Detailed notes on central nervous system physiology

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Central Nervous System Physiology - Detailed Notes

Sources: Guyton and Hall Textbook of Medical Physiology; Ganong's Review of Medical Physiology, 26th Ed.

1. Overview and Organization of the Nervous System

The CNS processes, integrates, and transmits information from external and internal sources to initiate physiological behaviors. It consists of the brain and spinal cord, working together with the peripheral nervous system (PNS).

Functional divisions:

Somatic nervous system - voluntary skeletal muscle control
Autonomic nervous system (ANS) - involuntary control of viscera, glands, smooth muscle; subdivided into sympathetic and parasympathetic
Enteric nervous system - intrinsic neural plexuses of the gut

The CNS is protected by the blood-brain barrier (BBB), cerebrospinal fluid (CSF), and the meninges.

2. The Neuron - Basic Structural and Functional Unit

Motor neuron with myelinated axon showing soma, dendrites, axon hillock, nodes of Ranvier, Schwann cells, and terminal buttons

2.1 Structural Components

Component	Structure	Function
Soma (cell body)	Contains nucleus, Nissl substance (RER), mitochondria	Metabolic center; protein synthesis
Dendrites	Multiple branching processes	Receive and integrate incoming signals; processed via dendritic spines
Axon hillock	Thickened base of axon	Site of action potential initiation (lowest threshold)
Initial segment	First portion of axon	Integrates inputs; determines firing
Axon	Long fibrous process, may be myelinated	Conducts impulses to presynaptic terminals
Terminal boutons (buttons)	Synaptic knobs at axon endings	Store and release neurotransmitters

2.2 Neuron Classification by Number of Processes

Unipolar - one process (e.g., invertebrate neurons)
Bipolar - two processes: one dendrite + one axon (e.g., retinal neurons, olfactory epithelium)
Pseudounipolar - single process splits into two (both function as axons); one to periphery, one to spinal cord. Classic example: dorsal root ganglion cells
Multipolar - one axon + many dendrites. Most CNS neurons; includes spinal motor neurons, hippocampal pyramidal cells, cerebellar Purkinje cells

2.3 Neuroglial Cells

Glia outnumber neurons ~10:1 and are not electrically excitable, but play essential supporting roles:

Astrocytes - structural support, BBB maintenance, ion buffering (K+), neurotransmitter uptake, synaptic modulation
Oligodendrocytes - myelinate CNS axons (one cell can myelinate multiple axons; contrast with Schwann cells in PNS, which myelinate one segment each)
Microglia - CNS immune cells; phagocytosis of debris and pathogens
Ependymal cells - line ventricles and central canal; involved in CSF production and circulation

3. Resting Membrane Potential

The resting membrane potential (RMP) of large nerve fibers is approximately -70 mV (inside negative relative to outside).

3.1 Ionic Basis

The Na⁺-K⁺ ATPase pump is central to establishing RMP:

Pumps 3 Na⁺ out for every 2 K⁺ in (electrogenic - net positive charge moves out)
Creates the following concentration gradients:

Ion	Outside (mEq/L)	Inside (mEq/L)	Ratio (in/out)
Na⁺	142	14	0.1
K⁺	4	140	35.0
Cl⁻	103	4	low inside
A⁻ (proteins)	-	high	impermeant

Leak channels: K⁺ leak channels allow continuous outward K⁺ diffusion down its concentration gradient, carrying positive charge out and contributing further to the negative interior. The membrane is about 100x more permeable to K⁺ than to Na⁺ at rest.

Nernst equilibrium potential for K⁺: approximately -94 mV
Nernst equilibrium potential for Na⁺: approximately +61 mV
RMP (-70 mV) lies between these values, reflecting the combined influence of both ions weighted by relative permeability (Goldman-Hodgkin-Katz equation).

Key point: Only 1/3,000,000 to 1/100,000,000 of the total positive charges inside the fiber need to be transferred to establish the -70 mV potential. This incredibly small ion movement allows the potential to reverse from -70 mV to +35 mV in as little as 1/10,000 of a second.

