TY  - CONF
AU  - Dinić, Jelena
AU  - Nešović, Marija
AU  - Divac Rankov, Aleksandra
AU  - Podolski-Renić, Ana
AU  - Stanković, Tijana
AU  - Dragoj, Miodrag
AU  - Jovanović, Mirna
AU  - Lazić, Katarina
AU  - Dimas, Kostas
AU  - Botta, Maurizio
AU  - Pešić, Milica
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6042
AB  - Zebrafish (Danio rerio) is an excellent model for studying toxicity and biological activities of novel compounds with anticancer potential. This model is widely utilized in biological research as it is comparable to human counterpart both molecularly and pathologically. As an in vivo system for toxicology, zebrafish has numerous advantages such as rapid and ex utero development, transparent embryos in early stages, high fecundity allowing high-throughput screening and cost effectiveness. Furthermore, evaluation of known toxic compounds in zebrafish revealed 63–100% predictability making zebrafish a very useful tool for studying toxic effects [1, 2]. In addition, embryonic zebrafish cancer models can be used for studying pathways and processes relevant to human malignancy including tumor-induced angiogenesis, tumor invasiveness, proliferation and migration. These models can be generated using transgenesis, gene inactivation, xenotransplantation, and cancerogenic induction. Herein, we present the results obtained in zebrafish toxicity studies of siramesine, a sigma receptor agonist with anticancer potential. Concentration dependent increase in lethality, induced by siramesine treatment, was observed in zebrafish embryos at 24 h post fertilization (hpf), 48 hpf and 72 hpf. Various concentration dependent toxic effects on embryo development were also observed, as well as decreased hatching rate in embryos treated with 5 µM and 10 µM siramesine at 72 hpf. Results obtained in zebrafish cancer model generated via xenotransplantation are also presented. This model was utilized to study the effect of Src tyrosine kinase inhibitor pro-LDS10 on the invasiveness of microinjected human glioblastoma cell line U87. Treatment with 5 µM pro-LDS10 resulted in significant reduction of U87 migratory potential at 4 days post injection.
PB  - COST Action CA17104
C3  - Abstract book: STRATAGEM CA17104: New diagnostic and therapeutic tools against multidrug-resistant tumours: First Working-Group Meeting WG1 - WG4; 2019 Jan 30-31; Turin, Italy
T1  - Evaluation of anticancer compounds activity and toxicity in zebrafish model
SP  - 34
EP  - 34
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6042
ER  - 

@conference{
author = "Dinić, Jelena and Nešović, Marija and Divac Rankov, Aleksandra and Podolski-Renić, Ana and Stanković, Tijana and Dragoj, Miodrag and Jovanović, Mirna and Lazić, Katarina and Dimas, Kostas and Botta, Maurizio and Pešić, Milica",
year = "2019",
abstract = "Zebrafish (Danio rerio) is an excellent model for studying toxicity and biological activities of novel compounds with anticancer potential. This model is widely utilized in biological research as it is comparable to human counterpart both molecularly and pathologically. As an in vivo system for toxicology, zebrafish has numerous advantages such as rapid and ex utero development, transparent embryos in early stages, high fecundity allowing high-throughput screening and cost effectiveness. Furthermore, evaluation of known toxic compounds in zebrafish revealed 63–100% predictability making zebrafish a very useful tool for studying toxic effects [1, 2]. In addition, embryonic zebrafish cancer models can be used for studying pathways and processes relevant to human malignancy including tumor-induced angiogenesis, tumor invasiveness, proliferation and migration. These models can be generated using transgenesis, gene inactivation, xenotransplantation, and cancerogenic induction. Herein, we present the results obtained in zebrafish toxicity studies of siramesine, a sigma receptor agonist with anticancer potential. Concentration dependent increase in lethality, induced by siramesine treatment, was observed in zebrafish embryos at 24 h post fertilization (hpf), 48 hpf and 72 hpf. Various concentration dependent toxic effects on embryo development were also observed, as well as decreased hatching rate in embryos treated with 5 µM and 10 µM siramesine at 72 hpf. Results obtained in zebrafish cancer model generated via xenotransplantation are also presented. This model was utilized to study the effect of Src tyrosine kinase inhibitor pro-LDS10 on the invasiveness of microinjected human glioblastoma cell line U87. Treatment with 5 µM pro-LDS10 resulted in significant reduction of U87 migratory potential at 4 days post injection.",
publisher = "COST Action CA17104",
journal = "Abstract book: STRATAGEM CA17104: New diagnostic and therapeutic tools against multidrug-resistant tumours: First Working-Group Meeting WG1 - WG4; 2019 Jan 30-31; Turin, Italy",
title = "Evaluation of anticancer compounds activity and toxicity in zebrafish model",
pages = "34-34",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6042"
}

Dinić, J., Nešović, M., Divac Rankov, A., Podolski-Renić, A., Stanković, T., Dragoj, M., Jovanović, M., Lazić, K., Dimas, K., Botta, M.,& Pešić, M.. (2019). Evaluation of anticancer compounds activity and toxicity in zebrafish model. in Abstract book: STRATAGEM CA17104: New diagnostic and therapeutic tools against multidrug-resistant tumours: First Working-Group Meeting WG1 - WG4; 2019 Jan 30-31; Turin, Italy
COST Action CA17104., 34-34.
https://hdl.handle.net/21.15107/rcub_ibiss_6042

Dinić J, Nešović M, Divac Rankov A, Podolski-Renić A, Stanković T, Dragoj M, Jovanović M, Lazić K, Dimas K, Botta M, Pešić M. Evaluation of anticancer compounds activity and toxicity in zebrafish model. in Abstract book: STRATAGEM CA17104: New diagnostic and therapeutic tools against multidrug-resistant tumours: First Working-Group Meeting WG1 - WG4; 2019 Jan 30-31; Turin, Italy. 2019;:34-34.
https://hdl.handle.net/21.15107/rcub_ibiss_6042 .

Dinić, Jelena, Nešović, Marija, Divac Rankov, Aleksandra, Podolski-Renić, Ana, Stanković, Tijana, Dragoj, Miodrag, Jovanović, Mirna, Lazić, Katarina, Dimas, Kostas, Botta, Maurizio, Pešić, Milica, "Evaluation of anticancer compounds activity and toxicity in zebrafish model" in Abstract book: STRATAGEM CA17104: New diagnostic and therapeutic tools against multidrug-resistant tumours: First Working-Group Meeting WG1 - WG4; 2019 Jan 30-31; Turin, Italy (2019):34-34,
https://hdl.handle.net/21.15107/rcub_ibiss_6042 .

