Nuero Unit 4

1. Learning – A lasting change in behavior or knowledge that results from experience, practice, or exposure.
2. Memory – The ability to encode, store, and retrieve information based on past experiences.
3. Memory trace – The physical or biochemical representation of a memory stored in the brain.
4. Acquisition – The initial stage of learning in which new information is first encoded.
5. Retrieval – The process of accessing stored memories.
6. Consolidation – The process by which fragile new memories become stable and long-lasting.
7. Reconsolidation – The re-stabilization of a memory after it has been recalled and temporarily destabilized.
8. Declarative memory – Conscious, explicit memories of facts and events ("knowing that").
9. Explicit memory – Memory requiring conscious retrieval.
10. Non-declarative memory – Memory expressed unconsciously through behavior ("knowing how").
11. Implicit memory – Memory expressed without awareness or intention.
12. Procedural memory – Skills and habits stored in long-term memory.
13. Semantic memory – Knowledge of facts, concepts, and general world knowledge.
14. Episodic memory – Personal, autobiographical memories tied to a specific time and place.
15. Autobiographical memory – Memory for one's own life events.
16. Skill learning – Acquiring the ability to perform tasks that require practice (e.g., riding a bike).
17. Priming – Exposure to a stimulus that influences response to a later stimulus without conscious awareness.
18. Conditioning – Learning associations between events.
19. Immediate memory – Very short holding of sensory events for fractions of a second.
20. Sensory memory – Temporary memory systems that hold sensory information.
21. Working memory – Short-term memory that holds information briefly for manipulation and immediate use.
22. Short-term memory – Storage lasting seconds to minutes, used for temporary information retention.
23. Long-term memory – Memory stored for days, years, or a lifetime.
24. Attention – Cognitive focus that enhances encoding into working memory.
25. Rehearsal – Repetition of information to maintain it in memory or consolidate it.
26. Encoding – The initial learning of information.
27. Storage – Keeping information in the brain over time.
28. Retrieval failure – Inability to access stored information.
29. Interference – Disruption of memory retrieval by competing information.
30. Neuroplasticity – The brain's ability to reorganize and change its connections and structure.
31. Synaptic plasticity – Long-term changes in the strength of synaptic connections.

SECTION 2 — MEMORY DISORDERS & CASE STUDIES

32. Amnesia – Loss of memory ability.
33. Retrograde amnesia – Loss of memories formed before an injury.
34. Anterograde amnesia – Inability to form new long-term memories after an injury.
35. Patient H.M. – Patient who underwent bilateral hippocampal removal and developed severe anterograde amnesia.
36. Bilateral temporal lobectomy – Surgical removal of both medial temporal lobes.
37. Hippocampal removal – Loss of hippocampal structures necessary for forming new declarative memories.
38. Intact procedural memory – Preservation of skill learning despite memory deficits.
39. Mirror-tracing task – A task in which H.M. showed procedural learning despite no conscious recollection.
40. Patient K.C. – Individual with loss of episodic memory but intact semantic memory.
41. Episodic amnesia – Inability to recall personal past experiences.
42. Semantic memory preservation – Retention of general knowledge despite episodic memory loss.
43. Patient J.K. – Individual with basal ganglia dysfunction and impaired procedural memory.
44. Basal ganglia dysfunction – Damage affecting habit and motor learning.
45. Procedural memory impairment – Inability to perform learned habits.
46. Korsakoff’s syndrome – Memory disorder linked to thiamine deficiency from alcoholism.
47. Thiamine deficiency – Lack of vitamin B1 impairing metabolism in neurons.
48. Chronic alcoholism – Long-term alcohol abuse causing nutritional deficits.
49. Confabulation – Unintentional fabrication of stories to fill memory gaps.
50. Frontal cortex atrophy – Degeneration of frontal lobe associated with Korsakoff’s.
51. Diencephalon damage – Injury to thalamus/hypothalamus contributing to memory problems.