4. The Action Potential (AP)

Action potential recording showing resting at -70 mV, depolarization overshoot to +35 mV, repolarization, and hyperpolarization

4.1 Stages of the Action Potential

1. Resting Stage (-70 mV)

Membrane is "polarized"
Voltage-gated Na⁺ channels closed but capable of opening
K⁺ leak channels open

2. Depolarization Stage

Threshold reached at approximately -55 mV
Massive opening of voltage-gated Na⁺ channels
Rapid Na⁺ influx drives membrane potential from -70 mV to approximately +35 mV (overshoot) in large fibers
Some CNS neurons only approach 0 mV without overshooting

3. Repolarization Stage

Within <1 ms, Na⁺ channels begin to close (inactivation gate closes)
Voltage-gated K⁺ channels open (delayed)
K⁺ rapidly exits, restoring negative potential

4. Hyperpolarization (Undershoot)

K⁺ channels remain open slightly longer than needed
Membrane potential briefly dips below -70 mV
Returns to resting level once K⁺ channels close

4.2 Voltage-Gated Channels

Voltage-gated Na⁺ channels have two gating components:

Activation gate (m gate) - opens rapidly when membrane depolarizes to threshold
Inactivation gate (h gate) - closes within a millisecond after activation, stopping Na⁺ influx (responsible for the absolute refractory period)

Voltage-gated K⁺ channels:

Delayed rectifier channels - open ~0.1-0.5 ms after depolarization
Their delayed opening underlies the repolarization phase and undershoot

4.3 Refractory Periods

Absolute refractory period - Na⁺ inactivation gates are closed; no stimulus can generate another AP regardless of strength. Lasts ~1-2 ms.
Relative refractory period - After-hyperpolarization phase; a stronger-than-normal stimulus can generate an AP. This limits the maximum firing frequency of a neuron.

4.4 All-or-Nothing Principle

Once an AP is elicited at any point on the membrane, depolarization travels over the entire membrane provided conditions are right. The "safety factor" - the ratio of AP amplitude to threshold - must be >1 for continued propagation.

4.5 Ionic Fluxes During an AP (Ganong's)

During depolarization: Na⁺ rushes in through voltage-gated Na⁺ channels
Peak of AP: Na⁺ permeability at maximum; approaches Na⁺ equilibrium potential (+61 mV)
Repolarization: K⁺ efflux via delayed rectifier K⁺ channels dominates

5. Conduction of Nerve Impulses

5.1 Unmyelinated Fibers - Continuous Conduction

Depolarization spreads by local circuit currents: inward Na⁺ current at a depolarized zone flows longitudinally inside the axon, then outward through adjacent resting membrane, depolarizing it to threshold. This proceeds continuously in both directions from the stimulus point.

5.2 Myelinated Fibers - Saltatory Conduction

In myelinated fibers, the myelin sheath (formed by Schwann cells in PNS, oligodendrocytes in CNS) acts as an electrical insulator. Ion exchange can only occur at nodes of Ranvier - the unmyelinated gaps between myelin segments (~1 mm apart).

Key features of saltatory conduction:

The AP "jumps" from node to node
Much faster conduction velocity (up to 120 m/s in large myelinated fibers vs 0.5-2 m/s in unmyelinated C fibers)
More energy efficient - fewer ions cross the membrane; less ATP needed by Na⁺-K⁺ pump to restore gradients

Conduction velocity is proportional to: fiber diameter and degree of myelination

Fiber Type	Diameter (μm)	Conduction (m/s)	Function
Aα	12-20	70-120	Motor, proprioception
Aβ	5-12	30-70	Touch, pressure
Aδ	2-5	12-30	Fast pain, cold
B	1-3	3-15	Preganglionic ANS
C	0.3-1	0.5-2	Slow pain, warmth

5.3 Re-Establishing Ionic Gradients After APs

Transmission of each AP slightly reduces the Na⁺/K⁺ gradients (Na⁺ enters, K⁺ exits). However, the change is so minute per impulse that 100,000 to 50 million impulses can be transmitted before gradients fail. The Na⁺-K⁺ ATPase continuously restores gradients using ATP. Pump activity increases approximately as the cube of intracellular Na⁺ concentration - a powerful feedback mechanism.

