Mouse Experiment: New Discoveries in Neurobiology

The Rodent Model: A Cornerstone of Neurobiological Research

Historical Perspective of Mouse Models in Neurobiology

Early Applications and Contributions

Early mouse research laid the foundation for modern neurobiology by providing a tractable organism for genetic manipulation, electrophysiological recording, and behavioral assessment. Researchers introduced targeted mutations to explore the role of specific proteins in synaptic transmission, establishing causal links between gene function and neuronal activity. Parallel advances in in‑vivo recording techniques allowed precise measurement of action potentials and local field potentials in freely moving animals, revealing dynamic patterns of network activity during learning tasks.

Key contributions of these initial studies include:

Development of transgenic lines expressing fluorescent markers, enabling visualization of neuronal morphology and connectivity.
Creation of knockout models for neurotransmitter receptors, which clarified the molecular basis of excitatory and inhibitory balance.
Implementation of conditioned fear and maze paradigms, providing quantitative metrics of memory formation and retrieval.
Introduction of optogenetic tools in mice, permitting reversible control of defined neuronal populations with light.
Mapping of cortical and subcortical circuits through viral tracers, producing detailed atlases of functional pathways.

These achievements demonstrated that mouse experimentation could bridge molecular genetics and systems-level neuroscience, establishing a platform for subsequent discoveries in brain function and disease.

Technological Advancements and Their Impact

Recent mouse studies have incorporated high‑resolution two‑photon microscopy, enabling real‑time observation of synaptic activity across cortical layers. The technique reduces tissue damage and provides quantitative metrics for plasticity, directly supporting the identification of novel neural pathways.

Advances in optogenetics now allow precise manipulation of specific neuronal populations with millisecond accuracy. Integration with genetically encoded calcium indicators produces simultaneous control and measurement, accelerating the validation of causal relationships between circuit dynamics and behavior.

Key technological developments influencing rodent neurobiology include:

Automated behavioral arenas equipped with machine‑learning classifiers for unbiased phenotype scoring.
In vivo electrophysiological probes featuring thousands of channels, delivering dense spatial sampling of neuronal firing patterns.
Cloud‑based data pipelines that standardize preprocessing, storage, and cross‑lab sharing of multimodal datasets.

Collectively, these tools transform experimental design, reduce variability, and expand the scope of discoveries attainable through mouse‑based investigations of brain function.

Groundbreaking Discoveries Through Mouse Experimentation

Neural Plasticity and Learning Mechanisms

Synaptic Modification in Memory Formation

Recent rodent investigations have revealed precise alterations at synaptic contacts that underlie the formation of new memories. Electrophysiological recordings demonstrate that experience‑dependent strengthening of excitatory connections, measured as long‑term potentiation, correlates with the acquisition phase of behavioral tasks. Conversely, long‑term depression emerges during extinction trials, indicating that bidirectional plasticity encodes both acquisition and loss of information.

Molecular analysis identifies a cascade of events that modify synaptic efficacy:

Calcium influx through NMDA receptors activates CaMKII, which phosphorylates AMPA‑receptor subunits.
Phosphorylation promotes insertion of additional AMPA receptors into the postsynaptic membrane, increasing conductance.
Local protein synthesis, driven by mTOR signaling, supplies scaffolding proteins that stabilize the expanded receptor pool.
Ubiquitin‑mediated degradation removes destabilized receptors, completing the remodeling cycle.

These processes converge on the structural reorganization of dendritic spines. High‑resolution imaging shows rapid spine enlargement during potentiation, followed by selective pruning when synaptic strength declines. The temporal profile of spine dynamics matches the time window for memory consolidation, suggesting that physical remodeling provides a substrate for long‑term storage.

Behavioral outcomes align with synaptic changes. Mice trained on spatial navigation tasks display enhanced LTP in hippocampal circuits, whereas pharmacological inhibition of CaMKII or mTOR impairs performance and prevents spine enlargement. Such findings link specific molecular interventions to observable deficits in memory encoding.

Collectively, the data establish a mechanistic framework in which activity‑driven receptor trafficking, protein synthesis, and cytoskeletal remodeling constitute the core of memory formation. Targeting these pathways offers a strategic avenue for therapeutic development aimed at cognitive dysfunction.

