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EEG in Rodents

At Ulysses Neuroscience Ltd., we provide advanced in vivo electrophysiology services using rodent EEG to support translational research and neuropharmacology programmes. Our European (HPRA) and North American (AAALAC) accredited platforms enable high-quality EEG studies in mice and rats, integrating behavioural, biomarker, PK/PD, and imaging readouts across a variety of disease models.

Why EEG Matters in Translational Research

Changes in rodent EEG, such as REM suppression, spectral shifts, and oscillatory activity modulation, are mirrored in humans following treatment with CNS-active compounds. This makes rodent EEG a powerful pharmacodynamic biomarker to bridge preclinical and clinical development, support early go/no-go decisions, and de-risk novel neurotherapeutics.

Who will find this platform useful?

  • Pharma & biotech companies developing CNS-active compounds

  • Clients equiring translational EEG biomarkers to align preclinical results with clinical endpoints
  • Partners seeking integrated EEG + behaviour + biomarker data to support IND-enabling studies

Why partner with ULYSSES?

  • Access to four complementary EEG platforms across mouse and rat

  • Expertise in epilepsy, psychedelics, schizophrenia, and depression

  • Synchronized HD video for behavioural correlation

  • Seamless integration with preclinical and clinical biomarker pipelines

  • Flexible study designs, expert scientific support, and full regulatory compliance

  • Audited and approved by major pharmaceutical sponsors

EEG Platforms Available

Changes in rodent EEG, such as REM suppression, spectral shifts, and oscillatory activity modulation, are mirrored in humans following treatment with CNS-active compounds. This makes rodent EEG a powerful pharmacodynamic biomarker to bridge preclinical and clinical development, support early go/no-go decisions, and de-risk novel neurotherapeutics.

1. Pinnacle Wireless EEG (Mouse and Rat):

2 EEG + 1 EMG channels / Wireless Bluetooth transmission / Sampling rate: 512–1024 Hz / Adjustable electrode placement / Synchronized HD video recording / Real-time monitoring / Analysis software specialized on sleep and seizures

Wireless EEG/EMG Recording with the Pinnacle System in Mice. The setup includes standard frontal and parietal surface electrodes connected to a lightweight removable headmount (top left and center). EEG signals are recorded continuously and synchronized with high-definition video tracking or behavioural correlation.

2. Pinnacle Tethered EEG (Mouse and Rat):


2 EEG + 1 EMG channels / Continuous long-term tethered recordings / Sampling rate up to 20 kHz / Adjustable electrode placement / Synchronized HD video recording /Real-time monitoring / Analysis software specialized on sleep and seizures

3. DSI Telemetry EEG (Mouse and Rat):

2 biopotential channels (EEG/EEG or EEG/EMG) / 24/7 RF telemetry recording / Sampling up to 1 kHz / Also collects animal activity and body temperature data

(Figure provided by Transpharmation)
24-Hour Sleep/Wake Profiling Using DSI Implantable Telemetry in Rats.
Implanted EEG/EMG electrodes (left and center) enable continuous recording from freely moving animals housed in dedicated telemetry boxes (right), with real-time data acquisition. Recordings included 1-hour baseline followed by 22 hours post-dose monitoring. EEG/EMG traces were scored to extract vigilance states: wakefulness, non-REM (NREM), and REM sleep.

4. Tainitec “TaiNi” EEG (Mouse):


Up to 16 recording channels / 1.5 g removable headmount (including battery) / Optimized for small mice / Sampling rate up to 20 kHz

(Figure provided by Transpharmation)
Sleep/Wake Profiling in Mice Using TAINI Wireless EEG Headmounts.
Lightweight head-mounted EEG systems allow continuous multi-channel recordings (up to 16 channels) in freely moving mice.

Models & Applications

Rodent EEG and Sleep Architecture Analysis

EEG and EMG telemetry recordings allow for automated, objective classification of vigilance states (Wake, NREM, REM). Spectral EEG analysis provides quantitative measures of drug-induced changes in brain oscillatory activity. These methods are essential for evaluating sedative/hypnotic activity, wake-promoting agents, and CNS engagement of psychoactive drugs.

