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1

Neurochemical correlates of 50‑kHz ultrasonic vocalizations in context induced response, reward processing, and appetitive social interactions

100%
Hamed A., Kursa M.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
A tool that most effectively determines the emotional states of rats is the registration and analysis of ultrasonic vocalizations (USVs). 50‑kHz USVs are a form of expression of positive emotions. USV measurement allows both identifying individual differences in processing information about the reward as well as reflecting, to a large extent, the level of individual motivation. We hypothesized that 50-kHz USV emission could have separate neurochemical backgrounds in different behavioral paradigms, as well as, some common neurochemical mechanisms reflected in examined neurotransmitters correlations. For example, re‑exposure to the context of morphine administration is associated with elevated serotonin concentrations in the amygdala, hippocampus, and medial prefrontal cortex (mPFC) and increased Glu/Gln ratio in the nucleus accumbens (Nacc). Machine learning based analysis indicates a strong correlation between serotonergic and glutamatergic systems in context‑induced conditioned response. In the case of social interaction paradigm, several neurochemical changes were detected. Depending on the duration of social interaction, neurotransmission pathways are activated in the cascade fashion. Thus, glutamatergic neurotransmission in amygdala, ventral tegmental area (VTA), Nacc, and hippocampus, and action in the serotonergic system in mPFC, Nacc, caudate, and putamen, dopaminergic neurotransmission in mPFC and hippocampus, and noradrenergic neurotransmission in the striatum, are activated under the influence of the elapsed time of social interaction.
2

Aspects of vegetation and soil relationships around athalassohaline lakes of Wadi El-Natrun, Western Desert, Egypt

81%
Abd El Ghani M., Hamdy R., Hamed A.
Journal of Biology and Earth Sciences
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2014
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tom 04
|
nr 1
3

Neural circuits in the central amygdala mediate socially transferred fear

81%
Rokosz K., Hamed A., Kondrakiewicz K., Knapska E.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Social complex behavior, like empathy, emerge over phylogeny from various precursors. One of the simplest is emotional contagion, i.e. sharing emotional states between individuals. Receiving signals of a potential danger may increase chances of survival, thus emotional contagion plays an important role in learning about external environment. The phenomenon is well described at the behavioral level, but the neural circuits necessary for sharing emotions are unknown. We designed a rat model of fear contagion and showed that a brief social interaction with a fearful cage mate promotes risk assessment behavior and activates the central amygdala (CeA) in an otherwise naïve rat. AIM(S): The purpose of this project was to elucidate the role of the CeA circuits involved in socially shared fear. METHOD(S): To investigate the functional outputs of the activated CeA neurons, we mapped neural circuits downstream from the CeA combining anterograde tracing with an imaging of activated neurons in transgenic “Venus” rats. To test the function of CeA “social fear” neurons, we optogenetically stimulated or inhibited subpopulation of CeA neurons activated by social interaction using c-fos-driven targeting of channelrhodopsin and halorhodopsin. RESULTS: In rats that socially shared fear of their partners, we observed strong activation of structures involved in anxiety and motor functions. Most of the activated cells received projections from the CeA. Optogenetic activation of the “social fear” neurons in a social context led to behavioral pattern resembling the one observed during social interaction with a fearful partner. Activation of neurons in non-social context induced exploration and risk assessment behavior (active fear). Inhibition of them had the opposite effects. CONCLUSIONS: The results suggest that the CeA neurons involved in socially transferred fear mediate active fear responses and anxiety-related behaviors in both social and non-social conditions.
4

Immunochtochemical analyses of GAT-1 in "trained" barrel hollows after whisker-shock task

81%
Jasinska M., Pyza E., Hamed A., Siucinska E.
Acta Neurobiologiae Experimentalis
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2011
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tom 71
|
nr S
Classical conditioning, which combines stimulation of a row of facial vibrissae (conditioned stimulus, CS) with a tail shock (unconditioned stimulus, UCS) expands the representation of “trained” whiskers and increases GABAergic measures in the hollows of “trained” barrels in the first somatosensory cortex (SI) of adult mouse. This study investigated how the appearance of the emotional effect of aversive learning (CS+UCS), i.e. aversive conditioned vocalization, affected the expression of puncta of a prominent high-affinity GABA plasma membrane transporter GAT-1 in the barrel cortex of mice 24 h after learning. We detected that application of aversive stimulation to the tail evoked of 6 – 18 kHz audible vocalization episodes. The aversive vocalization conditioned responses (CRs) during the interval in anticipation of the UCS in the first session of CS+UCS training were the largest in number and longest in duration in CS+UCS mice. Learning led to increased expression (54%) of neuronal and astroglial (GAT-1) puncta in the “trained” barrel hollows compared to controls. The electron microscopic observations confirmed that immunoreactivity for GAT-1+ puncta was localized: in single synaptic terminals present on symmetric synaptic specialization, on symmetric synapses of doublesynapse spines, and on astrocytic processes. Our data provide a causal link between vocalization conditioning, GAT-1 localized on GABAergic terminals and astrocyte networks and learning– dependent plasticity in the layer 4 of the adult SI cortex. MNiSW grant NN401018833 to ES.
5