SECTION 3 — HIPPOCAMPUS & SPATIAL MEMORY

52. Hippocampus – Brain structure essential for forming declarative memories.
53. CA1 region – Area critical for LTP expression and memory consolidation.
54. CA3 region – Area important for pattern completion and memory retrieval.
55. Dentate gyrus – Region involved in forming new memories and pattern separation.
56. Schaffer collaterals – Axons connecting CA3 to CA1 neurons and often used to study LTP.
57. Hippocampal place cells – Neurons that fire when an animal is in a specific location.
58. Spatial representation – Mental mapping of surroundings.
59. Cognitive map – Internal representation of spatial environment.
60. Environmental mapping – Hippocampal encoding of surroundings.
61. Context memory – Memory of the setting in which an event occurred.
62. Spatial navigation – Ability to move through an environment using memory.

SECTION 4 — SYNAPTIC BASIS OF MEMORY

63. Long-term potentiation (LTP) – Long-lasting increase in synaptic strength following high-frequency stimulation.
64. High-frequency stimulation – Rapid firing that induces LTP.
65. Tetanic stimulation – Burst of electrical activity used to induce LTP.
66. EPSP – Excitatory postsynaptic potential; depolarization of postsynaptic neuron.
67. Synaptic strengthening – Persistent increase in synaptic efficiency.
68. Hebbian learning – Theory stating synapses strengthen when pre- and postsynaptic neurons fire together.
69. Co-activation – Simultaneous firing of neurons required for LTP.
70. “Cells that fire together wire together” – Common summary of Hebbian learning.

LTP Mechanisms

71. Glutamate – Main excitatory neurotransmitter involved in LTP.
72. AMPA receptors – Receptors allowing Na+ entry and depolarization.
73. NMDA receptors – Receptors requiring depolarization to permit Ca2+ entry.
74. Mg²⁺ block – Magnesium ion that normally blocks the NMDA receptor channel.
75. Postsynaptic depolarization – Voltage change required to remove Mg²⁺ block.
76. Ca²⁺ influx – Entry of calcium that triggers molecular changes for LTP.
77. Calmodulin – Calcium-binding protein activating downstream pathways.
78. CaMKII – Kinase essential for LTP induction.
79. PKA – Protein kinase A; part of signaling cascade.
80. MAPK – Mitogen-activated protein kinase; involved in synaptic remodeling.
81. Protein synthesis – Creation of new proteins needed to stabilize long-term memory.
82. New AMPA receptor insertion – Mechanism that increases synaptic strength.
83. Synaptic remodeling – Structural changes in synapses to store memory.
84. Dendritic spine enlargement – Growth of postsynaptic spines associated with LTP.

LTD

85. Long-term depression (LTD) – Long-lasting weakening of synaptic strength.
86. Low Ca²⁺ activation – Signal that promotes LTD instead of LTP.
87. Protein phosphatases – Enzymes that remove phosphate groups to weaken synapses.
88. Synaptic weakening – Reduction in synaptic strength.
89. Pruning – Removal of unnecessary synaptic connections.
90. Circuit refinement – Tuning of neural pathways through LTP/LTD balance.

SECTION 5 — MEMORY STORAGE

91. Karl Lashley – Neuroscientist who searched for the “engram.”
92. Mass Action Principle – Memory loss depends on amount of cortex removed, not location.
93. Equipotentiality – Idea that all brain areas equally capable of storing memory.
94. Cortical damage – Injury affecting memory depending on extent.
95. Distributed memory storage – Memory stored across many brain regions.
96. Systems consolidation – Slow reorganization of memory across brain networks.