Environmental Enrichment and Brain Rewiring

Environmental enrichment in laboratory mice provides a combination of physical, social, and cognitive stimuli that drives measurable alterations in neural architecture. When rodents are housed with varied objects, running wheels, and group interactions, their cortical and hippocampal circuits exhibit increased dendritic arborization, higher spine density, and accelerated synaptogenesis. Parallel molecular analyses reveal up‑regulation of brain‑derived neurotrophic factor, enhanced expression of immediate‑early genes, and activation of signaling pathways associated with synaptic plasticity.

Key outcomes of enrichment‑driven rewiring include:

Expansion of granule cell layers in the dentate gyrus, reflecting adult neurogenesis.
Strengthening of long‑range connections between prefrontal and limbic regions, measurable by increased coherence in electrophysiological recordings.
Improvement in performance on spatial navigation and memory tasks, indicating functional benefits of structural changes.
Modulation of inhibitory interneuron networks, resulting in refined excitation‑inhibition balance.

These observations derive from controlled mouse experiments that compare standard cages with enriched environments. Quantitative imaging confirms that enriched subjects possess up to 30 % greater dendritic length in layer II/III pyramidal neurons relative to controls. Electrophysiological recordings demonstrate elevated long‑term potentiation magnitude, supporting the link between structural remodeling and enhanced synaptic efficacy.

The convergence of anatomical, molecular, and behavioral data establishes environmental enrichment as a potent driver of brain rewiring. Findings suggest that manipulations of the living environment can be leveraged to model neuroplasticity mechanisms relevant to recovery after injury, neurodevelopmental disorders, and age‑related cognitive decline.

Neurodegenerative Diseases: Unraveling Pathologies

Alzheimer's Disease: Amyloid and Tau Hypotheses

Recent murine investigations have provided quantitative data that reshape understanding of Alzheimer’s pathology. Transgenic mouse lines engineered to overproduce human amyloid‑β (Aβ) develop extracellular plaques that correlate with synaptic deficits and memory impairment measured in behavioral assays.

The amyloid hypothesis posits that accumulation of Aβ initiates neurodegeneration. Evidence from rodent studies includes:

Elevated soluble Aβ oligomers preceding plaque formation.
Synaptic loss detectable by electrophysiological recordings after oligomer exposure.
Cognitive decline reversible by antibodies that clear Aβ aggregates.

Parallel research on the tau hypothesis demonstrates that intracellular neurofibrillary tangles drive disease progression. Key observations in mouse models:

Expression of mutant tau leads to microtubule destabilization and axonal transport failure.
Hyperphosphorylated tau aggregates precede neuronal loss in regions analogous to human hippocampus.
Inhibition of kinases responsible for tau phosphorylation mitigates neurodegeneration and restores behavioral performance.

Combined analyses reveal interaction between the two pathways. Mice co‑expressing pathogenic Aβ and tau exhibit accelerated neurodegeneration compared with single‑transgene models, indicating synergistic toxicity. Intervention studies show that simultaneous targeting of Aβ deposition and tau phosphorylation yields greater functional recovery than monotherapies.

These findings underscore that mouse‑based neurobiological experiments now delineate precise mechanistic links between amyloid deposition, tau pathology, and cognitive deficits, guiding the design of multimodal therapeutic strategies.

Parkinson's Disease: Dopaminergic Neuron Loss

Parkinson’s disease is characterized by the progressive loss of dopamine‑producing neurons in the substantia nigra pars compacta, leading to motor dysfunction and non‑motor symptoms. The selective vulnerability of these cells underlies the clinical presentation and drives research aimed at uncovering the mechanisms of degeneration.

Murine investigations employ genetic mutations (e.g., α‑synuclein overexpression, LRRK2 variants) and toxin models (e.g., 6‑hydroxydopamine, MPTP) to reproduce dopaminergic cell loss. Recent experiments have refined temporal resolution of neuronal death, identified early alterations in mitochondrial dynamics, and demonstrated that microglial activation precedes overt neuronal loss. These studies also reveal that compensatory sprouting of remaining axons can temporarily sustain dopamine release before collapse.

Key observations from recent mouse work include:

Early disruption of calcium homeostasis within dopaminergic somata.
Up‑regulation of oxidative stress markers preceding cell death.
Activation of the NLRP3 inflammasome in microglia correlating with neuronal loss.
Synaptic remodeling in the striatum that modifies motor circuit output.
Efficacy of selective LRRK2 kinase inhibition in preserving neuronal integrity.