Up-regulation of PI3K‑Akt‑mTOR signaling pathway in neurons affects cognitive functions and social interactions in a mouse model

71%
Chwin N., Kiryk A., Bijoch L., Hamed A., Konopka W.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: The PI3K-Akt-mTOR pathway plays an important role in neuronal plasticity. In normal conditions, activity of this pathway is controlled by Pten phosphatase. AIM(S): We showed that loss of Pten gene in neurons evoked long-term up-regulation of PI3K-Akt-mTOR and temporarily improved learning and memory in mouse models. Moreover, we observed changes in mice vocalization during social interaction and in cellular physiology during electrophysiological recordings. METHOD(S): Mice model: Inactivation of Pten gene was investigated in 2 models: Pten/CaMKCreERT2, and Pten‑flox injected by AAV vectors. The mutation was restricted to forebrain and hippocampal neurons, respectively. Behavioral testing: Both models and respective controls were tested in a learning and memory test in IntelliCage. We measured spatial learning with appetitive behaviors. We also measured the ability to associate an aversive stimulus in the Contextual Fear Conditioning and social interaction in the Three Chamber Sociability and Social Novelty. Life span: Long‑term activity of the PI3K-Akt-mTOR pathway led to increased mortality of Pten/CaMKCreERT2 mutants. RESULTS: IntelliCage: We discovered better performance of Pten/CaMKCreERT2 mutants in the PL task. The memory improvement lasted to even 24 hours before the death. FC task: Mice developed stronger aversive memory than controls, manifested as increased freezing behavior. Both mutant models showed improved cognitive functions, and Pten/CaMKCreERT2 mice showed a decrease life span. CONCLUSIONS: Pten-flox-AAV mice developed enhanced contextual fear memory before neurodegeneration in hippocampus occurred and Pten-flox-AAV mice had intensified vocalizations with disturbed sound architecture in social interactions.
6

The influance of CRF and alpha-hellical CRF(9-41) on rat fear responses and amino acids concentration in the central nucleus of amygdala

51%
Skorzewska A., Bidzinski A., Hamed A., Lehner M., Turzynska D., Sobolewska A., Szyndler J., Maciejak P.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
In the previous study we showed that exogenous CRF (1 μg/rat, icv) enhanced rat-freezing responses and increased expression of CRFrelated immunoreactive complexes in the amygdala. On the other hand, a non-selective CRF receptor antagonist, α-helical CRF(9-41) (10 μg/rat, i.c.v.) decreased rat fear response and increased the concentration of GABA in the amygdala (in vitro). The aim of the present study was to examine the effects of CRF and α-helical CRF(9-41), on the freezing reaction in the conditioned fear test and the release of amino acids in the central nucleus of amygdala (CeA), using microdialysis technique. It was found that CRF increased the concentration of aspartate, glutamate and Glu/GABA ratio in the CeA, an effect that preceded an increased expression of anxiety-like responses, which appeared 15 min after drug administration. α-helical CRF(9-41), decreased rat freezing responses and increased the local concentration of GABA, during the fi rst 30 min of observation. The present data show an important role of CRF in the central nucleus of the amygdala in the integration of anxiety-related, biochemical and behavioural responses, and suggest an involvement of amino acids innervation of the CeA, in the effects of this neurohormone.
7

The valproic acid-induced effects on kynurenine pathway correlate with the changes in the central and peripheral concentration of amino acids

