ACTA NEUROBIOLOGIAE EXPERIMENTALIS (ISSN: 0065-1400 (PRINT), EISSN: 1689-0035) 涵盖神经科学的各个方面，从神经系统的分子和细胞神经生物学，到细胞和系统电生理学、脑成像、功能和比较神经解剖学、发育以及神经系统、行为和神经心理学向大脑衰老和病理学的演变，包括神经信息学和建模。

Acta Neurobiologiae Experimentalis covers various aspects of neuroscience, ranging from molecular and cellular neurobiology of the nervous system to cellular and systems electrophysiology, brain imaging, functional and comparative neuroanatomy, development, as well as the evolution of behavior and neuropsychology related to brain aging and pathology, including neuroinformatics and modeling.

《Acta Neurobiologiae Experimentalis》涵盖神经科学的各个方面，包括神经系统的分子和细胞神经生物学、细胞和系统电生理学、脑成像、功能和比较神经解剖学、发育、神经系统的行为和神经心理学，以及大脑衰老和病理学的演变，涉及神经信息学和建模等领域。

Acta Neurobiologiae Experimentalis

The concept that neural information is encoded in the firing rate of neurons has been the dominant paradigm in neurobiology for many years. This paradigm has also been adopted by the theory of artificial neural networks. Recent physiological experiments demonstrate, however, that in many parts of the nervous system, neural code is founded on the timing of individual action potentials. This finding has given rise to the emergence of a new class of neural models, called spiking neural networks. In this paper we summarize basic properties of spiking neurons and spiking networks. Our focus is, specifically, on models of spike-based information coding, synaptic plasticity and learning. We also survey real-life applications of spiking models. The paper is meant to be an introduction to spiking neural networks for scientists from various disciplines interested in spike-based neural processing.

Filip Ponulak 2

Andrzej Kasinski

Introduction to spiking neural networks: Information processing, learning and applications

脉冲神经网络导论：信息处理、学习和应用

Piperine is an amide alkaloid isolated from the black pepper plant. This study examined the pain‑relieving activity of piperine against paclitaxel (PTX)‑induced neuropathy. Male mice were divided into 6 groups: Sham‑operated group (remained intact), PTX group (PTX‑treated mice receiving normal saline), PTX+ piperine 10, 25, and 50 mg/kg groups (PTX‑treated mice receiving piperine) and positive control group (PTX‑treated mice receiving imipramine 10 mg/kg). Neuropathic pain was induced by PTX 2 mg/kg/day on days 1, 3, 5 and 7. On day 7, behavioral tests were conducted and serum levels of interleukin‑6 (IL‑6), tumor necrosis factor‑alpha (TNF‑α), malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) were assayed. PTX produced significant thermal hyperalgesia compared to the sham group. Piperine at all doses alleviated neuropathic pain, and significantly decreased IL‑6, TNF‑α, and MDA, but induced CAT and SOD activities compared to the control group. Piperine could confer beneficial effects against neuropathic pain, at least partially, via reduction of inflammatory and oxidative stress markers.

