Milica Cerovic, PhD

Peer-Reviewed Rublications

Cell Reports •

Coordinated Regulation of Synaptic Plasticity at Striatopallidal and Striatonigral Neurons Orchestrates Motor Control

All procedures involving animals were carried out in accordance with the Italian Ministry of Health’s directives (D.lgs 26/2014) regulating animal research. Mice were injected with 6-OHDA HBr (3.5 μg/μl) into the right medial forebrain bundle (MFB). Severity of dopamine denervation was estimated 9–14 days later by computing the number of ipsilateral over total spontaneous rotations of the body in 6-OHDA- and sham-lesioned mice. Only mice displaying a ratio of ipsilateral/total tight rotations >9

Blockade of the IL-1R1/TLR4 pathway mediates disease-modification therapeutic effects in a model of acquired epilepsy

We recently discovered that forebrain activation of the IL-1 receptor/Toll-like receptor (IL-1R1/TLR4) innate immunity signal plays a pivotal role in neuronal hyperexcitability underlying seizures in rodents. Since this pathway is activated in neurons and glia in human epileptogenic foci, it represents a potential target for developing drugs interfering with the mechanisms of epileptogenesis that lead to spontaneous seizures. The lack of such drugs represents a major unmet clinical need. We test
Biological Psychiatry •

Severe Intellectual Disability and Enhanced Gamma-Aminobutyric Acidergic Synaptogenesis in a Novel Model of Rare RASopathies

Dysregulation of Ras-extracellular signal-related kinase (ERK) signaling gives rise to RASopathies, a class of neurodevelopmental syndromes associated with intellectual disability. Recently, much attention has been directed at models bearing mild forms of RASopathies whose behavioral impairments can be attenuated by inhibiting the Ras-ERK cascade in the adult. Little is known about the brain mechanisms in severe forms of these disorders.

We performed an extensive characterization of a new brain
Nature •

SK channel modulation rescues striatal plasticity and control over habit in cannabinoid tolerance - Neuroscience

• None Hoffman, A.F., Oz, M., Caulder, T. & Lupica, C.R. Functional tolerance and blockade of long-term depression at synapses in the nucleus accumbens after chronic cannabinoid exposure. J. Neurosci. 23, 4815–4820 (2003).
• None Herkenham, M. et al. Characterization and localization of cannabinoid receptors in rat brain: a quantitative in vitro autoradiographic study. J. Neurosci. 11, 563–583 (1991).
• None Wang, Z. et al. Dopaminergic control of corticostriatal long-term synaptic depression i
Biological Psychiatry •

Derangement of Ras-Guanine Nucleotide-Releasing Factor 1 (Ras-GRF1) and Extracellular Signal-Regulated Kinase (ERK) Dependent Striatal Plasticity in L-DOPA-Induced Dyskinesia

Bidirectional long-term plasticity at the corticostriatal synapse has been proposed as a central cellular mechanism governing dopamine-mediated behavioral adaptations in the basal ganglia system. Balanced activity of medium spiny neurons (MSNs) in the direct and the indirect pathways is essential for normal striatal function. This balance is disrupted in Parkinson’s disease and in -3,4-dihydroxyphenylalanine ( -DOPA)-induced dyskinesia (LID), a common motor complication of current pharmacotherap
Frontiers •

Neuroinflammation and the Gut Microbiota: Possible Alternative Therapeutic Targets to Counteract Alzheimer’s Disease?

Alzheimer’s disease (AD) is a complex, multi-factorial disease affecting various brain systems. This complexity implies that successful therapies must be directed against several core neuropathological targets rather than single ones. The scientific community has made great efforts to identify the right AD targets beside the historic amyloid-β (Aβ). Neuroinflammation is re-emerging as determinant in the neuropathological process of AD. A new theory, still in its infancy, highlights the role of g

Molecular and cellular mechanisms of dopamine-mediated behavioral plasticity in the striatum

The striatum is the input structure of the basal ganglia system. By integrating glutamatergic signals from cortical and subcortical regions and dopaminergic signals from mesolimbic nuclei the striatum functions as an important neural substrate for procedural and motor learning as well as for reward-guided behaviors. In addition, striatal activity is significantly altered in pathological conditions in which either a loss of dopamine innervation (Parkinson’s disease) or aberrant dopamine-mediated