I. Brain Tissue Structure

(A) Cerebellum

    1. Cerebellar Cortex
        a. Molecular Layer
        b. Purkinje Cell Layer
        c. Granular Layer

    2. Cerebellar Medulla

(B) Cerebrum

    1. The cerebral cortex, the pivot of the nervous system, is typically divided into six layers:
        a. Molecular Layer (Layer I)
        b. External Granular Layer (Layer II)
        c. External Pyramidal Layer (Layer III)
        d. Internal Granular Layer (Layer IV)
        e. Internal Pyramidal Layer (Layer V)
        f. Multiform Layer (Layer VI)

    2. The cerebral white matter , composed of association , commissural , and projection fibers, serves the function of connecting various cerebral regions and linking them to lower centers.

II. Pathological Alterations

(A) Neurons

    1. Neuronal Degeneration: Characterized by neuronal swelling, atrophy, or vacuolization.

    2. Neuronal Necrosis: Evidenced by karyopyknosis, karyorrhexis, or karyolysis of the nucleus.

    3. Neuronal Inclusions: Presence of abnormal inclusions, such as Lewy bodies and neurofibrillary tangles.

(B) Glial Cells

    1. Astrocytes: Exhibit reactive hyperplasia, hypertrophy, or fibrosis.

    2. Oligodendrocytes: Demonstrate demyelination or cellular swelling.

    3. Microglia: Become activated, proliferate, or may form microglial nodules.

(C) Blood Vessels

    1. Vascular Wall Thickening: Caused by hyalinization or fibrinoid necrosis.

    2. Perivascular Space Enlargement: Resulting from perivascular edema or inflammatory cell cuffing.

    3. Vasculitis: Characterized by inflammatory cell infiltration or necrosis of the vessel wall.

(D) Inflammatory Responses

    1. Inflammatory Cell Infiltration: Involving lymphocytes, plasma cells, and/or macrophages.

    2. Granuloma Formation: Such as tuberculoid or fungal-like granulomas.

    3. Abscess Formation: Featuring pus accumulation and surrounding tissue necrosis.

(E) Neoplastic Lesions

    1. Tumor Cell Morphology: Assessment includes cellular atypia, mitotic figures, and invasive potential.

    2. Tumor Typing: Determination is based on cytomorphology and immunohistochemical profiling.

III. Common Staining Techniques for Brain Tissue and Their Pathological Descriptions

(A) H&E Staining:

The infarcted area shows loose, edematous tissue with dilated and congested capillaries. Neurons exhibit vacuolar degeneration, and some appear shrunken and triangular with pyknotic nuclei. Decreased Nissl staining and gliosis are evident.

(B) Nissl Staining:
Nissl bodies within neurons appear as dark blue granules against a light blue nucleus. A reduction in Nissl body count is observed in the infarction zone.

(C) Silver Impregnation:
Neurofilaments are typically stained deep brown or black, with a light yellow or brownish-yellow background. 

(D) TTC Staining:
Viable tissue stains red, while the infarcted area appears pale/white.

(E) LFB Staining:
Myelin sheaths are stained blue, against a colorless to light blue background.

(F) Congo Red Staining:
Amyloid proteins appear as pinkish-red plaques, often exhibiting apple-green birefringence under polarized light.

(G) Golgi Staining:
Neuronal and glial cell processes are stained black, against a colorless or light gray background.

(H) FJB Staining:
Degenerating neurons exhibit bright green fluorescence.

IV. Commonly Utilized Animal Models

(A) Cerebral Ischemia-Reperfusion Model (MCAO):
Manifests as neuronal necrosis, edema, and inflammatory cell infiltration.

(B) Alzheimer's Disease Model (AD):
Features as β-amyloid deposition forming senile plaques, primarily in the cerebral cortex and hippocampus. Significant neuronal loss in these regions leads to cerebral atrophy.

(C) Parkinson's Disease Model (PD):
Characterized by loss of dopaminergic neurons, activation of microglia with release of inflammatory factors, and the presence of Lewy bodies.

(D) Purulent Meningitis Model:
The subarachnoid space is filled with exudated neutrophils and scant fibrin. Vasculature is highly congested, and varying degrees of cerebral edema are present in the parenchyma.

(E) Stroke Model:
The ischemic area displays pale tissue, inflammatory cell infiltration, and extravasation of red blood cells.

(F) Epilepsy Model:
Exhibits hippocampal sclerosis, abnormal neuronal discharges, and gliosis.