TY  - JOUR
AU  - Ćirić, Jelena
AU  - Lazić, Katarina
AU  - Kapor, Slobodan
AU  - Perović, Milka
AU  - Petrović, Jelena
AU  - Pešić, Vesna
AU  - Kanazir, Selma
AU  - Šaponjić, Jasna
PY  - 2018
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0166432817312391
UR  - http://www.ncbi.nlm.nih.gov/pubmed/29170000
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3361
AB  - In order to find out the possible earliest biomarkers of Parkinson's disease (PD) cholinopathy, we followed the impact of bilateral pedunculopontine tegmental nucleus (PPT) lesion in rat on: the cortical and hippocampal sleep/wake states architectures, all sleep states related EEG microstructures, sleep spindles, the basal and stimulated locomotor activity. Sleep and basal locomotor activity in adult Wistar rats were followed during their inactive circadian phase, and throughout the same aging period. The bilateral PPT lesions were done by 0.1M ibotenic acid (IBO) during the surgical procedure for implantation of the electroencephalographic (EEG) and electromyographic (EMG) electrodes for chronic sleep recording. The cholinergic neuronal loss was identified by NADPH - diaphorase histochemistry. After all sleep and behavioral recording sessions, the locomotor activity was stimulated by d-amphetamine (d-AMPH) and the neuronal activity of striatum was followed by c-Fos immunolabeling. Impaired cholinergic innervation from the PPT was expressed earlier as sleep disorder then as movement disorder, and it was the earliest and long-lasting at hippocampal and thalamo-cortical level, and followed by a delayed "hypokinesia". This severe impact of a tonically impaired PPT cholinergic innervation was evidenced as the cholinergic interneuronal loss of the caudate putamen and as a suppressed c-Fos expression after stimulation by d-AMPH. In order how they occurred, the hippocampal non rapid eye movement (NREM) sleep disorder, altered high voltage sleep spindle (HVS) dynamics during rapid eye movement (REM) sleep in the hippocampus and motor cortex, and "hypokinesia" may serve as the biomarkers of PD cholinopathy onset and progression.
T2  - Behavioural Brain Research
T1  - Sleep disorder and altered locomotor activity as biomarkers of the Parkinson's disease cholinopathy in rat
VL  - 339
DO  - 10.1016/j.bbr.2017.11.021
SP  - 79
EP  - 92
ER  - 

@article{
author = "Ćirić, Jelena and Lazić, Katarina and Kapor, Slobodan and Perović, Milka and Petrović, Jelena and Pešić, Vesna and Kanazir, Selma and Šaponjić, Jasna",
year = "2018",
abstract = "In order to find out the possible earliest biomarkers of Parkinson's disease (PD) cholinopathy, we followed the impact of bilateral pedunculopontine tegmental nucleus (PPT) lesion in rat on: the cortical and hippocampal sleep/wake states architectures, all sleep states related EEG microstructures, sleep spindles, the basal and stimulated locomotor activity. Sleep and basal locomotor activity in adult Wistar rats were followed during their inactive circadian phase, and throughout the same aging period. The bilateral PPT lesions were done by 0.1M ibotenic acid (IBO) during the surgical procedure for implantation of the electroencephalographic (EEG) and electromyographic (EMG) electrodes for chronic sleep recording. The cholinergic neuronal loss was identified by NADPH - diaphorase histochemistry. After all sleep and behavioral recording sessions, the locomotor activity was stimulated by d-amphetamine (d-AMPH) and the neuronal activity of striatum was followed by c-Fos immunolabeling. Impaired cholinergic innervation from the PPT was expressed earlier as sleep disorder then as movement disorder, and it was the earliest and long-lasting at hippocampal and thalamo-cortical level, and followed by a delayed "hypokinesia". This severe impact of a tonically impaired PPT cholinergic innervation was evidenced as the cholinergic interneuronal loss of the caudate putamen and as a suppressed c-Fos expression after stimulation by d-AMPH. In order how they occurred, the hippocampal non rapid eye movement (NREM) sleep disorder, altered high voltage sleep spindle (HVS) dynamics during rapid eye movement (REM) sleep in the hippocampus and motor cortex, and "hypokinesia" may serve as the biomarkers of PD cholinopathy onset and progression.",
journal = "Behavioural Brain Research",
title = "Sleep disorder and altered locomotor activity as biomarkers of the Parkinson's disease cholinopathy in rat",
volume = "339",
doi = "10.1016/j.bbr.2017.11.021",
pages = "79-92"
}

Ćirić, J., Lazić, K., Kapor, S., Perović, M., Petrović, J., Pešić, V., Kanazir, S.,& Šaponjić, J.. (2018). Sleep disorder and altered locomotor activity as biomarkers of the Parkinson's disease cholinopathy in rat. in Behavioural Brain Research, 339, 79-92.
https://doi.org/10.1016/j.bbr.2017.11.021

Ćirić J, Lazić K, Kapor S, Perović M, Petrović J, Pešić V, Kanazir S, Šaponjić J. Sleep disorder and altered locomotor activity as biomarkers of the Parkinson's disease cholinopathy in rat. in Behavioural Brain Research. 2018;339:79-92.
doi:10.1016/j.bbr.2017.11.021 .

Ćirić, Jelena, Lazić, Katarina, Kapor, Slobodan, Perović, Milka, Petrović, Jelena, Pešić, Vesna, Kanazir, Selma, Šaponjić, Jasna, "Sleep disorder and altered locomotor activity as biomarkers of the Parkinson's disease cholinopathy in rat" in Behavioural Brain Research, 339 (2018):79-92,
https://doi.org/10.1016/j.bbr.2017.11.021 . .