• Full sleep-wake profiling
• Sleep latency and fragmentation
• qEEG analysis
• Hypnogram generation
• Repeated measures and crossover designs
• Integrated locomotor and temperature monitoring

(Figure provided by Transpharmation)
24-Hour Sleep/Wake Profiling Using DSI Implantable Telemetry in Rats.
The graphs show % amount of wake, NREM, and REM over time after administration (arrow) of vehicle or increasing doses of psilocybin (0.1, 0.3, 1.0, 10 mg/kg, IP). Psilocybin induced a dose-dependent suppression of REM sleep in the first 6 hours post-administration, with significant effects at 0.3 and 10 mg/kg.

(Figure provided by Transpharmation)
Sleep/Wake Profiling in Mice Using TAINI Wireless EEG Headmounts.
Quantified data (line and bar graphs) show psilocybin-induced dose-dependent suppression of REM sleep, particularly during the first 4–6 hours post-dosing (red arrow), with effects also on non-REM and wake dynamics. Ideal for acute dosing studies in fragile mouse strains.

Neuropsychiatric Models:
Depression and Schizophrenia

  1. Rodent Models: IFN-α model, Wistar-Kyoto rat, PCP-challenge
  2. Auditory (Steady-State Response ASSR):
    – Sensory gating readout disrupted by NMDA antagonists (e.g., PCP)

    – Quantified by signal-to-noise ratio (SNR) and phase-locking factor (PLF)

    – Drug rescue validation with investigational compounds

  3. Mismatch Negativity (MMN):– Measures pre-attentive auditory processing- Detects changes in EEG response to deviant stimuli- Useful for translational schizophrenia research

(Figure provided by Transpharmation)
Auditory Steady-State Response (ASSR) Disruption by Ketamine in Rats.
ASSR recordings were obtained using 40 Hz click-train stimulation in a sound-attenuated chamber. The experimental timeline included a 30-minute pre-treatment baseline (stim-off), followed by 10 sequential blocks of stim-on recordings post-administration of vehicle or ketamine (0.3–10 mg/kg, SC). The left panel shows the mean ASSR ratio (stim-on/stim-off) across all blocks, indicating dose-dependent disruption at the highest ketamine dose. Middle panel shows time-course of ASSR effects, with significant suppression across blocks for 10 mg/kg. Right panels show spectral EEG data: reduced 40 Hz power at high ketamine doses (amplitude in μV and % change vs. vehicle). ASSR was quantified as the ratio of 40 Hz power (stim-on / stim-off), serving as a translational biomarker of NMDA receptor dysfunction.

Psychedelic Research

Ulysses Neuroscience is fully licensed for Schedule I psychedelics and has a proven track record in evaluating the pharmacodynamic effects of classic and novel neuroplastogens. Our EEG-based assays provide key translational readouts:

  1. Gamma power enhancement
  2. REM sleep suppression
  3. Changes in spectral coherence and band-specific oscillations
  4. Dose–response profiles and time-course EEG shifts
  5. Combined EEG, behavioural, and biomarker analyses

Wireless EEG/EMG Recording with the Pinnacle System in Mice. The trace shows EEG gamma activity (30–80 Hz) over time from the parietal cortex at baseline and following subcutaneous administration of ketamine (15 mg/kg), demonstrating a marked increase in gamma power post-dose. Recordings were sampled at 512 Hz and processed with bandpass filtering.

(Figure provided by Transpharmation)
DSI Telemetry EEG in WKY Rats – Sleep/Wake Profiling After Psychedelic Administration
Wireless EEG/EMG telemetry was used to monitor sleep-wake states in Wistar-Kyoto (WKY) rats. Recordings spanned 24 hours post-dosing, enabling high-resolution staging of wakefulness, NREM, and REM sleep. Psilocybin (10 mg/kg, IP) induced REM suppression and increased wakefulness in line with known pharmacological effects. These data demonstrate the utility of WKY rats as a treatment-resistant depression model and confirm the sensitivity of EEG to detect psychedelic-induced alterations in sleep architecture.

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