Brain Rhythms, Sleep, Learning, Memory, and Language Notes

Electroencephalography (EEG) measures synchronous voltage fluctuations ( $\mu V$ range) from cortical pyramidal neurons.
Recording resolution: High temporal resolution ( $1000\,Hz$ ) but limited spatial resolution.
Rhythmic mechanisms: Driven by the Thalamus as a central pacemaker or collective neuronal oscillations via voltage-gated ion channels.
Pathological synchrony: Seizures and epilepsy are characterized by abnormal, high-amplitude, repetitive rhythmic activity.

Awake: Low voltage, fast EEG; vivid, external sensation; logical thought; voluntary movement.
Non-REM Sleep: High voltage, slow EEG; dull or absent sensation; logical, repetitive thought; occasional involuntary movement.
REM Sleep: Low voltage, fast EEG; vivid, internal sensation; vivid, illogical thought; muscle paralysis and Rapid eye movement (REM).

Serotonin (Raphe nuclei) and Norepinephrine (Locus coeruleus): High activity during wakefulness, low during SWS, very low in REM.
Acetylcholine (Brainstem): High during wakefulness and REM, low during SWS.
Pons Stimulation: Produces REM sleep and muscle atonia via IPSPs in spinal motoneurons.
PGO waves: (pontine – geniculate – occipital cortex) signal REM sleep entry.

Active brain regions during rest: Medial prefrontal cortex, posterior cingulate cortex, posterior parietal cortex, hippocampus, and lateral temporal cortex.
Functions: Internal thought, mind-wandering, autobiographical memory, and social cognition.

SCN: Master circadian oscillator located in the hypothalamus above the optic chiasm.
Zeitgebers: Environmental cues (primarily light) that entrain biological clocks.
Light sensor: Melanopsin-containing retinal ganglion cells project to the SCN to reset rhythms.

Declarative (explicit): Facts and events that can be stated.
Nondeclarative (implicit): Performance, skills, priming, and conditioning.
Temporal stages: Iconic ( $< 1\,sec$ ), short-term (STM), intermediate, and long-term (LTM).

Patient H.M (Henry Molaison): Temporal lobe surgery (removal of hippocampus and entorhinal cortex) resulted in severe anterograde amnesia for declarative LTM.
Key Findings: Spared procedural memory (e.g., mirror-tracing) and priming; memory consolidation (transfer to neocortex) involves the hippocampus, but storage does not.

Long-term Potentiation (LTP): Rapid stimulation increases synaptic efficacy via NMDA receptor activation, $Ca^{2+}$ influx, and protein kinase activation (PKA, PKC, CaMK, TK).
Long-term Depression (LTD): Low-frequency stimulation leads to small $Ca^{2+}$ entry, activating phosphatases to remove phosphate groups from kinases.
Consolidation: Long-lasting changes require CREB-mediated gene expression and new protein synthesis.

Broca’s Aphasia: Left inferior frontal gyrus damage; results in non-fluent, expressive speech deficits with intact comprehension.
Wernicke’s Aphasia: Left posterior superior temporal gyrus damage; results in fluent but unintelligible speech and loss of comprehension.
Arcuate fasciculus: Axon tract connecting Broca's and Wernicke's regions.
Wernicke-Geschwind Model: Defines pathways for repeating spoken and written words.

Left Hemisphere: Dominant for language ( $98\%$ of right-handed males), motor programming, and local perception.
Right Hemisphere: Dominant for attention, prosody (melody of speech), and global perception.
Corpus Callosum: Facilitates transfer between hemispheres; surgical callosotomy (Split brain) isolates information to individual hemispheres (e.g., Patient cannot name objects in the left visual field).