TY  - JOUR
AU  - Ćirić, Jelena
AU  - Lazić, Katarina
AU  - Kapor, Slobodan
AU  - Perović, Milka
AU  - Petrović, Jelena
AU  - Pešić, Vesna
AU  - Kanazir, Selma
AU  - Šaponjić, Jasna
PY  - 2018
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0166432817312391
UR  - http://www.ncbi.nlm.nih.gov/pubmed/29170000
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2932
AB  - In order to find out the possible earliest biomarkers of Parkinson's disease (PD) cholinopathy, we followed the impact of bilateral pedunculopontine tegmental nucleus (PPT) lesion in rat on: the cortical and hippocampal sleep/wake states architectures, all sleep states related EEG microstructures, sleep spindles, the basal and stimulated locomotor activity. Sleep and basal locomotor activity in adult Wistar rats were followed during their inactive circadian phase, and throughout the same aging period. The bilateral PPT lesions were done by 0.1M ibotenic acid (IBO) during the surgical procedure for implantation of the electroencephalographic (EEG) and electromyographic (EMG) electrodes for chronic sleep recording. The cholinergic neuronal loss was identified by NADPH - diaphorase histochemistry. After all sleep and behavioral recording sessions, the locomotor activity was stimulated by d-amphetamine (d-AMPH) and the neuronal activity of striatum was followed by c-Fos immunolabeling. Impaired cholinergic innervation from the PPT was expressed earlier as sleep disorder then as movement disorder, and it was the earliest and long-lasting at hippocampal and thalamo-cortical level, and followed by a delayed "hypokinesia". This severe impact of a tonically impaired PPT cholinergic innervation was evidenced as the cholinergic interneuronal loss of the caudate putamen and as a suppressed c-Fos expression after stimulation by d-AMPH. In order how they occurred, the hippocampal non rapid eye movement (NREM) sleep disorder, altered high voltage sleep spindle (HVS) dynamics during rapid eye movement (REM) sleep in the hippocampus and motor cortex, and "hypokinesia" may serve as the biomarkers of PD cholinopathy onset and progression.
T2  - Behavioural Brain Research
T1  - Sleep disorder and altered locomotor activity as biomarkers of the Parkinson's disease cholinopathy in rat
VL  - 339
DO  - 10.1016/j.bbr.2017.11.021
SP  - 79
EP  - 92
ER  - 

@article{
author = "Ćirić, Jelena and Lazić, Katarina and Kapor, Slobodan and Perović, Milka and Petrović, Jelena and Pešić, Vesna and Kanazir, Selma and Šaponjić, Jasna",
year = "2018",
abstract = "In order to find out the possible earliest biomarkers of Parkinson's disease (PD) cholinopathy, we followed the impact of bilateral pedunculopontine tegmental nucleus (PPT) lesion in rat on: the cortical and hippocampal sleep/wake states architectures, all sleep states related EEG microstructures, sleep spindles, the basal and stimulated locomotor activity. Sleep and basal locomotor activity in adult Wistar rats were followed during their inactive circadian phase, and throughout the same aging period. The bilateral PPT lesions were done by 0.1M ibotenic acid (IBO) during the surgical procedure for implantation of the electroencephalographic (EEG) and electromyographic (EMG) electrodes for chronic sleep recording. The cholinergic neuronal loss was identified by NADPH - diaphorase histochemistry. After all sleep and behavioral recording sessions, the locomotor activity was stimulated by d-amphetamine (d-AMPH) and the neuronal activity of striatum was followed by c-Fos immunolabeling. Impaired cholinergic innervation from the PPT was expressed earlier as sleep disorder then as movement disorder, and it was the earliest and long-lasting at hippocampal and thalamo-cortical level, and followed by a delayed "hypokinesia". This severe impact of a tonically impaired PPT cholinergic innervation was evidenced as the cholinergic interneuronal loss of the caudate putamen and as a suppressed c-Fos expression after stimulation by d-AMPH. In order how they occurred, the hippocampal non rapid eye movement (NREM) sleep disorder, altered high voltage sleep spindle (HVS) dynamics during rapid eye movement (REM) sleep in the hippocampus and motor cortex, and "hypokinesia" may serve as the biomarkers of PD cholinopathy onset and progression.",
journal = "Behavioural Brain Research",
title = "Sleep disorder and altered locomotor activity as biomarkers of the Parkinson's disease cholinopathy in rat",
volume = "339",
doi = "10.1016/j.bbr.2017.11.021",
pages = "79-92"
}

Ćirić, J., Lazić, K., Kapor, S., Perović, M., Petrović, J., Pešić, V., Kanazir, S.,& Šaponjić, J.. (2018). Sleep disorder and altered locomotor activity as biomarkers of the Parkinson's disease cholinopathy in rat. in Behavioural Brain Research, 339, 79-92.
https://doi.org/10.1016/j.bbr.2017.11.021

Ćirić J, Lazić K, Kapor S, Perović M, Petrović J, Pešić V, Kanazir S, Šaponjić J. Sleep disorder and altered locomotor activity as biomarkers of the Parkinson's disease cholinopathy in rat. in Behavioural Brain Research. 2018;339:79-92.
doi:10.1016/j.bbr.2017.11.021 .

Ćirić, Jelena, Lazić, Katarina, Kapor, Slobodan, Perović, Milka, Petrović, Jelena, Pešić, Vesna, Kanazir, Selma, Šaponjić, Jasna, "Sleep disorder and altered locomotor activity as biomarkers of the Parkinson's disease cholinopathy in rat" in Behavioural Brain Research, 339 (2018):79-92,
https://doi.org/10.1016/j.bbr.2017.11.021 . .

