Interrelationship of Psychotherapy, Psychocorrection and Psychoconsultation

Modern neurorehabilitation is focused primarily on the restoration of speech and cognitive mental processes, considering the rehabilitation of the individual as a task of psychotherapy. The article shows that a gentle attitude, a change in "body image" and neurotic experiences, characteristic of most patients with organic brain lesions, significantly affect the effectiveness of neuropsychological rehabilitation. Neurorehabilitation focuses on the restoration of speech and cognitive processes, considering the rehabilitation of the individual as an object of psychotherapy. On the basis of clinical cases, it has been shown that the weakened attitude, body image changes, and neurotic experiences characteristic of most patients with idiophrenic disease affect the effectiveness of neuropsychological rehabilitation. The article examines the theoretical and methodological principles and defines the main concepts of the topic. The relevance of the article is determined by the new innovative social needs in solving problems of a psychological nature, taking into account the neurological features of human thinking. Scientific intelligence in the field of neurorehabilitation provides grounds for determining the most effective methods of psychocorrection. The purpose of the study is to determine the relationship between psychotherapy, psychocorrection and psycho-counseling based on neurorehabilitation. After studying the data, it was determined that the ischemic attack of the brain was unspecified, it was suggested that the observed neurological symptoms (disorders of speech, movements, emotional sphere) are related to residual (residual) symptoms after a transient ischemic attack, which requires a detailed study.</p

Mitochondria Express α7 Nicotinic Acetylcholine Receptors to Regulate Ca2+ Accumulation and Cytochrome c Release: Study on Isolated Mitochondria

Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels that mediate synaptic transmission in the muscle and autonomic ganglia and regulate transmitter release in the brain. The nAChRs composed of α7 subunits are also expressed in non-excitable cells to regulate cell survival and proliferation. Up to now, functional α7 nAChRs were found exclusively on the cell plasma membrane. Here we show that they are expressed in mitochondria and regulate early pro-apoptotic events like cytochrome c release. The binding of α7-specific antibody with mouse liver mitochondria was revealed by electron microscopy. Outer membranes of mitochondria from the wild-type and β2−/− but not α7−/− mice bound α7 nAChR-specific antibody and toxins: FITC-labeled α-cobratoxin or Alexa 555-labeled α-bungarotoxin. α7 nAChR agonists (1 µM acetylcholine, 10 µM choline or 30 nM PNU-282987) impaired intramitochondrial Ca2+ accumulation and significantly decreased cytochrome c release stimulated with either 90 µM CaCl2 or 0.5 mM H2O2. α7-specific antagonist methyllicaconitine (50 nM) did not affect Ca2+ accumulation in mitochondria but attenuated the effects of agonists on cytochrome c release. Inhibitor of voltage-dependent anion channel (VDAC) 4,4′-diisothio-cyano-2,2′-stilbene disulfonic acid (0.5 µM) decreased cytochrome c release stimulated with apoptogens similarly to α7 nAChR agonists, and VDAC was co-captured with the α7 nAChR from mitochondria outer membrane preparation in both direct and reverse sandwich ELISA. It is concluded that α7 nAChRs are expressed in mitochondria outer membrane to regulate the VDAC-mediated Ca2+ transport and mitochondrial permeability transition

The effects of α7-specific ligands and DIDS on Ca²⁺ accumulation in mitochondria studied by flow cytometry.

<p><b>A</b> – purified liver mitochondria gated by size (Forward scatter) and granularity (Side scatter) in flow cytometry. <b>B</b> – binding of 0.1 µM acridine orange 10-nonyl bromide (NAO) to the gated mitochondria population; Control – the non-stained mitochondria. <b>C</b> – Ca²⁺ accumulation in mitochondria loaded with Fluo 3-AM. <b>D</b> – Ca²⁺ accumulated in mitochondria during 2 min after 1 min pretreatment with DIDS, acetylcholine, choline, PNU-282987 or MLA; data are shown as normalized mean fluorescence values of 5 independent experiments for each ligand; * – <i>P<0.05</i> compared to the fluorescence in the absence of α7 nAChR agonists or DIDS.</p

Cytochrome <i>c</i> release into mitochondria supernatants.

<p>Cyt <i>c</i> released from mitochondria in 2 min after addition of either 0.5 mM H₂O₂ or 90 µM CaCl₂ in the presence or absence of DIDS or α7 nAChR ligands. Each column corresponds to M±SE of three independent measurements. Mit – mitochondria without apoptogens; Contr – mitochondria treated with H₂O₂ or CaCl₂ only.</p

Connection of α7 nAChR and VDAC studied by sandwich assays.

<p>The schemes (<b>A, C</b>) and results of direct (<b>B</b>, n = 3) and reverse (<b>D</b>, n = 3) sandwich assays demonstrating the connection of α7 nAChR and VDAC in the outer membranes (OM) of the wild-type (WT) mitochondria. Anti-TOM22 – antibody against mitochondrial outer membrane translocase.</p