Ch 1. Brain Basics Brain Overview The brain is the literal “nerve-center” of the body, containing billions of neurons that simultaneously manage movement, thought, emotion, memory, and autonomic functions. Multitasking examples: throwing a ball while talking, planning dinner while shopping, day-dreaming while driving—all possible because the brain is partitioned into specialized regions working in parallel. Key principle: functional specialization + massive inter-connection = high-level cognition . Major Brain Landmarks and Lobes Cerebrum Largest brain portion; split into left & right hemispheres. Hemispheres connected by the corpus callosum (largest commissural tract). Surface layer = cerebral cortex ; deep folds (gyri & sulci) expand surface area, allowing more neurons → greater processing power. Lobes & Core Functions Frontal (above eyes) : voluntary movement, speech, memory, emotion, planning, problem-solving, personality.Parietal (top, behind frontal) : integrates skin sensations, taste, portions of visual processing (spatial aspects).Occipital (back) : primary & secondary visual processing, color/shape recognition, complex visual comprehension.Temporal (sides, level of eyes) : auditory interpretation, some visual processing.
• Hippocampus (curved, under cortex): encodes new memories.
• Amygdala (deep, anterior to hippocampus): integrates memory with emotion.Forebrain Structures: Limbic System & Basal Ganglia Limbic System (emotion & motivation regulation)Hippocampus & amygdala (temporal lobe). Thalamus : sensory integration & relay hub.Hypothalamus : hormonal control via pituitary; bodily homeostasis.Basal Ganglia Formed by portions of forebrain + midbrain. Regulate complex voluntary movements; provide excitatory/inhibitory feedback loops to motor cortex (fine motor skills, writing, instrument playing). Midbrain & Brainstem Components Midbrain (under thalamus) Coordinates eye movements (blink, focus). Generates auditory startle reflex. Contains nuclei that inhibit unwanted body movements & synchronize sensory ↔ motor signals. Brainstem = Midbrain + Pons + Medulla Core conduit between spinal cord & higher brain; houses life-support nuclei. Hindbrain: Cerebellum, Pons, Medulla Cerebellum Second-largest volume; holds >50 % of neurons . Two hemispheres, folded like cortex. Functions: coordinate voluntary movement, motor learning, spatial & temporal perception.
• Clinical example: cerebellar damage ⇒ jerky, arrhythmic gait; cannot touch finger to nose accurately. Pons (below cerebellum) : influences breathing & posture.Medulla (lowest brainstem) Connects brain ↔ spinal cord; controls swallowing, heart rate, breathing. Brain Evolution Originated from a simple neural tube (seen in lancelet Amphioxus ). Early vertebrate brain developed three bulges → forebrain, midbrain, hindbrain . Evolutionary expansions:Olfactory bulbs (chemical detection). Visual processing areas as image-forming eyes evolved. Cerebellum added for escape & orientation in active swimmers.Cerebral hemispheres ballooned; cortex folded in mammals, greatly amplifying neuron count & processing power. Neural Networks & Nerve Tracts Nerve tract : bundle of long-range axons linking regions (e.g., corpus callosum, anterior commissure).Neural network : ordered series of tracts + regions routing information in milliseconds.Movie-watching pathway example:Retina photoreceptors → optic nerve. Optic tract → thalamus (basic shape/color/motion coding). Thalamus → primary visual cortex (edge detection, binocular 3-D integration). Divergence into two streams:
• Temporal “what” : object identity.