SECTION 6 — ALZHEIMER’S DISEASE

97. Dementia – Progressive decline in memory plus cognitive impairments.
98. Alzheimer’s disease – Most common form of dementia, involving plaques, tangles, neuron loss.
99. Cognitive decline – Gradual loss of mental abilities.
100. Senile plaques – Extracellular deposits of β-amyloid protein.
101. β-amyloid – Peptide fragment accumulating in Alzheimer’s disease.
102. Amyloid precursor protein (APP) – Normal protein cleaved abnormally to form β-amyloid.
103. Amyloid aggregation – Clumping of β-amyloid into toxic plaques.
104. Neurofibrillary tangles – Intracellular tangles made of hyperphosphorylated tau.
105. Tau protein – Microtubule-associated protein that stabilizes axons.
106. Hyperphosphorylation – Excessive addition of phosphate groups causing tau to aggregate.
107. Hippocampal atrophy – Shrinking of hippocampus due to neuron loss.
108. Cortical thinning – Loss of cerebral cortex volume.
109. Enlarged ventricles – Fluid-filled cavities enlarge as brain shrinks.
110. Cholinergic neuron loss – Degeneration of ACh-producing neurons early in AD.
111. Basal nucleus of Meynert – Major source of cortical acetylcholine.
112. PET scan – Imaging showing reduced brain metabolism.
113. MRI scan – Structural imaging showing atrophy.
114. Decreased metabolic activity – Reduced brain function visible via PET.
115. Memory impairment – Difficulty forming and retrieving memories.
116. Executive dysfunction – Impaired planning, reasoning, decision-making.
117. Agnosia – Inability to recognize objects.
118. Apraxia – Inability to perform purposeful movements.
119. Aphasia – Impairment in language function.
120. Cholinesterase inhibitors – Drugs slowing ACh breakdown to treat AD symptoms.

SECTION 7 — LIMBIC SYSTEM & EMOTION

121. Limbic system – Group of brain structures related to emotion and memory.
122. James Papez – Neuroscientist who proposed original emotional circuit.
123. Papez circuit – Circuit believed to underlie emotional experience.
124. Cingulate gyrus – Involved in emotional processing.
125. Fornix – Major fiber pathway linking hippocampus to hypothalamus.
126. Mammillary bodies – Hypothalamic nuclei involved in memory.
127. Anterior thalamus – Relays limbic information to cortex.
128. Parahippocampal gyrus – Region crucial for memory and emotional context.
129. Emotional processing – Brain mechanisms for generating feelings.
130. “Stream of feeling” – Emotional response involving hypothalamus.
131. “Stream of thought” – Cognitive evaluation involving cortex.

SECTION 8 — HYPOTHALAMUS & EMOTION

132. Hypothalamus – Regulates autonomic and endocrine responses to emotion.
133. Classic hypothalamus – Region controlling homeostasis and hormonal release.
134. Emotional hypothalamus – Area generating physiological emotional responses.
135. Autonomic nervous system – Controls involuntary responses.
136. Sympathetic activation – Fight-or-flight response.
137. Parasympathetic activation – Rest-and-digest response.
138. Sham rage – Rage response in decorticate animals showing hypothalamus control.
139. Philip Bard experiment – Demonstrated hypothalamus generates coordinated rage behavior.
140. “Necessary” for emotion – Without hypothalamus, no emotional expression.
141. “Sufficient” for emotion – Hypothalamus alone can generate emotion even without cortex.

SECTION 9 — AMYGDALA & FEAR

142. Amygdala – Brain structure essential for fear learning and emotional significance.
143. Basolateral amygdala – Receives sensory input; forms associations.
144. Central nucleus of amygdala – Outputs fear responses (freezing, HR, BP changes).
145. Fear learning – Associating stimuli with emotional significance.
146. Fear response – Physiological reaction to threat.
147. Freeze response – Immobility behavior indicating fear.
148. Emotional salience – How important or threatening a stimulus is perceived.
149. Associative learning – Forming links between stimuli and outcomes.
150. Patient S.M. – Woman with bilateral amygdala destruction who cannot experience fear.
151. Urbach-Wiethe disease – Genetic disorder causing calcification of amygdala.
152. Loss of fear – Inability to feel fear or recognize fear in others.
153. Personal space impairment – Lack of discomfort in close proximity.
154. Fear facial recognition deficit – Inability to identify fear expressions.

SECTION 10 — FEAR CONDITIONING

155. Classical conditioning – Learning via association.
156. Conditioned stimulus (CS) – Previously neutral cue.
157. Unconditioned stimulus (US) – Naturally aversive cue (e.g., shock).
158. Conditioned response (CR) – Learned reaction (e.g., freezing to tone).
159. Tone-shock pairing – Standard fear conditioning paradigm.
160. Freezing behavior – Typical rodent fear response.
161. Somatosensory pain pathway – Carries shock information to amygdala.
162. Amygdala-dependent learning – Amygdala required for fear conditioning.
163. Hippocampal declarative memory – Required for conscious recollection, not for conditioned fear.
164. Dissociation of fear vs memory – Fear conditioning and declarative memory rely on different circuits.