6. Synaptic Transmission

6.1 Types of Synapses

Chemical synapses (most common in CNS):

Pre- and postsynaptic membrane separated by synaptic cleft (~20-40 nm wide)
One-way transmission (presynaptic → postsynaptic)
Subject to fatigue, pharmacological modulation, plasticity

Electrical synapses (gap junctions):

Direct cytoplasmic connections via connexins
Very fast, bidirectional transmission
Common in cardiac muscle, smooth muscle, some CNS neurons (e.g., inferior olive)

6.2 Synaptic Anatomy

Types of chemical synaptic contacts:

Axodendritic - most common; axon terminal contacts dendrite or dendritic spine
Axosomatic - axon contacts cell body (soma)
Axoaxonal - axon contacts another axon (mediates presynaptic inhibition/facilitation)

Presynaptic terminal contains:

Mitochondria (energy supply for neurotransmitter synthesis and vesicle recycling)
Synaptic vesicles - three types:
- Small clear vesicles: contain acetylcholine, glycine, GABA, or glutamate
- Small dense-core vesicles: contain catecholamines (dopamine, norepinephrine)
- Large dense-core vesicles: contain neuropeptides (synthesized in soma, transported by fast axoplasmic transport)

6.3 Steps in Chemical Synaptic Transmission

AP arrives at presynaptic terminal
Depolarization opens voltage-gated Ca²⁺ channels at active zones
Ca²⁺ influx (transmitter release begins within 200 μs)
Synaptic vesicles dock and fuse with presynaptic membrane via SNARE proteins (SNAP-25, synaptobrevin, syntaxin); neurexin-neuroligin interactions align pre- and postsynaptic elements
Exocytosis releases neurotransmitter into synaptic cleft
Neurotransmitter diffuses across cleft and binds to postsynaptic receptors
Receptor activation produces postsynaptic potential (EPSP or IPSP)
Neurotransmitter is removed by: reuptake (transporters), enzymatic degradation (e.g., AChE), or diffusion

Vesicle recycling: Small vesicles are recovered by endocytosis and refilled locally ("kiss-and-run" discharge is most common - vesicle briefly fuses, discharges contents, then reseals without full endocytosis).

6.4 Postsynaptic Potentials

Excitatory Postsynaptic Potential (EPSP):

Caused by opening of Na⁺/K⁺ channels (or other cation channels)
Net inward cation current → depolarization (more positive potential)
If summated EPSPs bring the axon hillock to threshold (~-55 mV), an AP fires

Inhibitory Postsynaptic Potential (IPSP):

Caused by opening of Cl⁻ channels (e.g., GABA-A receptor) or K⁺ channels
Cl⁻ influx (or K⁺ efflux) → hyperpolarization (more negative potential)
Makes it harder to reach threshold - inhibits firing

6.5 Summation

Type	Mechanism
Temporal summation	Multiple EPSPs from the same presynaptic neuron arriving in rapid succession; each builds on the residual depolarization of the previous one
Spatial summation	EPSPs from multiple presynaptic neurons arriving simultaneously; their depolarizations add at the axon hillock

On average, each neuron forms over 2,000 synaptic endings. The axon hillock integrates all inputs (summation of EPSPs and IPSPs) to determine whether an AP will be generated.

6.6 Inhibitory Mechanisms

Postsynaptic inhibition:

An inhibitory interneuron releases glycine or GABA onto the postsynaptic neuron
Produces IPSP via Cl⁻ or K⁺ channel opening
Example: reciprocal innervation - stretch receptor activation excites agonist motor neuron AND inhibits antagonist motor neuron via an inhibitory interneuron (direct/postsynaptic inhibition)

Presynaptic inhibition:

An inhibitory neuron synapses on an excitatory axon terminal (axoaxonal synapse)
GABA acting on GABA-A receptors increases Cl⁻ conductance in the excitatory terminal
This reduces the size of the AP invading the terminal, reducing Ca²⁺ influx, and thus less neurotransmitter is released
GABA-B receptors also open K⁺ channels and close Ca²⁺ channels at the terminal

Presynaptic facilitation: The opposite - activity at an axoaxonal synapse increases transmitter release from the excitatory ending.