The findings provide a mechanistic framework for therapeutic strategies that target mitochondrial protection, neuroinflammation, and synaptic stability. Translational relevance is reinforced by the alignment of murine phenotypes with human disease progression, supporting the use of these models to evaluate disease‑modifying interventions.

Psychiatric Disorders: Exploring Underlying Mechanisms

Depression: Serotonergic Pathways and Stress Responses

Recent rodent investigations have uncovered detailed relationships between serotonergic signaling and behavioral manifestations of depression. Experiments employing genetically engineered mice and pharmacological manipulations provide quantitative evidence linking alterations in serotonin transporter activity to measurable changes in mood‑related behaviors.

Key observations include:

Reduced expression of the serotonin transporter (SERT) correlates with heightened immobility in forced‑swim tests.
Up‑regulation of 5‑HT1A autoreceptors diminishes serotonergic firing rates, producing anxiety‑like phenotypes.
Selective deletion of tryptophan hydroxylase 2 (TPH2) in dorsal raphe nuclei leads to persistent depressive‑like states despite normal peripheral serotonin levels.

Stress exposure in these models activates the hypothalamic‑pituitary‑adrenal (HPA) axis, elevating corticosterone and disrupting feedback inhibition. Chronic unpredictable stress protocols reveal that prolonged glucocorticoid exposure down‑regulates 5‑HT2C receptor expression in the prefrontal cortex, thereby impairing serotonergic modulation of executive function. Simultaneously, stress‑induced epigenetic modifications of the SERT promoter reduce transcriptional efficiency, establishing a feed‑forward loop that sustains depressive behavior.

Integration of these findings suggests that therapeutic approaches targeting both serotonergic receptors and stress‑responsive pathways may achieve greater efficacy. Dual‑action compounds that restore SERT function while attenuating HPA axis hyperactivity demonstrate rapid reversal of depressive phenotypes in mouse trials, highlighting a promising direction for translational research.

Anxiety: Amygdala Function and Fear Conditioning

Recent rodent investigations have employed precise behavioral protocols to isolate neural substrates of anxiety, allowing direct measurement of amygdalar activity during controlled fear‑conditioning trials.

The amygdala integrates sensory input with affective valuation, directing autonomic and behavioral outputs that define anxious states. Within this structure, the basolateral complex processes conditioned stimuli, while the central nucleus orchestrates downstream motor and hormonal responses. Synaptic plasticity in these nuclei encodes the intensity and persistence of fear memories.

Fear conditioning follows a three‑phase sequence: acquisition, where a neutral cue becomes predictive of aversive shock; expression, marked by heightened freezing and physiological arousal; and extinction, during which repeated cue exposure without shock reduces the learned response. Each phase recruits distinct neuronal ensembles, and the transition between them reflects dynamic changes in amygdalar circuitry.

Key outcomes from recent mouse work include:

Optogenetic silencing of basolateral projections during acquisition abolishes later freezing, confirming causal involvement in memory formation.
In vivo calcium imaging reveals rapid, stimulus‑locked firing bursts in central nucleus neurons during expression, correlating with heart‑rate acceleration.
Conditional knockout of the NMDA‑receptor subunit NR2B in the amygdala impairs extinction learning, indicating a molecular requirement for synaptic remodeling.
Chemogenetic activation of inhibitory interneurons accelerates extinction, suggesting therapeutic avenues for anxiety disorders.

Collectively, these data delineate how amygdalar microcircuits encode, maintain, and suppress fear, providing a mechanistic framework for anxiety that stems directly from controlled mouse experimentation.

Emerging Technologies and Future Directions

Optogenetics: Precision Control of Neural Circuits

Manipulating Neuronal Activity in Live Animals

Recent investigations using rodent models have focused on direct control of neuronal circuits to uncover mechanisms of behavior and disease. By delivering light-sensitive proteins to specific cell populations, researchers achieve millisecond precision in activating or silencing neurons, allowing causal links between activity patterns and phenotypic outcomes. This approach, combined with genetically encoded calcium indicators, provides simultaneous manipulation and monitoring of circuit dynamics in awake, freely moving animals.

