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In this work, the Raman spectroscopy mapping technique is used for the analysis of mechanical strain in Bi 2 Se 3 thin films of various (3-400 nm) thicknesses synthesized by physical vapour deposition on amorphous quartz and single-layer graphene substrates. The evaluation of strain effects is based on the correlation analysis of in-plane (E 2 g ) and out-of-plane (A 2 1g ) Raman mode positions. For Bi 2 Se 3 films deposited on quartz, experimental datapoints are scattered along the line with a slope of ∼0.85, related to the distribution of hydrostatic strain. In contrast to quartz/Bi 2 Se 3 samples, for graphene/Bi 2 Se 3 heterostructures with the same thicknesses, an additional negative slope of ∼-0.85, which can be associated with the distribution of the in-plane ( a - b ) biaxial tensile strain due to the film-substrate lattice mismatch, is observed. The algorithm of phonon deformation potential (PDP) calculation based on the proposed strain analysis for the 3 nm thick Bi 2 Se 3 film deposited on the graphene substrate, where the strain is considered to be coherent across the thickness, is demonstrated. The PDPs for biaxial in-plane strain of the Bi 2 Se 3 3 nm film in in-plane and out-of-plane modes are equal to -7.64 cm -1 /% and -6.97 cm -1 /%, respectively., Competing Interests: There are no conflicts to declare., (This journal is © The Royal Society of Chemistry.)

We present Raman studies of graphene films grown on copper foil by atmospheric pressure CVD with n-decane as a precursor, a mixture of nitrogen and hydrogen as the carrier gas, under different hydrogen flow rates. A novel approach for the processing of the Raman spectroscopy data was employed. It was found that in particular cases, the various parameters of the Raman spectra can be assigned to fractions of the films with different thicknesses. In particular, such quantities as the full width at half maximum of the 2D peak and the position of the 2D graphene band were successfully applied for the elaborated approach. Both the G- and 2D-band positions of single layer fractions were blue-shifted, which could be associated with the nitrogen doping of studied films. The XPS study revealed the characteristics of incorporated nitrogen, which was found to have a binding energy around 402 eV. Moreover, based on the statistical analysis of spectral parameters and the observation of a G-resonance, the twisted nature of the double-layer fraction of graphene grown with a lower hydrogen feeding rate was demonstrated. The impact of the varied hydrogen flow rate on the structural properties of graphene and the nitrogen concentration is also discussed.

Arcain and a series of the partial modulators of polyamine binding sites of NMDA receptors (spermine- and adamantyl-containing polyamines IEM-1460, IEM-1490, IEM-1592, IEM-1755) do not display (in contrast to melipramine and memantine) antidepressant-like action in the forced swimming test and reserpine-induced depression test in rats. Compounds IEM-1460, IEM-1490, IEM-1592 increase the total time of immobilization in the Porsolt test, probably, by facilitating the development of stress-induced depression. It is supposed that the prodepressant activity of these compounds is mediated by NMDA-receptors having NR1/NR2C and NR1/NR2D subunit composition.

The experiments on rats showed that IEM-1460, IEM-1490, and IEM-1755 (bisammonium adamantyl-containing compounds possessing fast NMDA channel blocking activity) and polyamines (spermine and arcain) do not alter acquiring of the passive avoidance reaction. All these compounds improve, albeit with different efficacy, the memory traces impaired by scopolamine and/or electroshock: IEM-1755 eliminated amnesia induced by the electroshock, but enhanced the amnesia evoked by scopolamine. Arcain inhibited (for a short time and in a narrow dose range) the antiamnesic effect of IEM-1460. It is suggested that the antiamnesic effect of compounds from both groups is related to the ability of slowing down the NMDA receptor desensitization.

1. A whole-cell patch-clamp study of the effects of ambocarb, a novel nootropic beta-carboline, on sodium currents in rat acutely isolated hippocampal pyramidal neurons was performed. 2. Ambocarb potently and reversibly suppressed sodium currents in a concentration range of 3-300 mumol/L. The amount of block was dependent on the holding potential, with half-maximal inhibition values being 26 and 94 mumol/L at -80 and -120 mV, respectively. 3. Ambocarb induced a hyperpolarizing shift in the steady state availability curve, which indicates an increase in the proportion of inactivated sodium channels. This action is presumably mediated by promoting the development of inactivation and slowing the recovery of sodium channels from inactivation. 4. Because many neuroprotective drugs were shown to inhibit sodium currents, down-modulation of voltage-operated sodium channels that complements the known positive interaction of ambocarb and other related beta-carbolines with GABAA receptors may provide a promising strategy in the treatment of brain disorders associated with trauma and ischaemia.

