Limbic System 2 Flashcards
CA1 Hippocampal neurons exhibit
Long-Term Potentiation (LTP)
After receiving repeated inputs, they respond more to those inputs. (EPSPs get bigger)
Long-term potentiation of CA1 hippocampal neurons
The concept that neurons that fire together, wire together
Hebbian synapse
In LTP, glutamate binds with AMPA and NMDA receptors to open
Ca2+ channels
A 2nd messenger that signals the nucleus to produce more
AMPA receptors
Cells then become more responsive to
Subsequent excitation
The experimental support for this LTP model is that there is no LTP or learning in the presence of
NMDA agonists
Dendritic spine changes are associated with hippocampal
Long-term synaptic plasticity
New dendritic spines are observed within one hour of
LTP induction
In the dentate gyrus, blocking neurogenesis can block
Spatial learning
Neurogenesis is increased with
Exercise
Stimulates proliferation of progenitor cells, and enhances survival
LTP
A cue in the environment causes medial temporal lobe activation which causes activation of associated cortical areas
Memory retrieval
Hippocampal neurons participate in
Memory retrieval
Memory retrieval is also called
Reconsolidation
Suggestibility, bias, and flash-bulb memories that occur under situations of severe stress, surprise or importance
Memory retrieval (reconsolidation)
Natural tendency for all people to “fill in” missing pieces of experience with what they can infer or what they know
Confabulation
Seen with some memory disorders
-such as in the patient with bilateral temporal lobe removal
Confabulation
Removes confusion in our thought processes
Forgetting
Involves the prefrontal cortex inhibition of the hippocampus retrieval systems
Voluntary Forgetting
Highly superior autobiographical memory
Hyperthymesia
Increased grey matter in basal ganglia and increased white matter in the temporal lobe is characteristic of
Hyperthymesia
Tend to have some obsessive-compulsive tendencies, like organizing their thoughts
Patients with Hyperthymesia
Characterized by forgetfulness, anterograe and retrograde amnesia, and cognitive impairment
Alzheimer’s Disease
With Alzheimer’s disease, we see degeneration of the
Hippocampal and parahippocampal neurons
With Alzheimer’s disease, we also see loss of cholinergic cells in the
Basal forebrain nuclei (which project to cerebral cortex)
What are the three major acute signs of Wernicke-Korsakoff Syndrome?
Ataxia, Nystagmus, and Confusion (The Wernicke part)
Wernicke-Korsakoff affects the
Inferior Olive and Diencephalon
Wernike symptoms progress to learning and memory problems, which are the
Korsakoff components
Damage is to the mammillary bodies and the medial nuclei of the thalamus
Wernicke-Korsakoff Syndrome
Wernicke-Korsakoff Syndrome is caused by
Chronic alcoholism and malnutrition (esp B1 deficiency)
With Wernicke-Korsakoff Syndrome, we see anterograde and retrograde memory losses and confabulation with
Anosognosia (lack of realization)
The retrograde amnesia seen in Wernicke-Korsakoff is most likely due to damage to the
Prefrontal Cortex
Herpes virus in the DRG of CNs that in rare circumstances can move in the direction of the brain
Herpes Encephalitis