Toktam Sahranavard

Vahideh Ghorani

Fatemeh Forouzanfar

Samaneh Sadat Asadi Kakhki

Ebrahim Nikfar Dastaki

Ebrahim Golmakani

Ramin Rezaee

Piperine relieves neuropathic pain induced by paclitaxel in mice

胡椒碱缓解小鼠由紫杉醇引起的神经性疼痛

The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene is a critical tumor suppressor that plays an essential role in the development and functionality of the central nervous system. Located on chromosome 10 in humans and chromosome 19 in mice, PTEN encodes a protein that regulates cellular processes such as division, proliferation, growth, and survival by antagonizing the PI3K‑Akt‑mTOR signaling pathway. In neurons, PTEN dephosphorylates phosphatidylinositol‑3,4,5‑trisphosphate (PIP3) to PIP2, thereby modulating key signaling cascades involved in neurogenesis, neuronal migration, and synaptic plasticity. PTEN is crucial for embryonic neurogenesis, controlling the proliferation of neural progenitor cells and guiding the migration and proper lamination of neurons in cortical and hippocampal structures. It also regulates dendritic growth and axon guidance, ensuring correct neuronal connectivity. In postnatal neurogenesis, PTEN maintains the balance of stem cell proliferation and integration of new neurons into existing circuits, particularly in the hippocampal dentate gyrus. Animal models with PTEN deletion or mutation exhibit significant structural and functional neuronal abnormalities, including enlarged soma and dendritic hypertrophy, increased synaptic density, and altered synaptic plasticity mechanisms such as long‑term potentiation and long‑term depression. These changes lead to deficits in learning and memory tasks, as well as impairments in social behaviors. PTEN mutations are associated with neurodevelopmental disorders like intellectual disability, epilepsy, and autism spectrum disorders accompanied by macrocephaly. Understanding PTEN’s mechanisms offers valuable insights into its contributions to neurodevelopmental disorders and presents potential therapeutic targets for cognitive impairments and neurodegenerative diseases. Future research should focus on elucidating PTEN’s functions in mature neurons and its influence on established neuronal networks, which may have significant implications for memory enhancement and behavioral modifications.

Natalia Chwin

Anna Kiryk

The integral role of &lt;i&gt;PTEN&lt;/i&gt; in brain function: from neurogenesis to synaptic plasticity and social behavior

PTEN在脑功能中的整体作用：从神经发生到突触可塑性及社会行为

Both cannabinoid and opioid receptors are involved in pain behavior. The administration of morphine and cannabis in rats has been shown to decrease thyroid weight and thyroid‑stimulating hormone (TSH) levels. We hypothesized that the third ventricle, due to its adjacency to the hypothalamus, is involved in the modulation of hypothalamic‑pituitary‑thyroid axis activity and descending pain pathways. The present study examined the effect of intra‑third ventricle administration of morphine and cannabis agents on the modulation of pain behavior in normal, hypothyroid (increased serum TSH), and hyperthyroid (decreased serum TSH) rats using the tail‑flick test. The results indicated that intra‑third ventricle injection of AM251 (CB1 receptor antagonist) caused hyperalgesia, while intra‑third ventricle administration of ACPA (CB1 receptor agonist) and morphine produced analgesia in normal, hypothyroid, and hyperthyroid rats. A non‑effective dose of morphine (0.5 μg/rat) did not attenuate hyperalgesia induced by an effective dose of AM251. Co‑injection of ACPA and morphine into the third ventricle induced anti‑nociceptive effect in normal, hypothyroid, and hyperthyroid rats. An isobolographic analysis demonstrated a synergistic effect between ACPA and morphine in the production of the anti‑nociceptive effect. Consequently, the third ventricle may modulate pain behavior induced by cannabinoid and opioid receptors via descending pain pathways in normal, hypothyroid, and hyperthyroid rats.

Mohammad‑Reza Zarrindast

Fatemeh Khakpai

A synergistic analgesic effect of morphine in combination with the CB1 receptor agonist, ACPA, in normal, hypothyroid, and hyperthyroid male rats

吗啡与CB1受体激动剂ACPA联合使用对正常、甲状腺功能减退和甲状腺功能亢进雄性大鼠的协同镇痛作用

This study investigated the effects of sub‑chronic administration of lead (Pb) acetate on thiobarbituric acid reactive substances (TBA‑RS), total sulfhydryl content, protein carbonyl content, antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GSH‑Px]), acetylcholinesterase (AChE), and Na+K+‑ATPase in the cerebral structures of rats. Male Wistar rats aged 60 days were treated with saline (control group) or Pb (treatment group), at various doses, by gavage, once a day for 35 days. The animals were sacrificed twelve hours after the last administration, and the cerebellum, hippocampus and cerebral cortex were removed. The results showed that Pb did not alter the evaluated oxidative stress parameters. Furthermore, Pb (64 and/or 128 mg/kg) altered SOD in the cerebellum, cerebral cortex and hippocampus. Pb (128 mg/kg) altered CAT in the cerebellum and cerebral cortex and GSH‑Px in the cerebral cortex. Also, Pb (64 mg/kg and 128 mg/kg) altered GSH‑Px in the cerebellum. Moreover, Pb (128 mg/kg) increased AChE in the hippocampus and decreased Na+K+‑ATPase in the cerebellum and hippocampus. In conclusion, sub‑chronic exposure to Pb (occupational and environmental intoxication) altered antioxidant enzymes, AChE, and Na+K+‑ATPase, contributing to cerebral dysfunction.

