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001-es BibID:BIBFORM082078
035-os BibID:(WoS)000509325000003 (Scopus)85071744080 (PubMed)31469725
Első szerző:Kovács Adrienn (molekuláris biológus)
Cím:Orexinergic actions modify occurrence of slow inward currents on neurons in the pedunculopontine nucleus / Kovács Adrienn, Baksa Brigitta, Bayasgalan Tsogbadrakh, Szentesi Péter, Csemer Andrea, Pál Balázs
Dátum:2019
ISSN:0959-4965
Megjegyzések:Orexins are neuromodulatory peptides of the lateral hypothalamus which regulate homeostatic mechanisms including sleep-wakefulness cycles. Orexinergic actions stabilize wakefulness by acting on the nuclei of the reticular activating system, including the pedunculopontine nucleus. Orexin application to pedunculopontine neurons produces a noisy tonic inward current and an increase in the frequency and amplitudes of excitatory postsynaptic currents. In the present project, we investigated orexinergic neuromodulatory actions on astrocyte-mediated neuronal slow inward currents of pedunculopontine neurons and their relationships with tonic currents by using slice electrophysiology on preparations from mice. We demonstrated that, in contrast to several other neuromodulatory actions and in line with literature data, orexin predominantly elicited a tonic inward current. A subpopulation of the pedunculopontine neurons possessed slow inward currents. Independently from the tonic currents, actions on slow inward currents were also detected, which resembled other neuromodulatory actions: if slow inward currents were almost absent on the neuron, orexin induced an increase of the charge movements by slow inward currents, whereas if slow inward current activity was abundant on the neurons, orexin exerted inhibitory action on it. Our data support the previous findings that orexin elicits only inward currents in contrast with cannabinoid, cholinergic or serotonergic actions. Similar to the aforementioned neuromodulatory actions, orexin influences slow inward currents in a way depending on control slow inward current activity. Furthermore, we found that orexinergic actions on slow inward currents are similarly independent from its actions on tonic currents, as it was previously found with other neuromodulatory agonists.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
neuromodulation
orexin
pedunculopontine nucleus
slow inward current
tonic inward current
Megjelenés:Neuroreport. - 30 : 14 (2019), p. 933-938. -
További szerzők:Baksa Brigitta (1989-) (fogorvos) Bayasgalan, Tsogbadrakh (1983-) (Általános orvos) Szentesi Péter (1967-) (élettanász) Csemer Andrea (1994-) (molekuláris biológus) Pál Balázs (1975-) (élettanász)
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2.

001-es BibID:BIBFORM060026
Első szerző:Kovács Adrienn (molekuláris biológus)
Cím:Cholinergic and endocannabinoid neuromodulatory effects overlap on neurons of the pedunculopontine nucleus of mice / Adrienn Kovács, Csilla Bordás, Balázs Pál
Dátum:2015
Megjegyzések:The pedunculopontine nucleus (PPN) is a part of the reticular activating system and one of the main sources of the cholinergic fibers in the midbrain, while it is also subject to cholinergic modulation. This nucleus is known to be a structure that controls sleep-wake cycles, arousal, and locomotion. Neurons of the PPN are targets of several neuromodulatory mechanisms, which elicit heterogeneous pharmacological responses including hyperpolarization and depolarization, whereas lack of response can also be observed. In agreement with previous findings, we found that PPN neurons respond to the muscarinic agonist carbachol in a heterogeneous manner: they were depolarized and showed increased firing rate, decreased firing frequency, and were hyperpolarized, or showed no response. The heterogeneity of the muscarinic activation was similar to our previous observations with type 1 cannabinoid (CB1) receptor agonists; therefore, we investigated whether muscarinic and endocannabinoid modulatory mechanisms elicit the same action on a certain neuron. To achieve this, whole-cell patch clamp experiments were conducted on midbrain slices containing the PPN. Carbachol was applied first and, after recording the changes in the membrane potential and the firing frequency and achieving washout, the CB1 receptor agonist arachidonyl-2'-chloroethylamide (ACEA) was applied. A marked but not full overlap was observed: all neurons depolarized by carbachol were depolarized by the CB1 receptor agonist ACEA, and all neurons lacking response to carbachol lacked response to ACEA as well. However, neurons hyperpolarized by carbachol were depolarized, hyperpolarized, or not affected by the ACEA. These results indicate that endocannabinoid and muscarinic modulatory effects involve similar mechanisms of action.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
CB1 receptor
Muscarinic
Carbachol
arachidonyl-2'-chloroethylamide
reticular activating system
Megjelenés:Neuroreport. - 26 : 5 (2015), p. 273-278. -
További szerzők:Bordás Csilla Pál Balázs (1975-) (élettanász)
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3.