TY  - JOUR
AU  - Lazić, Katarina
AU  - Ćirić, Jelena
AU  - Šaponjić, Jasna
PY  - 2018
UR  - http://doi.wiley.com/10.1111/jsr.12758
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3140
AB  - On the basis of our previous studies and the important role of the thalamo-cortical network in states of unconsciousness, such as anaesthesia and sleep, and in sleep spindles generation, we investigated sleep spindles (SS) and high-voltage sleep spindle (HVS) dynamics during non-rapid eye movement (NREM) and rapid eye movement (REM) sleep following different types of general anaesthesia in both physiological controls and in a rat model of Parkinson's disease (PD) cholinopathy, to follow the impact of anaesthesia on post-anaesthesia sleep at the thalamo-cortical level through an altered sleep spindle dynamics. We recorded 6 hr of spontaneous sleep in all rats, both before and 48 hr after ketamine/diazepam or pentobarbital anaesthesia, and we used 1 hr of NREM or REM sleep from each to validate visually the automatically detected SS or HVS for their extraction and analysis. In the controls, SS occurred mainly during NREM, whereas HVS occurred only during REM sleep. Ketamine/diazepam anaesthesia promoted HVS, prolonged SS during NREM, induced HVS of increased frequency during REM, and increased SS/HVS densities during REM versus NREM sleep. Pentobarbital anaesthesia decreased the frequency of SS during NREM and the HVS density during REM sleep. Although the pedunculopontine tegmental nucleus lesion prolonged SS only during NREM sleep, in these rats, ketamine/diazepam anaesthesia suppressed HVS during both sleep states, whereas pentobarbital anaesthesia promoted HVS during REM sleep. The different impacts of two anaesthetic regimens on the thalamo-cortical regulatory network are expressed through their distinct sleep spindle generation and dynamics that are dependent on the NREM and REM state regulatory neuronal substrate.
T2  - Journal of Sleep Research
T1  - Sleep spindle dynamics during NREM and REM sleep following distinct general anaesthesia in control rats and in a rat model of Parkinson’s disease cholinopathy
DO  - 10.1111/jsr.12758
ER  - 

@article{
author = "Lazić, Katarina and Ćirić, Jelena and Šaponjić, Jasna",
year = "2018",
abstract = "On the basis of our previous studies and the important role of the thalamo-cortical network in states of unconsciousness, such as anaesthesia and sleep, and in sleep spindles generation, we investigated sleep spindles (SS) and high-voltage sleep spindle (HVS) dynamics during non-rapid eye movement (NREM) and rapid eye movement (REM) sleep following different types of general anaesthesia in both physiological controls and in a rat model of Parkinson's disease (PD) cholinopathy, to follow the impact of anaesthesia on post-anaesthesia sleep at the thalamo-cortical level through an altered sleep spindle dynamics. We recorded 6 hr of spontaneous sleep in all rats, both before and 48 hr after ketamine/diazepam or pentobarbital anaesthesia, and we used 1 hr of NREM or REM sleep from each to validate visually the automatically detected SS or HVS for their extraction and analysis. In the controls, SS occurred mainly during NREM, whereas HVS occurred only during REM sleep. Ketamine/diazepam anaesthesia promoted HVS, prolonged SS during NREM, induced HVS of increased frequency during REM, and increased SS/HVS densities during REM versus NREM sleep. Pentobarbital anaesthesia decreased the frequency of SS during NREM and the HVS density during REM sleep. Although the pedunculopontine tegmental nucleus lesion prolonged SS only during NREM sleep, in these rats, ketamine/diazepam anaesthesia suppressed HVS during both sleep states, whereas pentobarbital anaesthesia promoted HVS during REM sleep. The different impacts of two anaesthetic regimens on the thalamo-cortical regulatory network are expressed through their distinct sleep spindle generation and dynamics that are dependent on the NREM and REM state regulatory neuronal substrate.",
journal = "Journal of Sleep Research",
title = "Sleep spindle dynamics during NREM and REM sleep following distinct general anaesthesia in control rats and in a rat model of Parkinson’s disease cholinopathy",
doi = "10.1111/jsr.12758"
}

Lazić, K., Ćirić, J.,& Šaponjić, J.. (2018). Sleep spindle dynamics during NREM and REM sleep following distinct general anaesthesia in control rats and in a rat model of Parkinson’s disease cholinopathy. in Journal of Sleep Research.
https://doi.org/10.1111/jsr.12758

Lazić K, Ćirić J, Šaponjić J. Sleep spindle dynamics during NREM and REM sleep following distinct general anaesthesia in control rats and in a rat model of Parkinson’s disease cholinopathy. in Journal of Sleep Research. 2018;.
doi:10.1111/jsr.12758 .

Lazić, Katarina, Ćirić, Jelena, Šaponjić, Jasna, "Sleep spindle dynamics during NREM and REM sleep following distinct general anaesthesia in control rats and in a rat model of Parkinson’s disease cholinopathy" in Journal of Sleep Research (2018),
https://doi.org/10.1111/jsr.12758 . .