Magda Helena Soratto Heitich Ferrazza

Débora Delwing‑Dal Magro

Eloise Salamaia

Thales Ercole Guareschi

Luis Felipe Fernandes Erzinger

Thayná Patachini Maia

Cassiana Siebert

Tiago Marcon dos Santos

Angela Terezinha De Souza Wyse

Gabriela Borgmann

Katherine Plautz

Daniela Delwing‑de Lima

Sub‑chronic administration of lead alters markers of oxidative stress, acetylcholinesterase and Na+K+‑ATPase activities in rat brain

亚慢性铅暴露对大鼠脑中氧化应激标志物、乙酰胆碱酯酶和Na+K+‑ATP酶活性的影响

Brain-derived neurotrophic factor (BDNF) is involved in the maintenance of dopamine level and the survival of dopaminergic neurons, which may affect the functionality of brain structures responsible for motor and cognitive function. The aim of the study was to assess the association of individual and combined single nucleotide polymorphism (SNP) in the rs6265 BDNF (Val66Met), rs397595 DAT (SLC6A3), and rs4680 COMT (Val158Met) genes with early‑onset of Parkinson’s disease (PD) patients. Moreover, we assessed the association between the BDNF Val66Met polymorphism and the level of BDNF protein in the serum of patients with PD and controls. The study involved 163 patients with idiopathic PD divided into early onset (&lt;55 years) and late‑onset (&gt;55 years) groups and 91 healthy age‑matched people (Control). The SNP were determined using the TaqMan Real‑Time PCR method. Serum BDNF levels were determined by ELISA assay. The risk of developing early PD in people with the BDNF genotype AG increases threefold in comparison with the carriers of the BDNF genotype GG. In PD patients and healthy people with the BDNF genotypes AG and AA, a lower serum BDNF level was found compared to those with the BDNF genotype GG in both groups. The results of our study indicate that the presence of the Val66Met BDNF gene polymorphism is associated with reduced blood BDNF levels and an elevated risk of developing early‑onset PD. This effect appears to be more pronounced in men.

Iwona Przybylska

Jarosław Marusiak

Beata Toczyłowska

Adam Stępień

Bogdan Brodacki

Józef Langfort

Małgorzata Chalimoniuk

Association between the Val66Met (rs6265) polymorphism of the brain-derived neurotrophic factor (BDNF) gene, BDNF protein level in the blood and the risk of developing early‑onset Parkinson’s disease

脑源性神经营养因子基因Val66Met (rs6265)多态性、血清BDNF蛋白水平与早发性帕金森病发病风险的相关性

Alzheimer’s disease (AD) is an age‑related, progressive decline in cognitive ability. Accumulation and deposition of amyloid‑β (Aβ) is still the best‑known cause of AD that worsens over time. It is unclear whether the increase in Aβ production or the inefficiency of the degradation system causes the accumulation of β‑fibrils during AD development. This research investigated Aβ‑producing and clearance pathways in different stages of AD. For this purpose, patients were categorized into four experimental groups: patients with mild cognitive impairment, patients with moderate cognitive decline, patients with very severe cognitive decline, and healthy patients as control. Levels of Aβ‑40, soluble amyloid precursor protein beta (sAPPβ), matrix metalloproteinase‑9 (MMP‑9), matrix metalloproteinase‑3 (MMP‑3), neprilysin (NEP), angiotensin‑converting enzyme (ACE), and insulin‑degrading enzyme (IDE) were determined by ELISA kits and immunoblotting in serum samples. According to the results, the levels of Aβ‑40 and sAPPβ increased in AD patients from an early stage, and levels were maintained in progressive AD stages. MMP‑9 also increased in the early stage, but its content decreased with disease development. MMP‑3 was significantly higher in the three stages of AD compared to the control patients. However, IDE, NEP, and ACE enzymes as clearing systems decreased in all studied AD samples, with their reductions more remarkable in the middle and late stages. The results showed that multiple Aβ‑degrading enzymes such as NEP and IDE in AD patients decline as AD progresses, while Aβ‑40 and sAPPβ increased from the early stage of the disease. Therefore, it could be concluded that detection of the dementia phase is a critical step for therapeutic strategies.

