Hippocampus reveives sensory inputs that first go to entorhinal cortex and pyriform regions. 

2 afferent pathways: perforant and alveolar

other minor inputs: septal nuclei, cerebral cortex (mainly cingulate gyrus) and monoamines from brainstem (retic formation)

Hippocampus and declarative memory

short term -> long term 

"consolidation"

Long Term Potentiation: Calcium enters via NMDA receptors and activates protein kinases, they induce LTP by:

a. altering efficieny of AMPA receptors

b. causing new receptors to be forms

CA1 susceptible to hypoxia during birth which leads to seizure activity

THIAMINE DEFICIENCY

excess alcohol or vitamin D deficiency, which causes learning problems

-involved in learning, emotion, and behavior

-acts as a relay to the hippocampal area

-lesion causes septal rage

main output: hypothalamus

other outputs: prefrontal cortex, anterior cingulate gyrus, mammillary bodies, and medial thalamus

Nuclei of Amygdala:

centromedial, basolateral, and central

1. Centromedial:

major inputs - olfactory tract and piriform cortex 

major outputs - medial hypothalamus

2. basolateral:

major input - association cortex (auditory)

major output - prefrontal cortex, directly or indirectly (via MD thalamic nucleus)

3. central

major inputs - visceral and taste afferents (n. solitarius)

major outputs - lateral hypothalamus and PAG

stria terminalis - medial hypothalamus

ventral amygdalofugal pathways - lateral hypothalamus

- modulate diurnal endocrine cycles

- feeding behavior

- aggressive behavior

- fear conditioning (via auditory pathways)

lesion to amygdala

symptoms: tameness, lack of fear, hypersexuality, bulemia, oral tendencies, hypermetamorphosis

lesion in amygdala

patient can draw any emotion except fear

patient can't express fear 

violence related version of MAO-A gene

has reduced volume and activity of the anterior cingulate cortex which is part of a circuit that regulates impulsive aggression