TY  - THES
AU  - Lazić, Katarina
PY  - 2017
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=5775
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:17640/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1025173682
UR  - http://nardus.mpn.gov.rs/123456789/9462
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3295
AB  - U ovoj doktorskoj disertaciji ispitivan je uticaj ketamin/diazepam i pentobarbital opšte anestezije na EEG mikrostrukturu i obrazac disanja tokom anestezije, kao i na arhitekturu spavanja i strukturu prelaznih stanja, EEG mikrostrukturu i dinamiku epizoda svih faza spavanja nakon anestezije, kako u fiziološkim kontrolama, tako i u eksperimentalnom modelu holinergičke neuropatologije Parkinsonove bolesti (bilateralna lezija PPT jedra).Rezultati ove doktorske disertacije pokazali su da je ketamin/diazepam anestezija operativnog nivoa izazvala ozbiljan poremećaj respiratornog obrasca i EEG mikrostrukture tokom anestezije. Međutim, jednako vreme potrebno za uspostavljanje stabilne anestezije u pacova sa bilateralnom lezijom PPT jedra kao i dugotrajni suprimirajući efekti na povećanu NREM beta i teta amplitudu (elektrofiziološki markeri deficita holinergičkih neurona PPT jedra) nakon anestezije, ukazuju da je ova anestezija potencijalno povoljnija, kako za ulazak u anesteziju, tako i za NREM fazu spavanja nakon operativnih zahvata kod gerijatrijskih pacijenata, kao i pacijenata obolelih od Parkinsonove i Alchajmerove bolesti.Nasuprot ketamin/diazepam anesteziji, pentobarbital anestezija ima povoljnije dejstvo na REM fazu spavanja nakon anestezije, kako kod fizioloških kontrola, tako i u eksperimentalnom modelu holinergičke neuropatologije Parkinsonove bolesti na osnovu: dugotrajnih poremećaja REM spavanja i strukture prelaznih stanja kod fizioloških kontrola koje izaziva ketamin/diazepam anestezija; suprimirajućih efekata obe anestezije operativnog nivoa na produženu REM/REM1 fazu spavanja i poremećaj njihove EEG mikrostrukture kod bilateralne lezije PPT jedra; suprimirajućeg efekta pentobarbital anestezije na povećani broj NREM/REM/NREM prelaza uzrokovanih lezijom PPT jedra; kao i na osnovu EEG mikrostrukture tokom stabilne pentobarbital anestezije, koja se ne razlikuje u poređenju PPT lezije i fiziološke kontrole.
AB  - The aim of this doctoral dissertation was to follow the impact of ketamine/diazepam and pentobarbital anesthesia on the EEG microstructure and respiratory pattern during anesthesia, and on the post-anesthesia sleep/wake states architecture and transition structure, EEG microstructure across sleep, and all the sleep state episodes dynamics in the physiological condition, as well as during the PPT cholinergic neuropathology (the experimental model of Parkinson’s disease cholinergic neuropathology). Ketamine/diazepam anesthesia induces more alterations in the EEG microstructure and respiratory pattern than does the pentobarbital anesthesia in the PPT lesioned rats. In addition, the equal time required to establish an anesthetized state in the PPT lesioned vs. control rats, and the long-term suppressive effect on augmented NREM beta and theta amplitudes (the hallmarks of PPT cholinergic neuronal loss in rat) suggest ketamine/diazepam anesthesia as potentially more beneficial both for anesthesia induction and for post-anesthesia NREM sleep in the surgical procedures of the elderly, and Parkinson’s, and Alzheimer’s patients. In contrast to the ketamine/diazepam anesthesia the pentobarbital anesthesia is much more beneficial for the post-anesthesia REM sleep in physiological conditions as well as during the PPT cholinergic neuropathology on the basis of: the long-lasting REM sleep and transition structure disorders in physiological controls, induced by the ketamine/diazepam; the abolishing effects of both anesthetic regimens on the post-anesthesia prolonged REM/REM1 sleep and on their EEG microstructure disorders in the PPT lesioned rats; the abolishing effect of pentobarbital on the increased NREM/REM/NREM transitions, caused by the PPT lesion; and the equal EEG microstructure during stable pentobarbital anesthesia in the PPT lesioned rats versus controls.
PB  - Belgrade: University of Belgrade, Faculty of Biology
T2  - University of Belgrade, Faculty of Biology
T1  - Uticaj opšte anestezije na spavanje u eksperimentalnom modelu holinergičke neuropatologije Parkinsonove bolesti - mogući rizici postoperativnog oporavka
T1  - Impact of general anesthesia on sleep in the experimental model of Parkison's disease neuropathology - possible risks of postoperative recovery
SP  - 1
EP  - 106
UR  - https://hdl.handle.net/21.15107/rcub_nardus_9462
ER  - 

@phdthesis{
author = "Lazić, Katarina",
year = "2017",
abstract = "U ovoj doktorskoj disertaciji ispitivan je uticaj ketamin/diazepam i pentobarbital opšte anestezije na EEG mikrostrukturu i obrazac disanja tokom anestezije, kao i na arhitekturu spavanja i strukturu prelaznih stanja, EEG mikrostrukturu i dinamiku epizoda svih faza spavanja nakon anestezije, kako u fiziološkim kontrolama, tako i u eksperimentalnom modelu holinergičke neuropatologije Parkinsonove bolesti (bilateralna lezija PPT jedra).Rezultati ove doktorske disertacije pokazali su da je ketamin/diazepam anestezija operativnog nivoa izazvala ozbiljan poremećaj respiratornog obrasca i EEG mikrostrukture tokom anestezije. Međutim, jednako vreme potrebno za uspostavljanje stabilne anestezije u pacova sa bilateralnom lezijom PPT jedra kao i dugotrajni suprimirajući efekti na povećanu NREM beta i teta amplitudu (elektrofiziološki markeri deficita holinergičkih neurona PPT jedra) nakon anestezije, ukazuju da je ova anestezija potencijalno povoljnija, kako za ulazak u anesteziju, tako i za NREM fazu spavanja nakon operativnih zahvata kod gerijatrijskih pacijenata, kao i pacijenata obolelih od Parkinsonove i Alchajmerove bolesti.Nasuprot ketamin/diazepam anesteziji, pentobarbital anestezija ima povoljnije dejstvo na REM fazu spavanja nakon anestezije, kako kod fizioloških kontrola, tako i u eksperimentalnom modelu holinergičke neuropatologije Parkinsonove bolesti na osnovu: dugotrajnih poremećaja REM spavanja i strukture prelaznih stanja kod fizioloških kontrola koje izaziva ketamin/diazepam anestezija; suprimirajućih efekata obe anestezije operativnog nivoa na produženu REM/REM1 fazu spavanja i poremećaj njihove EEG mikrostrukture kod bilateralne lezije PPT jedra; suprimirajućeg efekta pentobarbital anestezije na povećani broj NREM/REM/NREM prelaza uzrokovanih lezijom PPT jedra; kao i na osnovu EEG mikrostrukture tokom stabilne pentobarbital anestezije, koja se ne razlikuje u poređenju PPT lezije i fiziološke kontrole., The aim of this doctoral dissertation was to follow the impact of ketamine/diazepam and pentobarbital anesthesia on the EEG microstructure and respiratory pattern during anesthesia, and on the post-anesthesia sleep/wake states architecture and transition structure, EEG microstructure across sleep, and all the sleep state episodes dynamics in the physiological condition, as well as during the PPT cholinergic neuropathology (the experimental model of Parkinson’s disease cholinergic neuropathology). Ketamine/diazepam anesthesia induces more alterations in the EEG microstructure and respiratory pattern than does the pentobarbital anesthesia in the PPT lesioned rats. In addition, the equal time required to establish an anesthetized state in the PPT lesioned vs. control rats, and the long-term suppressive effect on augmented NREM beta and theta amplitudes (the hallmarks of PPT cholinergic neuronal loss in rat) suggest ketamine/diazepam anesthesia as potentially more beneficial both for anesthesia induction and for post-anesthesia NREM sleep in the surgical procedures of the elderly, and Parkinson’s, and Alzheimer’s patients. In contrast to the ketamine/diazepam anesthesia the pentobarbital anesthesia is much more beneficial for the post-anesthesia REM sleep in physiological conditions as well as during the PPT cholinergic neuropathology on the basis of: the long-lasting REM sleep and transition structure disorders in physiological controls, induced by the ketamine/diazepam; the abolishing effects of both anesthetic regimens on the post-anesthesia prolonged REM/REM1 sleep and on their EEG microstructure disorders in the PPT lesioned rats; the abolishing effect of pentobarbital on the increased NREM/REM/NREM transitions, caused by the PPT lesion; and the equal EEG microstructure during stable pentobarbital anesthesia in the PPT lesioned rats versus controls.",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "University of Belgrade, Faculty of Biology",
title = "Uticaj opšte anestezije na spavanje u eksperimentalnom modelu holinergičke neuropatologije Parkinsonove bolesti - mogući rizici postoperativnog oporavka, Impact of general anesthesia on sleep in the experimental model of Parkison's disease neuropathology - possible risks of postoperative recovery",
pages = "1-106",
url = "https://hdl.handle.net/21.15107/rcub_nardus_9462"
}