7. Major Neurotransmitter Systems

Neurotransmitter	Type	Receptor Types	Location	Effect
Glutamate	Amino acid	AMPA, NMDA, Kainate, mGluR	Widespread (main excitatory)	Excitation, LTP, memory
GABA	Amino acid	GABA-A (ionotropic, Cl⁻), GABA-B (metabotropic, K⁺/Ca²⁺)	Widespread (main inhibitory)	Inhibition
Glycine	Amino acid	GlyR (ionotropic, Cl⁻)	Spinal cord, brainstem	Inhibition (reciprocal innervation)
Acetylcholine (ACh)	Quaternary amine	Nicotinic (ionotropic), Muscarinic (metabotropic)	NMJ, basal forebrain, ANS	Excitation (NMJ), varied (muscarinic)
Dopamine	Catecholamine	D₁-D₅ (metabotropic)	Substantia nigra (→ striatum), VTA (→ limbic)	Reward, motor control, motivation
Norepinephrine	Catecholamine	α₁, α₂, β₁, β₂ (metabotropic)	Locus coeruleus (→ cortex)	Arousal, attention, stress
Serotonin (5-HT)	Indoleamine	5-HT1-7	Raphe nuclei (→ widespread)	Mood, sleep, pain modulation
Histamine	Imidazole	H₁-H₄	Hypothalamus	Wakefulness
Endorphins/Enkephalins	Neuropeptides	μ, δ, κ opioid receptors	Throughout CNS	Pain modulation, reward

8. Receptor Types and Signal Transduction

Ionotropic Receptors (Fast Synaptic Transmission)

Ligand-gated ion channels
Response in milliseconds
Examples: AMPA, NMDA, GABA-A, nAChR, GlyR

Metabotropic Receptors (Slow Synaptic Transmission)

G protein-coupled receptors (GPCRs)
Activate intracellular second messengers (cAMP, IP₃, DAG)
Response in seconds to minutes; longer-lasting effects
Examples: GABA-B, mGluR, muscarinic, adrenergic, dopaminergic, serotonergic

9. Higher CNS Functions

9.1 Cerebral Cortex

The cortex is organized into 6 layers and divided into functional areas (Brodmann areas):

Primary motor cortex (M1) - precentral gyrus (area 4); voluntary movement; somatotopically organized as the motor homunculus
Primary somatosensory cortex (S1) - postcentral gyrus (areas 3, 1, 2); body sensation; sensory homunculus
Primary visual cortex (V1) - occipital lobe (area 17); retinotopic mapping
Primary auditory cortex (A1) - superior temporal gyrus (area 41/42); tonotopic mapping
Broca's area - left inferior frontal gyrus (areas 44, 45); speech production
Wernicke's area - left posterior superior temporal gyrus (area 22); speech comprehension
Prefrontal cortex - executive function, planning, working memory, personality

9.2 Basal Ganglia

Components: striatum (caudate + putamen), globus pallidus (GP), subthalamic nucleus (STN), substantia nigra (SN)

Function: modulation of voluntary movement initiation and suppression; habit formation; reward

Two pathways:

Direct pathway: cortex → striatum → GPi → thalamus → cortex (net facilitatory - promotes movement)
Indirect pathway: cortex → striatum → GPe → STN → GPi → thalamus → cortex (net inhibitory - suppresses movement)

Dopamine from the substantia nigra pars compacta facilitates direct and inhibits indirect pathway → net movement facilitation.

Dopamine loss (Parkinson's disease): reduced direct, increased indirect → thalamic suppression → bradykinesia, rigidity, tremor.

9.3 Cerebellum

Three functional divisions:

Vestibulocerebellum (flocculonodular lobe) - balance, eye movement (input from vestibular system)
Spinocerebellum (vermis + intermediate hemispheres) - limb coordination, corrects ongoing movements (input from spinal cord)
Cerebrocerebellum (lateral hemispheres) - motor planning and timing (input from cortex)

Cerebellar output is always inhibitory (Purkinje cells → deep cerebellar nuclei → thalamus → cortex) or excitatory via excitatory deep nuclear cells to brainstem/thalamus.

9.4 Thalamus

The thalamus is the principal relay station for sensory and motor information to the cortex:

Nucleus	Input	Cortical Projection
VPL	Spinal cord (body sensation)	Somatosensory cortex
VPM	Trigeminal (face sensation)	Somatosensory cortex
MGN	Inferior colliculus	Auditory cortex
LGN	Retina	Visual cortex
VL	Cerebellum, basal ganglia	Motor cortex
MD	Prefrontal cortex, limbic	Prefrontal cortex

The thalamus also regulates sleep-wake transitions via thalamocortical oscillations.