Complementary chemogenetic strategies employ engineered receptors activated by inert ligands, delivering reversible modulation over minutes to hours. The technique simplifies experimental logistics, enabling chronic studies of neuronal influence on learning, stress responses, and neurodegeneration without the need for implanted hardware. Both optogenetic and chemogenetic methods require rigorous validation of expression specificity, dose–response relationships, and off‑target effects.

Key methodological considerations include:

Precise targeting of viral vectors or transgenic lines to avoid unintended cell populations.
Calibration of stimulation parameters (intensity, frequency, duration) to replicate physiological firing patterns.
Integration of behavioral assays with electrophysiological or imaging readouts for multimodal validation.
Implementation of appropriate control groups, such as sham‑stimulated or ligand‑only cohorts, to isolate the effect of neuronal manipulation.

The convergence of these technologies in mouse experiments has generated reproducible insights into synaptic plasticity, circuit reorganization after injury, and the cellular basis of psychiatric disorders. By refining manipulation protocols and expanding the repertoire of effectors, the field moves toward comprehensive mapping of functional neuroarchitecture in living organisms.

Probing Behavior and Cognition

The latest rodent investigations in neurobiology employ sophisticated behavioral assays to dissect cognitive processes. Researchers integrate automated tracking, high‑resolution video analysis, and machine‑learning classifiers to quantify exploration, decision‑making, and social interaction with millisecond precision. These techniques reveal distinct neural signatures associated with reward anticipation, spatial navigation, and pattern discrimination.

Key outcomes from these experiments include:

Identification of prefrontal‑striatal circuits that encode trial‑by‑trial learning rates.
Demonstration that optogenetic silencing of hippocampal place cells disrupts maze performance without affecting motor function.
Evidence that neuromodulatory tone modulates risk‑assessment behavior, measurable through variable‑delay operant tasks.

Collectively, the data refine models of how discrete neuronal ensembles support complex cognition, offering a framework for translating mouse findings into broader neurobiological theory.

CRISPR-Cas9: Genetic Engineering for Disease Modeling

Gene Editing for Targeted Mutations

Gene editing enables precise alterations of mouse genomes to interrogate neural circuitry and disease mechanisms. Researchers introduce targeted mutations by delivering programmable nucleases—most commonly CRISPR‑Cas9 or base editors—into embryonic stem cells or zygotes. The resulting alleles mimic human neurogenetic disorders, allowing direct assessment of molecular and behavioral phenotypes.

The workflow typically includes:

Design of guide RNAs that flank the desired locus.
Validation of cleavage efficiency in vitro.
Microinjection or electroporation of nuclease components into fertilized eggs.
Screening of offspring for correct edits using PCR and sequencing.
Phenotypic characterization through electrophysiology, imaging, and behavioral assays.

Advanced strategies such as homology‑directed repair introduce single‑base changes without leaving selectable markers, preserving native gene regulation. Conditional alleles, generated by flanking exons with loxP sites, permit temporal control of mutation expression via Cre recombinase, facilitating studies of developmental versus adult neuronal functions.

Off‑target assessment relies on whole‑genome sequencing or GUIDE‑seq to ensure that observed neurobiological effects stem from the intended modification. Integration of edited mouse lines with in‑vivo recording technologies yields high‑resolution data on synaptic transmission, network oscillations, and circuit plasticity.

By coupling precise genomic edits with comprehensive functional readouts, investigators uncover causal links between specific genetic variants and neural phenotypes, advancing the understanding of brain disorders and informing therapeutic development.

Correcting Pathogenic Variants

Recent rodent investigations have revealed mechanisms underlying neuronal dysfunction, emphasizing the need to eliminate disease‑causing genetic alterations. Targeted correction of pathogenic variants restores normal protein function, directly linking genotype to phenotype in experimental models.

Precise genome editing tools enable this correction. CRISPR‑Cas9 introduces double‑strand breaks at defined loci, while base editors convert single nucleotides without creating lesions. Antisense oligonucleotides modulate splicing to bypass deleterious exons. Each approach reduces the expression of mutant alleles and promotes the synthesis of functional proteins.

CRISPR‑Cas9 mediated knock‑in of wild‑type sequences
Adenine or cytosine base editors for point‑mutation repair
Prime editing for insertion or deletion of pathogenic segments
Antisense oligonucleotide delivery for exon skipping

Application of these methods in mouse models consistently yields phenotypic rescue. Behavioral assays demonstrate restored motor coordination, electrophysiological recordings show normalized synaptic transmission, and histological analysis confirms preservation of neuronal architecture. The reproducibility of these outcomes validates the strategy as a translational bridge to human neurodegenerative disorders.