Lazić, K.. (2017). Uticaj opšte anestezije na spavanje u eksperimentalnom modelu holinergičke neuropatologije Parkinsonove bolesti - mogući rizici postoperativnog oporavka. in University of Belgrade, Faculty of Biology
Belgrade: University of Belgrade, Faculty of Biology., 1-106.
https://hdl.handle.net/21.15107/rcub_nardus_9462

Lazić K. Uticaj opšte anestezije na spavanje u eksperimentalnom modelu holinergičke neuropatologije Parkinsonove bolesti - mogući rizici postoperativnog oporavka. in University of Belgrade, Faculty of Biology. 2017;:1-106.
https://hdl.handle.net/21.15107/rcub_nardus_9462 .

Lazić, Katarina, "Uticaj opšte anestezije na spavanje u eksperimentalnom modelu holinergičke neuropatologije Parkinsonove bolesti - mogući rizici postoperativnog oporavka" in University of Belgrade, Faculty of Biology (2017):1-106,
https://hdl.handle.net/21.15107/rcub_nardus_9462 .

TY  - JOUR
AU  - Ćirić, Jelena
AU  - Lazić, Katarina
AU  - Petrović, Jelena
AU  - Kalauzi, A
AU  - Šaponjić, Jasna
PY  - 2017
UR  - http://www.oatext.com/sleep-spindles-as-an-early-biomarker-of-rem-sleep-disorder-in-a-rat-model-of-parkinsons-disease-cholinopathy.php
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3296
AB  - Rhythmic oscillations of neuronal populations, generated by different mechanisms, are present at several levels of the central nervous system and serve many important physiological or reflect pathological functions. Understanding the role of brain oscillations as possible biomarkers of brain function and plasticity is still a challenge, and despite extensive research, their role is still not well established. We recently demonstrated that the hallmarks of earlier aging onset during impaired thalamo-cortical cholinergic innervation (in a rat model of Parkinson’s disease cholinopathy) were consistently expressed, from 3 and one half to 5 and one half months of age, through increased electroencephalographic (EEG) sigma activity amplitude during rapid eye movement (REM) sleep, as a unique aging induced REM sleep phenomenon. In addition, there was altered motor cortical drive during non-rapid-eye-movement (NREM) and REM sleep. In order to explain this new aging-induced REM sleep phenomenon, we analyzed possible differences between control REM sleep spindle activity and REM sleep spindle activity at the onset of REM sleep “enriched“ with sigma activity (at 4 and one half months of age), following bilateral pedunculopontine tegmental nucleus (PPT) cholinergic neuronal loss in the rat. We analzyed differences in spindle density, duration, and frequency. We demonstrated in young adult Wistar rats with the severely impaired PPT cholinergic innervation the alterations in sleep spindle dynamics and pattern during REM sleep in the motor cortex as the earliest biomarkers for the onset of their altered aging processes.
T2  - Translational Brain Rhythmicity
T1  - Sleep spindles as an early biomarker of REM sleep disorder in a rat model of Parkinson’s disease cholinopathy
IS  - 1
VL  - 2
DO  - 10.15761/TBR.1000111
SP  - 1
EP  - 11
ER  - 

@article{
author = "Ćirić, Jelena and Lazić, Katarina and Petrović, Jelena and Kalauzi, A and Šaponjić, Jasna",
year = "2017",
abstract = "Rhythmic oscillations of neuronal populations, generated by different mechanisms, are present at several levels of the central nervous system and serve many important physiological or reflect pathological functions. Understanding the role of brain oscillations as possible biomarkers of brain function and plasticity is still a challenge, and despite extensive research, their role is still not well established. We recently demonstrated that the hallmarks of earlier aging onset during impaired thalamo-cortical cholinergic innervation (in a rat model of Parkinson’s disease cholinopathy) were consistently expressed, from 3 and one half to 5 and one half months of age, through increased electroencephalographic (EEG) sigma activity amplitude during rapid eye movement (REM) sleep, as a unique aging induced REM sleep phenomenon. In addition, there was altered motor cortical drive during non-rapid-eye-movement (NREM) and REM sleep. In order to explain this new aging-induced REM sleep phenomenon, we analyzed possible differences between control REM sleep spindle activity and REM sleep spindle activity at the onset of REM sleep “enriched“ with sigma activity (at 4 and one half months of age), following bilateral pedunculopontine tegmental nucleus (PPT) cholinergic neuronal loss in the rat. We analzyed differences in spindle density, duration, and frequency. We demonstrated in young adult Wistar rats with the severely impaired PPT cholinergic innervation the alterations in sleep spindle dynamics and pattern during REM sleep in the motor cortex as the earliest biomarkers for the onset of their altered aging processes.",
journal = "Translational Brain Rhythmicity",
title = "Sleep spindles as an early biomarker of REM sleep disorder in a rat model of Parkinson’s disease cholinopathy",
number = "1",
volume = "2",
doi = "10.15761/TBR.1000111",
pages = "1-11"
}

Ćirić, J., Lazić, K., Petrović, J., Kalauzi, A.,& Šaponjić, J.. (2017). Sleep spindles as an early biomarker of REM sleep disorder in a rat model of Parkinson’s disease cholinopathy. in Translational Brain Rhythmicity, 2(1), 1-11.
https://doi.org/10.15761/TBR.1000111

Ćirić J, Lazić K, Petrović J, Kalauzi A, Šaponjić J. Sleep spindles as an early biomarker of REM sleep disorder in a rat model of Parkinson’s disease cholinopathy. in Translational Brain Rhythmicity. 2017;2(1):1-11.
doi:10.15761/TBR.1000111 .