9.5 Hypothalamus

Controls homeostasis via the ANS and endocrine system:

Temperature regulation - anterior hypothalamus cools; posterior warms
Feeding and satiety - lateral hypothalamus (hunger); ventromedial nucleus (satiety)
Thirst and water balance - osmoreceptors trigger ADH release (posterior pituitary)
Circadian rhythms - suprachiasmatic nucleus (SCN)
Autonomic regulation - coordinates sympathetic and parasympathetic responses
Hormone regulation - controls anterior pituitary via releasing/inhibiting hormones (TRH, CRH, GnRH, GHRH, somatostatin, dopamine)

9.6 Limbic System

Structures: hippocampus, amygdala, cingulate gyrus, parahippocampal gyrus, mammillary bodies, fornix

Functions:

Hippocampus - formation of declarative (explicit) memory (consolidation from short to long-term)
Amygdala - emotional processing (fear, aggression), emotional memory
Cingulate gyrus - attention, emotion regulation, pain

10. Sensory Physiology

10.1 General Principles

Receptor potential - graded potential generated by sensory stimulus; not all-or-nothing
Adequate stimulus - the specific type of energy a receptor is specialized to detect
Sensory coding: intensity is coded by AP frequency and number of recruited fibers; modality by labeled-line specificity; location by receptive field topography

10.2 Somatosensory Pathways

Dorsal column-medial lemniscal pathway:

Modalities: fine touch, vibration, proprioception, two-point discrimination
First-order neurons: dorsal root ganglia → dorsal columns (ipsilateral) → decussates at medulla
Second-order: medial lemniscus → contralateral thalamus (VPL)
Third-order: VPL → somatosensory cortex

Spinothalamic (anterolateral) pathway:

Modalities: pain, temperature, crude touch
First-order neurons: dorsal root ganglia → dorsal horn → decussates in spinal cord
Second-order: contralateral spinothalamic tract → thalamus (VPL)
Third-order: VPL → somatosensory cortex

10.3 Pain

Fast (sharp) pain - Aδ fibers; spinothalamic tract; localized
Slow (burning/aching) pain - C fibers; spinothalamic tract; diffuse
Referred pain - visceral pain perceived at somatic location due to convergence of visceral and somatic afferents on same spinal neurons (e.g., cardiac ischemia → left arm/jaw)
Gate control theory (Melzack and Wall) - Aβ (touch) fibers activate inhibitory interneurons in dorsal horn that suppress pain transmission by C/Aδ fibers

Endogenous analgesia system:

Periaqueductal gray (PAG) → raphe nuclei → spinal cord
Releases serotonin and enkephalins → inhibits pain transmission
Opioids act at μ receptors throughout this system

11. Motor Control

11.1 Spinal Motor Circuits

Motor unit = one α-motor neuron + all muscle fibers it innervates
Smaller motor units: fine control (extraocular, hand)
Larger motor units: powerful movements (limb, postural)

Stretch reflex (myotatic reflex):

Muscle spindle Ia afferents → monosynaptic EPSP on α-motor neuron → muscle contraction
Simultaneously activates Renshaw cells for recurrent inhibition (limits overfiring)
Inhibitory interneuron → IPSP on antagonist motor neuron = reciprocal innervation

Golgi tendon organ (GTO) - inverse myotatic reflex:

Ib afferents from GTO → inhibitory interneuron → IPSP on agonist motor neuron
Prevents excessive tension; protects muscle from damage

11.2 Descending Motor Pathways

Pathway	Origin	Decussation	Function
Corticospinal (pyramidal)	Motor cortex	Medullary pyramids (~85%)	Voluntary fine motor control, especially distal limbs
Rubrospinal	Red nucleus (midbrain)	Immediately	Distal limb control (less dominant in humans)
Reticulospinal	Reticular formation	Bilateral	Proximal limb and axial muscle control, posture
Vestibulospinal	Vestibular nuclei	Ipsilateral	Postural reflexes, extension tone
Tectospinal	Superior colliculus	Contralateral	Head and eye movements (orienting reflex)

12. Autonomic Nervous System (ANS)

12.1 Anatomical Organization

Feature	Sympathetic	Parasympathetic
Outflow	Thoracolumbar (T1-L2)	Craniosacral (CN III, VII, IX, X; S2-4)
Preganglionic fiber	Short	Long
Postganglionic fiber	Long	Short
Ganglion location	Paravertebral/prevertebral	Near/in target organ
Preganglionic NT	ACh (nAChR)	ACh (nAChR)
Postganglionic NT	NE (most); ACh (sweat glands, some vessels)	ACh (mAChR)