SECTION 11 — MOTIVATION, REWARD, ADDICTION

165. Dopamine – Neurotransmitter involved in reward, motivation, and movement.
166. Reward processing – Brain evaluation of pleasurable stimuli.
167. Motivation circuits – Networks driving goal-directed behavior.
168. Reinforcement learning – Learning based on consequences.
169. Reward prediction error – Difference between expected and actual reward.

Dopamine pathways

170. Mesolimbic pathway – VTA → nucleus accumbens; reward and pleasure.
171. Mesocortical pathway – VTA → prefrontal cortex; cognition and planning.
172. Nigrostriatal pathway – Substantia nigra → striatum; movement control.
173. VTA (ventral tegmental area) – Source of dopamine neurons for reward.
174. Nucleus accumbens – Critical structure for reward and addiction.
175. Ventral striatum – Region mediating motivation.
176. Basal ganglia – Structures controlling movement and habits.
177. Prefrontal cortex – Decision-making and impulse control.
178. Hippocampus (context) – Provides contextual information to reward system.

Addiction

179. Drug reinforcement – Drugs strengthen behavior that leads to their use.
180. Dopamine elevation – All addictive drugs increase DA in nucleus accumbens.
181. Disinhibition – Removing inhibitory control to increase dopamine activity.
182. GABA interneuron inhibition – Opiates inhibit GABA, increasing dopamine firing.
183. Cocaine – Blocks dopamine reuptake.
184. Amphetamine – Causes dopamine release.
185. Nicotine – Stimulates ACh receptors on VTA neurons to increase DA.
186. Opiates – Activate opioid receptors and increase dopamine via disinhibition.
187. Craving – Strong desire to use a drug.
188. Withdrawal – Negative symptoms when drug is removed.
189. Dopamine downregulation – Reduced DA receptor expression from chronic drug use.
190. D2 receptor reduction – Marker of addiction-related changes.

SECTION 12 — LANGUAGE & APHASIA

Language anatomy

191. Broca’s area – Region in left frontal lobe for speech production.
192. Wernicke’s area – Left temporal lobe region for language comprehension.
193. Arcuate fasciculus – Fiber bundle connecting Broca’s and Wernicke’s.
194. Primary auditory cortex – Processes sound information.
195. Primary visual cortex – Processes visual input.
196. Temporal lobe – Involved in language comprehension and memory.
197. Frontal lobe – Involved in language production and planning.

Aphasias

198. Broca’s aphasia – Non-fluent speech with preserved comprehension.
199. Non-fluent aphasia – Difficulty producing speech.
200. Agrammatism – Difficulty forming grammatically correct sentences.
201. Wernicke’s aphasia – Fluent but meaningless speech with impaired comprehension.
202. Fluent aphasia – Fluent output lacking meaningful content.
203. Word salad – Disorganized, nonsensical speech.
204. Paraphasias – Incorrect word substitutions.
205. Anosognosia – Unawareness of one's own deficits.
206. Conduction aphasia – Damage to arcuate fasciculus causing repetition difficulty.
207. Repetition deficit – Inability to repeat spoken words.

SECTION 13 — LATERALIZATION & SPLIT BRAIN

208. Hemispheric lateralization – Division of cognitive functions between hemispheres.
209. Corpus callosum – Major fiber tract connecting hemispheres.
210. Split-brain surgery – Severing corpus callosum to treat epilepsy.
211. Epilepsy treatment – Purpose of split-brain surgery.
212. Optic chiasm – Crossing of optic nerves.
213. Right visual field – Processed by left hemisphere.
214. Left visual field – Processed by right hemisphere.
215. Left hemisphere (“interpreter”) – Creates verbal explanations for actions.
216. Right hemisphere (visuospatial) – Handles spatial processing and emotion.
217. Prosody – Emotional tone and rhythm of speech.
218. Spatial cognition – Ability to process spatial relationships.
219. Consciousness definition – Awareness and ability to communicate that awareness.