Ćirić, Jelena, Lazić, Katarina, Petrović, Jelena, Kalauzi, A, Šaponjić, Jasna, "Sleep spindles as an early biomarker of REM sleep disorder in a rat model of Parkinson’s disease cholinopathy" in Translational Brain Rhythmicity, 2, no. 1 (2017):1-11,
https://doi.org/10.15761/TBR.1000111 . .

TY  - JOUR
AU  - Lazić, Katarina
AU  - Petrović, Jelena
AU  - Ćirić, Jelena
AU  - Kalauzi, Aleksandar
AU  - Šaponjić, Jasna
PY  - 2017
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0031938416306308
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3297
AB  - Postoperative sleep disorders, particularly the REM sleep disorder, may have a significant deleterious impact on postoperative outcomes and may contribute to the genesis of certain delayed postoperative complications. We have followed the effect of distinct anesthesia regimens (ketamine/diazepam vs. pentobarbital) over 6days following the induction of a stable anesthetized state in adult male Wistar rats, chronically instrumented for sleep recording. In order to compare the effect of both anesthetics in the physiological controls vs. the rats with impaired pedunculopontine tegmental nucleus (PPT) cholinergic innervation, during the operative procedure for the implantation of EEG and EMG electrodes, the bilateral PPT lesion was conducted using ibotenic acid (IBO). We have followed in particular post-anesthesia REM sleep. Our results show the distinct EEG microstructure of the motor cortex during the different stable anesthetized states, and their distinct impact on post-anesthesia REM sleep. In contrast to pentobarbital anesthesia, the ketamine/diazepam anesthesia potentiated the long-lasting post-anesthesia REM statewith higher muscle tone (REM1) vs. REM state with atonia (REM2). Whereas both anesthesias prolonged the post-anesthesia REM sleep duration, the long-term prolongation of the REM1 state was demonstrated only after the ketamine/diazepam anesthesia, first due to the increased number of REM1 episodes, and then due to the prolonged REM1 episodes duration. On the other hand, whereas both anesthetic regimens abolished the prolonged post-anesthesia REM/REM1 sleep and the EEG microstructure disorder during REM sleep, only the pentobarbital abolished the increased NREM/REM/NREM transitions, caused by the PPT lesion. In addition, in the PPT lesioned rats, the ketamine/diazepam anesthesia decreased the Wake/NREM/Wake transitions while the pentobarbital anesthesia decreased the Wake/REM/Wake transitions. Our present study suggests pentobarbital anesthesia as being highly beneficial for post-anesthesia REM sleep in the physiological condition as well as during PPT cholinergic neuropathology.
T2  - Physiology & Behavior
T1  - REM sleep disorder following general anesthesia in rats.
VL  - 168
DO  - 10.1016/j.physbeh.2016.10.013
SP  - 41
EP  - 54
ER  - 

@article{
author = "Lazić, Katarina and Petrović, Jelena and Ćirić, Jelena and Kalauzi, Aleksandar and Šaponjić, Jasna",
year = "2017",
abstract = "Postoperative sleep disorders, particularly the REM sleep disorder, may have a significant deleterious impact on postoperative outcomes and may contribute to the genesis of certain delayed postoperative complications. We have followed the effect of distinct anesthesia regimens (ketamine/diazepam vs. pentobarbital) over 6days following the induction of a stable anesthetized state in adult male Wistar rats, chronically instrumented for sleep recording. In order to compare the effect of both anesthetics in the physiological controls vs. the rats with impaired pedunculopontine tegmental nucleus (PPT) cholinergic innervation, during the operative procedure for the implantation of EEG and EMG electrodes, the bilateral PPT lesion was conducted using ibotenic acid (IBO). We have followed in particular post-anesthesia REM sleep. Our results show the distinct EEG microstructure of the motor cortex during the different stable anesthetized states, and their distinct impact on post-anesthesia REM sleep. In contrast to pentobarbital anesthesia, the ketamine/diazepam anesthesia potentiated the long-lasting post-anesthesia REM statewith higher muscle tone (REM1) vs. REM state with atonia (REM2). Whereas both anesthesias prolonged the post-anesthesia REM sleep duration, the long-term prolongation of the REM1 state was demonstrated only after the ketamine/diazepam anesthesia, first due to the increased number of REM1 episodes, and then due to the prolonged REM1 episodes duration. On the other hand, whereas both anesthetic regimens abolished the prolonged post-anesthesia REM/REM1 sleep and the EEG microstructure disorder during REM sleep, only the pentobarbital abolished the increased NREM/REM/NREM transitions, caused by the PPT lesion. In addition, in the PPT lesioned rats, the ketamine/diazepam anesthesia decreased the Wake/NREM/Wake transitions while the pentobarbital anesthesia decreased the Wake/REM/Wake transitions. Our present study suggests pentobarbital anesthesia as being highly beneficial for post-anesthesia REM sleep in the physiological condition as well as during PPT cholinergic neuropathology.",
journal = "Physiology & Behavior",
title = "REM sleep disorder following general anesthesia in rats.",
volume = "168",
doi = "10.1016/j.physbeh.2016.10.013",
pages = "41-54"
}

Lazić, K., Petrović, J., Ćirić, J., Kalauzi, A.,& Šaponjić, J.. (2017). REM sleep disorder following general anesthesia in rats.. in Physiology & Behavior, 168, 41-54.
https://doi.org/10.1016/j.physbeh.2016.10.013

Lazić K, Petrović J, Ćirić J, Kalauzi A, Šaponjić J. REM sleep disorder following general anesthesia in rats.. in Physiology & Behavior. 2017;168:41-54.
doi:10.1016/j.physbeh.2016.10.013 .

Lazić, Katarina, Petrović, Jelena, Ćirić, Jelena, Kalauzi, Aleksandar, Šaponjić, Jasna, "REM sleep disorder following general anesthesia in rats." in Physiology & Behavior, 168 (2017):41-54,
https://doi.org/10.1016/j.physbeh.2016.10.013 . .