12.2 Key Physiological Effects

Target Organ	Sympathetic Effect	Parasympathetic Effect
Heart rate	↑ (β₁)	↓ (M₂)
Heart contractility	↑ (β₁)	↓ (M₂)
Bronchioles	Dilate (β₂)	Constrict (M₃)
Pupils	Dilate (α₁, mydriasis)	Constrict (M₃, miosis)
GI motility	↓ (β₂, α₂)	↑ (M₃)
Bladder detrusor	Relax (β₂)	Contract (M₃)
Bladder sphincter	Contract (α₁)	Relax (M₃)
Blood vessels (skin)	Constrict (α₁)	Dilate (M)
Adrenal medulla	Releases Epi/NE	-

13. Sleep and the Reticular Activating System (RAS)

The ascending reticular activating system (ARAS) projects from brainstem reticular formation to thalamus and cortex, maintaining wakefulness
Key neurotransmitters for arousal: norepinephrine (locus coeruleus), serotonin (raphe), acetylcholine (pedunculopontine/LDT), histamine (TMN), orexin (hypothalamus)

Sleep stages:

NREM (Non-REM) sleep:
- Stage 1 (N1): transition, theta waves (4-8 Hz)
- Stage 2 (N2): sleep spindles (12-14 Hz), K-complexes
- Stage 3 (N3): slow-wave sleep (SWS), delta waves (<4 Hz); growth hormone released
REM sleep: low-voltage, fast EEG (desynchronized); dreaming, eye movements, muscle atonia (inhibition of spinal motor neurons); memory consolidation

14. Synaptic Plasticity and Memory

Long-Term Potentiation (LTP):

Repeated high-frequency stimulation of a synapse → persistent increase in synaptic strength
Key mechanism: NMDA receptor activation requires simultaneous presynaptic glutamate release AND postsynaptic depolarization (coincidence detection) to unblock the Mg²⁺ plug; Ca²⁺ enters → activates CaMKII → AMPA receptor phosphorylation and insertion into postsynaptic membrane

Long-Term Depression (LTD):

Low-frequency stimulation → persistent decrease in synaptic strength
Involves AMPA receptor endocytosis

Types of memory:

Declarative (explicit) - episodic (events) and semantic (facts); hippocampus-dependent
Non-declarative (implicit) - procedural (motor skills, cerebellum), classical conditioning (amygdala/cerebellum), priming (neocortex)

15. Blood-Brain Barrier and Cerebrospinal Fluid

Blood-Brain Barrier (BBB):

Formed by tight junctions between cerebral capillary endothelial cells + astrocytic foot processes + pericytes
Highly selective: allows lipid-soluble molecules (O₂, CO₂, alcohol, steroids) and small uncharged molecules (glucose via GLUT1, amino acids via specific transporters)
Excludes: most drugs, large molecules, charged/hydrophilic substances, bacteria
Absent in circumventricular organs (area postrema, median eminence, posterior pituitary, subfornical organ) - these sense blood-borne signals

Cerebrospinal Fluid (CSF):

Produced by choroid plexus (~500 mL/day); total volume ~150 mL
Composition: low protein, low cells, glucose ~2/3 of plasma glucose
Circulation: lateral ventricles → interventricular foramina (of Monro) → 3rd ventricle → cerebral aqueduct (of Sylvius) → 4th ventricle → subarachnoid space via foramina of Luschka and Magendie → reabsorbed at arachnoid granulations into dural sinuses
Functions: mechanical cushion, CNS homeostasis (ionic, metabolic), waste removal

Key References:

Guyton and Hall Textbook of Medical Physiology (Guyton and Hall, Ch. 5 - Membrane Potentials/Action Potentials)
Ganong's Review of Medical Physiology, 26th Ed. (Ganong's, Ch. 4 - The Neuron; Ch. 6 - Synaptic & Junctional Transmission)

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CNS Physiology Notes

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What's included:

Styled with a clean navy/blue academic theme
Table of contents with all 15 sections linked
All tables formatted with alternating row colors
Both neuron diagram and action potential graph images embedded
Covers: neuron anatomy, resting membrane potential, action potentials, saltatory conduction, synaptic transmission, neurotransmitter systems, cerebral cortex/basal ganglia/cerebellum/thalamus/hypothalamus, sensory pathways, motor control, ANS, sleep, memory/LTP, and the BBB/CSF

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