• Parietal “where” : spatial location. Visual cortex sends feedback to thalamus ⇒ continual refinement (thalamo-cortical loop). Brain Waves (EEG Rhythms) Rhythmic activity from thalamo-cortical loops detectable as brain waves . Frequency bands (with typical cortical origins & states):Alpha 8!\text{–}!13\,\text{Hz} (parietal/occipital, relaxed eyes-closed).Beta 14!\text{–}!30\,\text{Hz} (frontal/parietal during sensory processing, concentration).Theta 4!\text{–}!7\,\text{Hz} (light sleep).Delta <3.5\,\text{Hz} (deep sleep). Typical scalp amplitudes:
• Alpha & Delta 20\text{–}200\,\mu\text{V}
• Beta & Theta 5\text{–}10\,\mu\text{V} Neural Circuits: Columns, Excitation & Inhibition Cortical microcircuit : neurons arranged in stacked layers forming vertical columns dedicated to specific features (e.g., a single pixel, pitch, or tactile point).Signal flow : feed-forward down the column; each relay transforms information (edges → shapes → faces).Lateral connectivity : neurons talk to neighboring columns, allowing dynamic modulation (context-dependent perception).Neuron types Excitatory \approx80\% (e.g., pyramidal cells): push postsynaptic neurons toward firing.Inhibitory \approx20\% (local interneurons): suppress activity; essential for tuning & preventing runaway excitation (epilepsy if imbalanced).Recurrent network motifs Feed-forward inhibition : column A excites its own path while inhibiting neighbors → sharper contrast.Feedback inhibition : downstream excitation loops back via interneurons to dampen earlier layers → stability & timing.Neuron Anatomy Soma (cell body) : nucleus + protein machinery.Dendrites : branched receivers; thousands of synapses per neuron.Axon : single long output cable; can span >1\,\text{m}; ends in axon terminals .Myelin (oligodendrocyte/Schwann cell sheath) : increases conduction speed via saltatory transmission between nodes of Ranvier .Glial Cells (≈ equal numbers to neurons in primate cortex) Astrocytes : ion buffering, nutrient supply, synapse formation/cleanup.Microglia : immune surveillance, phagocytosis, synaptic pruning.Ependymal cells : secrete cerebrospinal fluid.Oligodendrocytes : form myelin in CNS (Schwann cells in PNS).Ion Channels & Action Potentials Resting potential \approx -70\,\text{mV} (inside negative). Synaptic inputs depolarize or hyperpolarize dendritic membrane. If summed depolarization reaches threshold (voltage-gated Na⁺ channels open), an action potential fires—an all-or-nothing electrical pulse propagating down the axon. Synapses & Neurotransmission Chemical synapse components : presynaptic axon terminal, synaptic cleft, postsynaptic density.Sequence:Action potential arrives → voltage-gated Ca²⁺ channels open. Ca²⁺ triggers fusion of synaptic vesicles → neurotransmitter release. NTs diffuse <1\,\mu\text{m} across cleft → bind postsynaptic receptors. Receptors open/close ion channels → postsynaptic potential. Termination: enzymatic breakdown or reuptake into presynaptic terminal; astrocytes assist by “mopping up.” Receptor families Ionotropic : receptor = part of ion channel (fast, ms scale).Metabotropic : receptor triggers G-protein cascade → indirect channel modulation or gene effects (slower, modulatory).Neurotransmitters: Glutamate & GABA Glutamate (excitatory; \approx50\% of synapses)AMPA receptors : fast, transient depolarization.NMDA receptors : slower, require multiple spikes & Mg²⁺ unblock; crucial for synaptic plasticity, learning & memory.GABA (inhibitory)GABA_A (ionotropic) : Cl⁻ influx → hyperpolarization.GABA_B (metabotropic) : K⁺ efflux → hyperpolarization.Receptors & Molecular Signaling (Hormones, Neuromodulators) Hormones (e.g., cortisol, estradiol) carry systemic information; can act on membrane receptors or, if lipid-soluble, intracellular receptors → act as transcription factors.Neuromodulators (e.g., endocannabinoids) fine-tune neurotransmission—often suppress release probability.Prostaglandins : small lipids raising pain sensitivity during inflammation.Signal transduction : ligand binding → conformational change → intracellular cascade (second messengers, kinases, ion balance shifts, gene regulation).Genes, Gene Expression & Neurological Disorders All neurons share identical DNA; functional diversity arises from differential gene expression . Chromatin remodeling (tight vs. open) controls which genes are accessible; reversible → neurons adapt to environment & hormones. Alleles : sequence variations ⇒ protein variants with differing efficacy.Example: Tay-Sachs disease —mutations in HEX A gene → defective β-hexosaminidase A; toxic lipid accumulation, fatal neurodegeneration. Advances in whole-genome sequencing will clarify genetic contributions to brain disorders within the next decade.