TY  - JOUR
AU  - Petrović, Jelena
AU  - Ćirić, Jelena
AU  - Lazić, Katarina
AU  - Kalauzi, Aleksandar
AU  - Šaponjić, Jasna
PY  - 2013
UR  - http://www.scopus.com/inward/record.url?eid=2-s2.0-84881370170&partnerID=tZOtx3y1
UR  - http://www.sciencedirect.com/science/article/pii/S0014488613000605
UR  - http://www.ncbi.nlm.nih.gov/pubmed/23481548
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3298
AB  - The pedunculopontine tegmental nucleus (PPT) represents a major aggregation of cholinergic neurons in the mammalian brainstem, which is important in the generation and maintenance of REM sleep. We investigated the effects of unilateral and bilateral PPT lesions on sleep and all the conventional sleep-state related EEG frequency bands amplitudes, in an attempt to find the EEG markers for the onset and progression of PPT cholinergic neuronal degeneration. The experiments were performed on 35 adult male Wistar rats, chronically implanted for sleep recording. During the surgical procedure for EEG and EMG electrodes implantation, the unilateral or bilateral PPT lesion was produced under ketamine/diazepam anesthesia, by the stereotaxically guided microinfusion of 100 nl 0.1M ibotenic acid (IBO) into PPT. We applied Fourier analysis to signals acquired throughout 6h of recordings, and each 10s epoch was differentiated as a Wake, NREM or REM state. We also calculated the group probability density estimates (PDE) of all Wake, NREM and REM conventional EEG frequency amplitudes, and the number of all the transition states using MATLAB 6.5. Our results show that the unilateral or bilateral PPT lesions did not change the sleep/wake architecture, but did change the sleep/wake state transitions structure and the sleep/state related "EEG microstructure". Unilateral or bilateral PPT lesions sustainably increased Wake/REM and REM/Wake transitions from 14 to 35 days after lesions. This was followed by decreased NREM/REM and REM/NREM transitions from 28 days only in the case of the bilateral PPT lesion. The unilateral PPT lesion augmented both Wake theta and REM beta while it also attenuated the relative amplitude of the Wake delta frequency, with a delay of one week. Following a bilateral PPT lesion there was augmentation of the relative amplitude of the Wake, NREM, and REM beta and REM gamma frequency which occurred simultaneously to NREM and Wake delta attenuation. We have shown that the PPT cholinergic neuronal loss sustainably increased the number of the Wake/REM and REM/Wake transitions and augmented sleep-states related cortical activation that was simultaneously expressed by the high frequency amplitude augmentation, as well as Wake and NREM delta frequency attenuation.
T2  - Experimental Neurology
T1  - Lesion of the pedunculopontine tegmental nucleus in rat augments cortical activation and disturbs sleep/wake state transitions structure.
VL  - 247
DO  - 10.1016/j.expneurol.2013.02.007
SP  - 562
EP  - 71
ER  - 

@article{
author = "Petrović, Jelena and Ćirić, Jelena and Lazić, Katarina and Kalauzi, Aleksandar and Šaponjić, Jasna",
year = "2013",
abstract = "The pedunculopontine tegmental nucleus (PPT) represents a major aggregation of cholinergic neurons in the mammalian brainstem, which is important in the generation and maintenance of REM sleep. We investigated the effects of unilateral and bilateral PPT lesions on sleep and all the conventional sleep-state related EEG frequency bands amplitudes, in an attempt to find the EEG markers for the onset and progression of PPT cholinergic neuronal degeneration. The experiments were performed on 35 adult male Wistar rats, chronically implanted for sleep recording. During the surgical procedure for EEG and EMG electrodes implantation, the unilateral or bilateral PPT lesion was produced under ketamine/diazepam anesthesia, by the stereotaxically guided microinfusion of 100 nl 0.1M ibotenic acid (IBO) into PPT. We applied Fourier analysis to signals acquired throughout 6h of recordings, and each 10s epoch was differentiated as a Wake, NREM or REM state. We also calculated the group probability density estimates (PDE) of all Wake, NREM and REM conventional EEG frequency amplitudes, and the number of all the transition states using MATLAB 6.5. Our results show that the unilateral or bilateral PPT lesions did not change the sleep/wake architecture, but did change the sleep/wake state transitions structure and the sleep/state related "EEG microstructure". Unilateral or bilateral PPT lesions sustainably increased Wake/REM and REM/Wake transitions from 14 to 35 days after lesions. This was followed by decreased NREM/REM and REM/NREM transitions from 28 days only in the case of the bilateral PPT lesion. The unilateral PPT lesion augmented both Wake theta and REM beta while it also attenuated the relative amplitude of the Wake delta frequency, with a delay of one week. Following a bilateral PPT lesion there was augmentation of the relative amplitude of the Wake, NREM, and REM beta and REM gamma frequency which occurred simultaneously to NREM and Wake delta attenuation. We have shown that the PPT cholinergic neuronal loss sustainably increased the number of the Wake/REM and REM/Wake transitions and augmented sleep-states related cortical activation that was simultaneously expressed by the high frequency amplitude augmentation, as well as Wake and NREM delta frequency attenuation.",
journal = "Experimental Neurology",
title = "Lesion of the pedunculopontine tegmental nucleus in rat augments cortical activation and disturbs sleep/wake state transitions structure.",
volume = "247",
doi = "10.1016/j.expneurol.2013.02.007",
pages = "562-71"
}

Petrović, J., Ćirić, J., Lazić, K., Kalauzi, A.,& Šaponjić, J.. (2013). Lesion of the pedunculopontine tegmental nucleus in rat augments cortical activation and disturbs sleep/wake state transitions structure.. in Experimental Neurology, 247, 562-71.
https://doi.org/10.1016/j.expneurol.2013.02.007

Petrović J, Ćirić J, Lazić K, Kalauzi A, Šaponjić J. Lesion of the pedunculopontine tegmental nucleus in rat augments cortical activation and disturbs sleep/wake state transitions structure.. in Experimental Neurology. 2013;247:562-71.
doi:10.1016/j.expneurol.2013.02.007 .

Petrović, Jelena, Ćirić, Jelena, Lazić, Katarina, Kalauzi, Aleksandar, Šaponjić, Jasna, "Lesion of the pedunculopontine tegmental nucleus in rat augments cortical activation and disturbs sleep/wake state transitions structure." in Experimental Neurology, 247 (2013):562-71,
https://doi.org/10.1016/j.expneurol.2013.02.007 . .