51%
Maciejak P., Szyndler J., Turzynska D., Sobolewska A., Kolosowska K., Lehner M., Wislowska-Stanek A., Skorzewska A., Hamed A., Plaznik A.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Despite its widespread use, the mechanisms of valproic acid (VPA) action are not fully understood. In the current study, we have examined the peripheral and central effects of VPA administration on the metabolic pathway of tryptophan (TRP): concentration of its centrally active metabolites, kynurenine (KYN) and kynurenic acid (KYNA). Moreover, the role of a displacement of TRP from serum albumin binding sites, and changes in the peripheral and central concentration of amino acid including glutamate (GLU), GABA, alanine (ALA), glutamine (GLTM), glycine (GLY), aspartate (ASP), were also studied. We found that VPA administration produced a progressive and strong increase in the central concentration of KYNA, KYN and TRP. Simultaneously, TRP concentration in plasma declined while the peripheral increase of KYNA in plasma was weaker and occurred earlier than in the hippocampus. We also observed that administration of ibuprofen to rats, a prototypic drug used to study drug binding to serum albumin, strongly increased the amount of a free serum and hippocampal TRP concentration, to a degree similar to the effect of VPA. Moreover, we found that the most pronounced changes in the concentration of amino acids caused by administration of VPA include an increase of GLU and a decrease of ALA in the plasma as well as a decrease of ASP and an increase of GABA in the brain. The factor analysis revealed that the changes in the concentrations of TRP, determined both in the plasma and in the hippocampus grouped strongly with the changes in the plasma concentrations of GLU and the central concentration of ASP. Our results showed that administration of VPA strongly modifies the activity of the kynurenine pathway with significant changes in TRP, KYN and KYNA levels in the CNS. The reason for this may be a strong VPA-induced displacement of TRP from its binding sites to plasma albumin. It appears also that the changes in TRP evoked by VPA administration due to competition for transport into the brain, may result in a shift in the central and peripheral balance between branched-chain (BCAA) and aromatic amino acids (AAA). This may lead to a decrease in BCAA transport to the brain, leading to a deficit of BCAAs as a donor of amino groups to the process of GLU resynthesis from pyruvate. Changes in the BCAA/ AAA ratio, arising as a consequence of changes in the TRP level, could explain an observed increase in the plasma concentrations of GLU and a decrease in the ASP concentrations in the brain that occurred after administration of VPA. In sum, given the neuroprotective role of KYNA, the current study suggests that stimulation of the kynurenine pathway may also apply to the central and peripheral concentration of amino acids. The modification of the activity of the kynurenine pathway may at least in part contribute to the related antiepileptic and neuroprotective mechanisms of VPA action.
8

The effects of protein synthesis inhibitor on the expression and re-consolidation on pentylenetetrazol kindler seizuresp.322

42%
Maciejak P., Szyndler J., Turzynska D., Sobolewska A., Taracha E., Skorzewska A., Lehner M., Krzascik P., Hamed A., Bidzinski A., Plaznik A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
In the present study the effects of a protein synthesis inhibitor, cycloheximide (125 μg, i.c.v.), on the expression and reconsolidation of pentylenetetrazol-induced kindled seizures, were studied in rats. Cycloheximide given repeatedly (every second day) to fully kindled rats, immediately after 4 consecutive sessions of PTZ-seizures, did not modify the strength of subsequent fi ts of convulsions. On the other hand, the protein synthesis inhibitor signifi cantly attenuated the strength of convulsions when the drug was administered 1 h before the PTZ injection, every second day for 5 consecutive experimental sessions. However, when cycloheximide was omitted in a consecutive session, PTZ induced a fully developed fi t of tonicclonic convulsions, indicating that cycloheximide-induced changes in seizure intensity were transitory, not related to a stable modifi cation in the function of neuronal circuits responsible for kindling seizures. The present fi ndings suggest that the mechanisms underlying epileptogenesis are very resistant to modifi cation, and as such, are not the subject to permanent changes even under the infl uence of protein synthesis inhibition. One possible reason may be the depth and multiplicity of changes induced by seizures (i.e. alterations in enzymes, receptors, structural proteins, growth factors, etc.), that may cause permanent biochemical and morphological alterations in the brain that give rise to the kindled seizures.
9

Colocalisation of glucocorticoid and 5-HT1A receptor immunoreakrivity-expressing cells in the brain structures of low and high anxiety rats

42%
Lebner M., Taracha E., Maciejak P., Szyndler J., Skorzewska A., Turzynska D., Sobolewska A., Wiskowska-Stanek A., Hamed A., Bidzinski A., Plaznik A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
In recent years we have elaborated an animal model to examine the neurochemical background of differences in the individual responses to conditioned aversive stimuli, using the strength of a rat contextual fear test, as a discriminating variable: low responders (LR), i.e. rats with duration of a freezing response one standard error, or more, below the mean value and high responders (HR), i.e. rats with duration of a freezing response one standard error, or more, above the mean value. It was found that 1.5 h after a testing session of contextual fear test, the LR animals showed a higher density of 5-HT1A and glucocorticoid immunoreactivity-expressing cells (GRsir) in the cortical M2 area and hippocampal dentate gyrus as well as an increased number co-expressing 5-HT1A /GRs-ir in the same areas. The HR rats had a signifi cantly higher concentration of 5-HT1A and GRs-ir in the basolateral amygdala. The present data add more arguments for the neurobiological background of differences in individual responses to aversive conditioned stimuli.
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