Katarzyna Ziętal

Propranolol is a non-selective β-adrenergic receptor antagonist widely used in cardiovascular medicine and anxiety-related conditions; however, its central neurochemical mechanisms remain incompletely understood. This study investigated the effects of long-term propranolol administration on anxiety-like behavior and hypothalamic neurotransmission in rats. Adult male Sprague–Dawley rats received propranolol in drinking water at doses of 1, 2.5, or 5 mg/kg b.w./day for 33 days. Behavioral effects were assessed using the Open Field Test (OF) and Elevated Plus Maze (EPM). Hypothalamic concentrations of amino acids, e.g., γ-aminobutyric acid (GABA) as well as monoamines, and their metabolites were determined by high-performance liquid chromatography with electrochemical detection (HPLC-ED). Long-term propranolol treatment induced a significant anxiolytic-like effect, reflected by increased exploration of open arms in the EPM, without affecting locomotor activity in the OF. Neurochemical analyses revealed a significant increase in hypothalamic GABA levels and a marked reduction in noradrenergic turnover, as indicated by decreased MHPG/NA ratios. Propranolol also increased hypothalamic serotonin concentrations, whereas dopaminergic turnover remained unchanged. These findings demonstrate that long-term propranolol administration produces neurochemical changes within the hypothalamus involving noradrenergic, serotonergic, and GABAergic signaling pathways. The results suggest that the anxiolytic-like effects of propranolol extend beyond β-adrenergic receptor blockade and may be mediated by coordinated modulation of multiple neurotransmitter systems involved in stress regulation and emotional processing. The study provides new evidence linking chronic propranolol exposure to selective hypothalamic neurochemical remodeling associated with reduced anxiety-like behavior.

The study aimed to evaluate the effect of betanin—a bioactive, natural pigment found in beetroot and prickly pear—on cognitive function, motor performance, and neurotransmission in a mouse model of Parkinson’s disease (PD). Aged mice with PD-like symptoms induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were pretreated with betanin (50 or 100 mg/kg b.w./day) via drinking water. Behavioural tests assessed motor skills, anxiety-related behaviour, and spatial memory. Biochemical analyses of central nervous system structures were conducted using high-performance liquid chromatography (HPLC) to determine neurotransmitter levels and metabolites. Betanin improved motor and cognitive functions in MPTP-treated mice. While learning ability remained unchanged, the 50 mg/kg dose alleviated spatial memory deficits. Biochemically, betanin moderately limited dopamine depletion and significantly influenced dopamine metabolism and serotonin levels. These findings suggest that betanin, as a functional food component, may exert neuroprotective effects and support cognitive and motor function in neurodegenerative conditions such as PD.

Parkinson’s disease is one of the most common neurodegenerative disorders characterized by a multitude of motor and non-motor clinical symptoms resulting from the progressive and long-lasting abnormal loss of nigrostriatal dopaminergic neurons. Currently, the available treatments for patients with Parkinson’s disease are limited and exert only symptomatic effects, without adequate signs of delaying or stopping the progression of the disease. Atsttrin constitutes the bioengineered protein which ultrastructure is based on the polypeptide chain frame of the progranulin (PGRN), which exerts anti-inflammatory effects through the inhibition of TNFα. The conducted preclinical studies suggest that the therapeutic implementation of Atsttrin may be potentially effective in the treatment of neurodegenerative diseases that are associated with the occurrence of neuroinflammatory processes. The aim of the proposed study was to investigate the effect of direct bilateral intracerebral administration of Atsttrin using stereotactic methods in the preclinical C57BL/6 mouse model of Parkinson’s disease inducted by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication. The analysis of the dose dependency effects of the increasing doses of Atsttrin has covered a number of parameters and markers regarding neurodegenerative processes and inflammatory responses including IL-1α, TNFα, IL-6, TH, and TG2 mRNA expressions. Accordingly, the evaluation of the changes in the neurochemical profile included DA, DOPAC, 3-MT, HVA, NA, MHPG, 5-HT, and 5-HIAA concentration levels. The intracerebral administration of Atsttrin into the striatum effectively attenuated the neuroinflammatory reaction in evaluated neuroanatomical structures. Furthermore, the partial restoration of monoamine content and its metabolic turnover were observed. In this case, taking into account the previously described pharmacokinetic profile and extrapolated bioavailability as well as the stability characteristics of Atsttrin, an attempt was made to describe as precisely as possible the quantitative and qualitative effects of increasing doses of the compound within the brain tissue microenvironment in the presented preclinical model of the disease. Collectively, this findings demonstrated that the intracerebral administration of Atsttrin may represent a potential novel therapeutic method for the treatment of Parkinson’s disease.