Future work will integrate multiplexed editing to address polygenic contributions, refine delivery vectors for central nervous system targeting, and combine genetic correction with pharmacological modulation. Such advances aim to convert laboratory discoveries into therapeutic interventions for patients suffering from genetically driven neurological disease.

Advanced Imaging Techniques: Visualizing Brain Activity

Two-Photon Microscopy for Deep Brain Imaging

Two‑photon fluorescence microscopy enables optical sectioning at depths exceeding 600 µm in living mouse brain tissue. By employing near‑infrared pulsed lasers, the technique confines excitation to the focal volume, reducing out‑of‑focus photodamage and allowing repeated imaging of neuronal structures over weeks.

Key technical features include:

Pulse parameters: 80‑100 fs pulse width, repetition rates of 80 MHz, and average powers below 30 mW at the sample preserve viability.
Scanning strategies: Resonant galvanometer scanners achieve frame rates of 30 Hz, supporting calcium‑indicator dynamics.
Detection optics: Non‑descanned photomultiplier tubes collect scattered photons efficiently, extending usable depth.

In mouse models, two‑photon microscopy has revealed:

Layer‑specific dendritic spine turnover during learning tasks.
Activity‑dependent vascular remodeling in the somatosensory cortex.
Real‑time migration of microglial processes in response to injury.

Implementation considerations:

Cranial window preparation: Chronic glass windows provide stable optical access while minimizing inflammation.
Fluorophore selection: Red‑shifted indicators (e.g., jRGECO1a) improve signal‑to‑noise at greater depths.
Motion correction: Real‑time image registration compensates for respiration‑induced brain movement.

Recent advancements integrate adaptive optics to correct wavefront distortions, further extending imaging depth to the hippocampal formation. Combined with genetically encoded voltage sensors, the approach captures subthreshold membrane events across cortical layers, delivering unprecedented insight into circuit function during behavioral experiments.

Functional MRI in Awake Mice

Functional magnetic resonance imaging (fMRI) of awake mice provides direct access to brain activity without the confounding effects of anesthesia. The approach combines head-fixation, habituation protocols, and high‑field scanners to capture blood‑oxygen‑level‑dependent (BOLD) signals while the animal remains conscious and responsive to sensory or behavioral tasks.

Technical implementation requires a lightweight restraint system that secures the skull while permitting limited movement of the body. Mice undergo a multi‑day acclimation schedule during which they learn to tolerate the restraint and acoustic environment of the scanner. Imaging parameters typically include gradient‑echo echo‑planar sequences with repetition times of 1–2 s and spatial resolutions of 0.2–0.3 mm, enabling detection of voxel‑wise activation patterns across the entire brain.

Key advantages of awake imaging over anesthetized protocols include:

Preservation of natural neuronal dynamics;
Ability to correlate BOLD responses with voluntary behavior;
Detection of rapid state‑dependent changes in functional connectivity;
Compatibility with longitudinal studies of disease progression.

The method has revealed stimulus‑evoked activation maps for visual, somatosensory, and olfactory pathways, identified intrinsic network architectures analogous to those observed in larger mammals, and quantified alterations in connectivity associated with genetic models of neurodegeneration. These findings expand the mechanistic understanding of circuit function and dysfunction in rodent neurobiology.

By eliminating anesthesia‑induced suppression, awake mouse fMRI establishes a robust platform for translational investigations, linking cellular‑level manipulations with whole‑brain functional outcomes and accelerating the discovery pipeline in neurobiological research.

Ethical Considerations and Challenges

Animal Welfare in Research

Humane Treatment and Experimental Design

The ethical framework governing rodent studies now mandates strict compliance with institutional and federal regulations that prioritize animal welfare while preserving scientific validity. Researchers must obtain protocol approval from an oversight committee, demonstrate that procedures minimize pain and distress, and implement refinement techniques such as environmental enrichment, analgesia, and humane endpoints. Continuous monitoring of physiological and behavioral indicators ensures that interventions remain within acceptable welfare thresholds.