Sinan Yousif Saleh

Leila Sadeghi

Gholamreza Dehghan

Investigation of amyloid‑β peptide production and clearance pathways in different stages of Alzheimer’s disease

阿尔茨海默病不同阶段中淀粉样β肽生成与清除途径的研究

The thalamic reticular nucleus controls information processing in thalamocortical neurons. GABAergic neurons present in this nucleus express the α3 subunit of post‑synaptic GABAA receptors, which bind GABA from globus pallidus neurons. Pallidal neurons, in turn, have dopaminergic D4 receptors in their axon terminals. The thalamic reticular nucleus connects reciprocally with the thalamus, and it receives afferents from the brain cortex, as well as from other brain structures that have an important role in the modulation of the thalamic network. Based on the above, the purpose of this study was to assess the electrophysiological and molecular effects of unilateral lesion of the globus pallidus on the electric activity of the thalamic reticular nucleus. Two‑month‑old male rats were used. The right globus pallidus was lesioned with quinolinic acid. Seven days after the lesion, ipsilateral turning was registered, confirming the lesion. Afterward, electrophysiological evaluation of the right thalamic reticular nucleus’ electrical activity was performed. Subsequently, mRNA expression for D4 receptors and subunit α3, as well as protein content were assessed in the right reticular nucleus. Pallidum lesion caused an increase in firing frequency and decreased firing bursts of reticular neurons. In addition, dopaminergic D4 mRNA, as well as protein increased. In contrast, GABAergic GABAA subunit α3 expression was suppressed, but protein content increased. These results show that the globus pallidus regulates firing in reticular neurons through D4 receptors and subunit α3 of GABAA receptor in the reticular nucleus of the thalamus.

Lizette Montoya-Gress

Lizbeth Juárez-Rojas

Julio Almanza-Pérez

Eunice Farfán-García

Luis Gómez-Quiroz

Mehdi Ommati

Reza Heidari

Enrique Querejeta-Villagómez

Alberto Alatorre-Pérez

Socorro Retana-Márquez

Changes in D&lt;sub&gt;4&lt;/sub&gt; and GABA&lt;sub&gt;A&lt;/sub&gt; subunit α3 receptors in the thalamic reticular nucleus caused by unilateral lesion of the globus pallidus

苍白球单侧损伤引起的丘脑网状核D<sub>4</sub>和GABA<sub>A</sub>亚基α3受体变化

Abbreviation	Acta Neurobiol Exp (Wars)
Journal Impact	1.50
Quartiles(Global)	NEUROSCIENCES(Q4)

Publication Information	Publisher: Nencki Institute of Experimental Biology，Publishing cycle: Quarterly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1970，Proportion of original research papers: 98.00%，Self Citation Rate:0.00%， Gold OA Rate: 89.57%
Average review cycle	网友分享经验：>12周，或约稿
Average recruitment ratio	网友分享经验：较易

Acta Neurobiologiae Experimentalis

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Introduction to spiking neural networks: Information processing, learning and applications

Piperine relieves neuropathic pain induced by paclitaxel in mice

The integral role of <i>PTEN</i> in brain function: from neurogenesis to synaptic plasticity and social behavior

A synergistic analgesic effect of morphine in combination with the CB1 receptor agonist, ACPA, in normal, hypothyroid, and hyperthyroid male rats

Sub‑chronic administration of lead alters markers of oxidative stress, acetylcholinesterase and Na+K+‑ATPase activities in rat brain

Piperine relieves neuropathic pain induced by paclitaxel in mice

The integral role of <i>PTEN</i> in brain function: from neurogenesis to synaptic plasticity and social behavior

Association between the Val66Met (rs6265) polymorphism of the brain-derived neurotrophic factor (BDNF) gene, BDNF protein level in the blood and the risk of developing early‑onset Parkinson’s disease

Investigation of amyloid‑β peptide production and clearance pathways in different stages of Alzheimer’s disease

Changes in D<sub>4</sub> and GABA<sub>A</sub> subunit α3 receptors in the thalamic reticular nucleus caused by unilateral lesion of the globus pallidus

ISSN	0065-1400, 1689-0035
h-index	60