SECTION 14 — SCHIZOPHRENIA

220. Schizophrenia – Psychiatric disorder involving hallucinations, delusions, and cognitive dysfunction.
221. “Split mind” misconception – Incorrect belief that schizophrenia is multiple personalities.
222. Positive symptoms – Added abnormal behaviors (hallucinations, delusions).
223. Negative symptoms – Loss of normal function (flat affect, reduced motivation).
224. Cognitive symptoms – Problems with thinking, memory, and executive function.
225. Hallucinations – Perceptions without external stimuli.
226. Delusions – False beliefs.
227. Paranoia – Irrational fear of harm.
228. Disorganized speech – Incoherent or tangential speech patterns.
229. Flat affect – Reduced emotional expression.
230. Working memory deficits – Impairment in holding and manipulating information.

Neural causes

231. Enlarged ventricles – Sign of brain volume loss.
232. Temporal cortex thinning – Tissue loss in temporal lobes.
233. Prefrontal cortex dysfunction – Impaired decision-making and cognition.
234. Abnormal dendrites – Disorganized neuron structure.
235. Hippocampal abnormalities – Structural or functional changes in hippocampus.

Dopamine theory

236. Hyperactive mesolimbic DA – Excess dopamine causing positive symptoms.
237. Hypoactive mesocortical DA – Low dopamine causing negative symptoms.
238. D2 receptor overactivation – Excess stimulation causing hallucinations/delusions.
239. D1 receptor underactivation – Reduced PFC function.

Treatments

240. Typical antipsychotics – First-generation drugs blocking D2 receptors.
241. Atypical antipsychotics – Second-generation drugs with fewer motor side effects.
242. Third-generation antipsychotics – Drugs stabilizing dopamine (e.g., Abilify).
243. Chlorpromazine – First antipsychotic drug; blocks dopamine receptors.
244. Haloperidol – Potent D2 antagonist used for positive symptoms.
245. Clozapine – Atypical antipsychotic effective in treatment-resistant cases.
246. Risperidone – Atypical antipsychotic treating both positive and negative symptoms.
247. Olanzapine – Atypical antipsychotic with broad receptor targets.
248. Aripiprazole – Partial D2 agonist balancing dopamine levels.
249. Tardive dyskinesia – Irreversible involuntary movements from long-term antipsychotic use.
250. Parkinsonian side effects – Movement problems due to dopamine blockade.

SECTION 15 — DEPRESSION

251. Major depressive disorder – Mood disorder involving persistent sadness and loss of interest.
252. Unipolar depression – Depression without manic episodes.
253. Monoamine hypothesis – Theory that depression is caused by low serotonin and norepinephrine.
254. Serotonin (5-HT) – Neurotransmitter affecting mood and cognition.
255. Norepinephrine (NE) – Neurotransmitter involved in arousal and mood.
256. Reserpine – Drug that depletes monoamines and can induce depression.
257. MAO inhibitors – Antidepressants preventing breakdown of monoamines.
258. SSRIs – Selective serotonin reuptake inhibitors; increase serotonin levels.
259. Serotonin transporter – Protein responsible for serotonin reuptake.
260. Short allele (S allele) – Variant linked to increased depression risk under stress.
261. Long allele (L allele) – Variant associated with lower risk.
262. Gene-environment interaction – Combined influence of genes and life experiences.
263. Childhood abuse risk factor – Early trauma increasing depression likelihood.
264. Impaired neurogenesis – Reduced formation of new neurons in hippocampus.
265. HPA axis dysfunction – Stress system abnormalities contributing to depression.
266. Reduced hippocampal volume – Shrinking of hippocampus seen in depression.
267. Reduced amygdala volume – Structural changes associated with mood disorders.
268. Reduced cortical thickness – Loss of neurons/volume in cortex.
269. Decreased metabolic activity (PET) – Lower brain activity seen in depressed patients.