Experimental design must integrate methodological rigor with humane considerations. Core elements include:

Power analysis to determine the smallest sample size capable of detecting biologically meaningful effects, thereby reducing unnecessary animal use.
Random allocation of subjects to treatment groups to prevent selection bias.
Blinded assessment of outcomes to eliminate observer bias.
Standardized housing and handling to limit variability unrelated to the experimental variable.
Predefined humane endpoints that trigger immediate cessation of procedures when distress exceeds predefined limits.

Data collection protocols should employ automated or objective measurement tools whenever possible, decreasing handling frequency and associated stress. Documentation of all welfare interventions and deviations from the original plan is essential for reproducibility and ethical accountability. By aligning humane treatment with robust experimental architecture, investigators generate reliable neurobiological insights while upholding the highest standards of animal care.

Reducing, Refining, and Replacing (3Rs)

The application of the 3Rs framework—Reduction, Refinement, and Replacement—has become integral to contemporary rodent studies that uncover neural mechanisms. Reduction emphasizes statistical power and experimental design to achieve reliable results with the smallest feasible cohort. Refinement focuses on procedures that minimize pain, stress, and physiological disruption, employing advanced imaging, automated monitoring, and humane endpoints. Replacement encourages the adoption of alternative models, such as organ‑on‑a‑chip systems, computational simulations, and invertebrate assays, whenever they can address the same scientific question.

Implementing these principles in mouse‑based neurobiology research yields several practical benefits:

Smaller sample sizes without compromising data integrity, achieved through longitudinal tracking and within‑subject analyses.
Enhanced animal welfare through analgesic protocols, enriched housing, and non‑invasive recording techniques.
Accelerated discovery cycles by integrating in silico predictions and cell‑culture platforms that reduce reliance on whole‑animal experiments.

Collectively, the 3Rs drive methodological rigor, ethical compliance, and resource efficiency, shaping a research environment where innovative neural insights emerge alongside responsible animal stewardship.

Limitations of Mouse Models

Translational Gaps to Human Conditions

Recent rodent investigations have revealed molecular pathways that regulate synaptic plasticity, neuronal survival, and circuit remodeling. These mechanisms are central to understanding disease progression, yet their relevance to human neuropathology remains uncertain.

Key factors that hinder direct translation include:

Species‑specific gene expression patterns that alter protein function.
Divergent immune system responses influencing neuroinflammation.
Differences in brain size, connectivity, and developmental timelines.
Limited availability of human‑equivalent biomarkers for validating mouse findings.

Addressing these gaps requires a systematic approach:

Align experimental endpoints with clinically measurable outcomes, such as cerebrospinal fluid protein levels or functional imaging signatures.
Incorporate human‑derived cellular models (e.g., induced pluripotent stem cell neurons) to test mouse‑identified targets under physiologically relevant conditions.
Employ cross‑species computational models that adjust for anatomical and temporal scaling, enabling prediction of human responses from rodent data.
Validate candidate interventions in large‑animal models that bridge the gap between murine physiology and human anatomy before proceeding to clinical trials.

By integrating these strategies, researchers can convert discoveries from mouse studies into actionable insights for treating neurological disorders in patients.

Species-Specific Differences in Brain Structure and Function

The current rodent investigation uncovers neural traits that differ markedly between species. Comparative analysis reveals that mice possess a proportionally larger olfactory bulb, a condensed neocortical surface, and a distinct pattern of hippocampal connectivity relative to primates and rats. These structural variations correspond to divergent sensory priorities and behavioral repertoires.

Key structural distinctions identified:

Olfactory bulb volume: mouse > rat > primate (percentage of total brain mass).
Prefrontal cortical thickness: primate > mouse ≈ rat (layer organization).
Corpus callosum size: primate > rat > mouse (inter‑hemispheric integration capacity).

Functionally, electrophysiological recordings demonstrate species‑specific firing dynamics. Mouse cortical neurons exhibit higher baseline firing rates and shorter refractory periods, supporting rapid sensorimotor cycles. In contrast, primate neurons display prolonged integration windows, facilitating complex decision‑making processes. Synaptic plasticity assays show that mice achieve long‑term potentiation with fewer stimulation pairs, indicating a lower threshold for synaptic strengthening.

These findings emphasize that extrapolation from mouse data to other mammals requires adjustment for morphological and electrophysiological disparities. Recognizing these species‑specific parameters enhances the translational relevance of neurobiological research derived from rodent models.