neurological disorders such as amnesia. There are two types of amnesia, anterograde and retrograde. Anterograde amnesia is inability in forming new information, while retrograde refers to the loss of the past memory. As suggested by Cipolotti and Bird (2006), hippocampus’s lesions are

Synaptic plasticity refers to a process through which the brain undergoes neural changes due to alterations in synaptic strength. Many studies have demonstrated that these synapses have the ability to strengthen or weaken on account of synaptic activity. In other words, an increase in synaptic activity will further strengthen that connection, making it more sensitive to a particular stimulus. Conversely, a decrease in synaptic activity will weaken the connection such that it loses its sensitivity to a given stimulus. The neuronal events that result in the strengthening or weakening of a synapse are explained through two mechanisms – Long-Term Potentiation (LTP) and Long-Term Depression (LTD). In fact, scientists believe that the coupling of these two mechanisms essentially contributes to memory and learning of an individual.

After a new memory is learnt, it enters the process of encoding during which the memory is labile and capable of disruption until it becomes stabilised over a period of time (Nader & Einarsson, 2010; Nader et al, 2000). This process is called consolidation and originally consisted of the theory that once stabilised in the brain, it remains fixed (Suzuki et al, 2004). This theory has been rebutted by the acceptance of reconsolidation, a theory that imposes the ideology that when memories are retrieved, through similar experiences (Lee, 2009), they become labile until,

Doctors and scientists dispute the exact role of the hippocampus, but agree that it has an essential role in the formation of new memories about personally experienced events. Some researchers prefer to consider the hippocampus as part of a larger medial temporal lobe memory system responsible for declarative memory. When a long-term, declarative memory is made, certain neuronal connections in the temporal lobe are strengthened, and others are weakened. These changes are fairly permanent, however some may take weeks or months before they are complete

The amygdala is known to learn from exposure to fear and store assessment of threat–related stimuli. The prefrontal cortex is involved in extinction and the retention of fear and is connected to the amygdala. Finally, the hippocampus encodes the context during fear learning process and sends it to the amygdala. People with PTSD have hyper-activity in the amygdala, while having hypo-activity in the prefrontal cortex and there is reduction of the hippocampus volume. This reduction may limit proper evaluation and categorization of the experience. A study on Vietnam soldiers revealed that lesions in the amygdala and prefrontal cortex resulted in the absence of PTSD. To get further into the molecular level studies been done on the hormonal system. “Stress is known to contribute to the pathogenesis of a variety of disorders, including the majority of psychiatric like major depression and posttraumatic stress disorder.” (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3825244/pdf/DM30-02-343616.pdf). Research has revealed evidence that a hormonal system known as the hypothalamic-pituitary-adrenal (HPA) axis is the one that gets disrupted in people with PTSD. The hormonal system is involved in normal stress reactions, so the disruption of this system in people with PTSD creates this “false alarm”. It has been suggested by some scientist that the dysfunction of the HPA system results in hippocampal damage in people with PTSD. Damage in the hormones is caused by damage to

Previous research displays a relationship between defensive behavior and fear, anxiety and stress. Several animal models have been developed to model aspects of anxiety and stress related disorders. Of these, self-enhanced fear learning (SEFL) is based on foot shock fear conditioning, but is a maladaptive form of hyperreactive fear, modeling Posttraumatic Stress Disorder (PTSD). In the model, animals are exposed to a severe stressor in one context, changing how a future mild stressor is processed in a distinct context. The enhancement in fear learning is not caused by generalization between the two contexts. Our laboratory uses the SEFL model to study the neurobiological mechanisms driving PTSD.