001-es BibID:BIBFORM109964
035-os BibID:(scopus)85148082398 (wos)000935540500006
Első szerző:Maamrah, Baneen (molekuláris biológus)
Cím:KCNQ4 potassium channel subunit deletion leads to exaggerated acoustic startle reflex in mice / Maamrah Baneen, Pocsai Krisztina, Bayasgalan Tsogbadrakh, Csemer Andrea, Pál Balázs
Dátum:2023
ISSN:0959-4965
Megjegyzések:The potassium voltage-gated channel subfamily Q member 4 (KCNQ4) subunit forms channels responsible for M-current, a muscarine-sensitive potassium current regulating neuronal excitability. In contrast to other KCNQ subunits, its expression is restricted to the cochlear outer hair cells, the auditory brainstem and other brainstem nuclei in a great overlap with structures involved in startle reflex. We aimed to show whether startle reflexis affected by the loss of KCNQ4 subunit and whether these alterations are similar to the ones caused by brainstem hyperexcitability. Young adult KCNQ4 knockout mice and wild-type littermates, as well as mice expressing hM3D chemogenetic actuator in the pontine caudal nucleus and neurons innervating it were used for testing acoustic startle. The acoustic startle reflex was significantly increased in knockout mice compared with wild-type littermates. When mice expressing human M3 muscarinic (hM3D) in nuclei related to startle reflex were tested, a similar increase of the first acoustic startle amplitude and a strong habituation of the further responses was demonstrated. We found that the acoustic startle reflex is exaggerated and minimal habituation occurs in KCNQ4 knockout animals. These changes are distinct from the effects of the hyperexcitability of nuclei involved in startle. One can conclude that the exaggerated startle reflex found with the KCNQ4 subunit deletion is the consequence of both the cochlear damage and the changes in neuronal excitability of startle networks.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Neuroreport. - 34 : 4 (2023), p. 232-237. -
További szerzők:Pocsai Krisztina (1978-) (élettanász) Bayasgalan, Tsogbadrakh (1983-) (Általános orvos) Csemer Andrea (1994-) (molekuláris biológus) Pál Balázs (1975-) (élettanász)
Pályázati támogatás:TKP2020-NKA-04
Egyéb
2020-4.1.1-TKP2020
Egyéb
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4.

001-es BibID:BIBFORM031839
035-os BibID:(PMID)10923648
Első szerző:Monory Krisztina
Cím:Characterization of N,N(Me)2-Dmt-Tic-OH, a delta selective opioid dipeptide antagonist / Krisztina Monory, Sharon D. Bryant, István Kertész, Gianfranco Balboni, Remo Guerrini, Géza Tóth, Severo Salvadori, Lawrence H. Lazarus, Anna Borsodi
Dátum:2000
ISSN:0959-4965
Megjegyzések:N,N(Me)2-Dimethyl-tyrosine-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid-OH (N,N(Me)2-Dmt-Tic-OH) is a very selective delta opioid dipeptide with elevated antagonist activity. We have radiolabelled this compound by catalytic tritiation of the N,N(Me)2-Dmt(3',5'-I2)-Tic-OH precursor. The ligand labelled rat brain membranes with a Kd value of 0.42 nM and a Bmax of 63.12 fmol/mg protein. The new tritiated ligand showed high affinity for the delta opioid receptor whereas its binding at mu and kappa opioid receptors was weak. N,N(Me)2-Dmt-Tic-OH was able to inhibit the agonist-stimulated binding of the non-hydrolysable GTP analogue ¿35SGTPgammaS, thus attenuating the activation of G proteins via opioid receptors. This simple opioid dipeptide in both normal and labelled form may serve as a useful tool to study delta opioid receptors in vitro and in vivo.
Tárgyszavak:Természettudományok Kémiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Neuroreport. - 11 : 10 (2000), p. 2083-2086. -
További szerzők:Bryant, Sharon D. Kertész István (1966-) (vegyész) Balboni, Gianfranco Guerrini, Remo Tóth Géza Salvadori, Severo Lazarus, Lawrence H. Borsodi Anna
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM040111
Első szerző:Szőke Éva
Cím:Interacting effects of capsaicin and anandamide on intracellular calcium in sensory neurones / Szdke, E., Balla, Z., Csernoch, L., Czeh, G., Szolcsanyi, J.
Dátum:2000
ISSN:0959-4965
Megjegyzések:Capsaicin (100 nM to 1 microM) and anandamide (200 nM to 10 microM) caused a transient increase in fluorescence of fura-2 loaded cultured small trigeminal neurones of rats measured with a ratiometric technique. The percentage of cells responding to capsaicin at 100 nM, 330 nM and 1 microM was 47.4%, 45.3%, and 70.4%, respectively. Averaged peak value of fluorescense ratio (R) at 340 and 380 nm excitation was slightly dose dependent. Peaks of anandamide-induced transients were R = 0.2 at 200 nM and 0.16 at 10 microM. Near 40% of capsaicin-sensitive cells responded also to anandamide. Anandamide (200 nM) inhibited the capsaicin-induced calcium influx. The results suggest that anandamide increases intracellular calcium and inhibits capsaicin-evoked calcium transients.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuroreport. - 11 : 9 (2000), p. 1949-1952. -
További szerzők:Balla Zsolt Csernoch László (1961-) (élettanász) Czéh Gábor Szolcsányi János (Pécs)
Internet cím:elektronikus változat
Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM030614
Első szerző:Weisz Júlia
Cím:Right prefrontal activation produced by arterial baroreceptor stimulation : a PET study / Weisz J., Emri M., Fent J., Lengyel Z., Márián T., Horváth G., Bogner P., Trón L., Adám G.
Dátum:2001
ISSN:0959-4965
Megjegyzések:This study was performed to test the hypothesis of greater right hemispheric involvement in the processing of baroreceptor stimuli. Carotid sinus baroreceptors were stimulated by rhythmically decreasing air pressure in a neck chamber, and under control conditions the thorax was stimulated in a similar manner. Changes in regional cerebral blood flow (rCBF) were measured by PET. Baroreceptor stimulation resulted in rCBF increase in the right anterior-inferior prefrontal cortex (Brodmann areas (BA) 10/44/47) and bilaterally in BA 6/8. We conclude that in at least some stages of baroreceptor information processing the right hemisphere plays a greater role than the left hemisphere.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Neuroreport. - 12 : 15 (2001), p. 3233-3238. -
További szerzők:Emri Miklós (1962-) (fizikus) Fent János Lengyel Zsolt (nukleáris medicina szakorvos) Márián Teréz (1950-) (radiobiológus) Horváth G. Bogner Péter (1963-) (radiológus) Trón Lajos (1941-) (biofizikus) Ádám György
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