Serotonin evokes the depolarization and the membrane resistance lowering of rat dorsal root ganglion neurones when a K(+)--conductance of the neuronal membranes is blocked by Cs+ intracellular injection. These 5-HT3-effects ere diminished and removed by preliminary superfusion of the ganglions with saline containing busperone or its structural analogues. The effects of camphorimide analogues of buspirone (campirone, pyricapirone) could not be reproduced in case of the protein kinase A blockade by tolbutamide (100 microM/l). It is suggested that camphorimide analogues are the 5-HT3 receptor blockers while busperone and ipsapirone modulate 5-HT3 receptor affinity by decreasing the protein kinase A activity.

The authors studied the action of lithium ions on the responses of rat dorsal root ganglion neurons and frog spinal motoneurons evoked by monoamine agonists using the microelectrode technique. Lithium ions reversibly inhibit the depolarizing responses of spinal sensory neurons and motoneurons evoked by activation of muscarinic choline-, alpha 1-adreno-, and 5-hydroxytryptamine2 receptors, but enhance the hyperpolarizing neuronal responses evoked by activation of 5-hidroxytryptamine1A receptors.

The nootropic drugs--nootropil, aethimizol, diethylaminoethanol, and ambocarb diminished of amnesia of active avoidance habit evoked by maximal electroconvulsive shock in the rats. At the same time tested nootropic drugs potentiated the frog spinal motoneurons responses mediated by NMDA, but not non NMDA glutamate receptors activation. It was discussed the role of NMDA-potentiating nootropic drugs action in their anti-amnestic action.

The double bath method has been used to study reflex inhibition of cholinergic transmission in the guinea-pig ileum segment. It is shown that adenosine, noradrenaline, 5-methylfurmethide as well as acute hypoxia, which affect the oral part of the intestine are able to evoke two kinds of effects in its anal part firstly, the depression of cholinergic transmission, and secondly, the stimulation of non-adrenergic, non-cholinergic contractions. A preliminary treatment with capsaicin and with hexamethonium on the oral part of the gut prevents these effects, and the chymotrypsin abolishes these effects. A mechanism of this reflex descending inhibition of cholinergic transmission is realised apparently through the stimulation of the chemoreceptors in afferent capsaicin-sensitive nerves with participation of cholinergic interneurons and activation of the inhibitory, most probably vasoactive intestinal peptidergic (VIP) neurons in the enteric plexuses.

By using intracellular technique the authors studied the responses of frog spinal motoneurones and rat dorsal root ganglion evoked by GABA, L-aspartate and dopamine in the presence of 5-hydroxytryptamine and its 1A-agonists or without them. It is shown that buspirone, campirone and serotonin increase the GABA effects but inhibit the effects of aspartate via the GABA- and NMDA-receptors modulation.

Experiments on anaesthetized rats showed that buspirone, its structural analogies (ipsapirone, campirone and levopirone) and active metabolite 1-(2-pyrimidinyl)-piperazine (0.1-30 mg/kg i.v.) produced bradycardia, hyperpnea and changed the arterial pressure level. Arterial pressure either increased or decreased that was determined by its initial level. The hypotension produced by all these drugs was of a central origin and mediated by hydroxytryptamine-1A-receptors. The pressor response resulted from activation of predominantly hydroxytryptamine-2-receptors of vascular smooth muscles.

Monoamines, their agonists and antagonists have been investigated for their influence on responses of spinal motoneurons in frog mediated by NMDA-glutamate receptors (late components of dorsal root polysynaptic EPSP's and depolarizing responses evoked by L-aspartate). Monoamine responses which promoted an increase of intracellular concentration of cAMP and Ca2+ in the motoneurons (activation of alpha- and beta-adrenoreceptors, D1-dopamine and 5-hydroxytryptamine-receptors) reinforced the studied spinal motoneuron responses of frog. These responses were weakened by the monoamine action which led to a decrease of the intracellular concentration of cAMP and Ca2+ (activation of D2-dopamine and 5-hydroxytryptamine1A-receptors). The monoamine effects were inhibited by specific monoamine antagonists, tolbutamide and trifluoperazine. It is supposed that NMDA receptor-channel complex is exposed by cAMP- and Ca(2+)-calmodulin-dependent phosphorylation induced by activation of membrane monoamine receptors.

The anxiolytic activity of serotonin agonists (buspirone, ipsapirone, campirone, caplapirone, 1-pyrimidinyl-piperazine) determined in rats on 3 experimental models of anxiety closely correlates with the degree of inhibition of impulse release of 3H-serotonin by electrically stimulated slices of the midbrain raphe dorsal nucleus (r = +0.85) but not the slices of the cerebral hemispheric cortex (r = +0.60) of the rats. The anxiolytic activity of neuroleptics (chlorpromazine, trifluorperazine), antidepressant (amitriptyline, imipramine) and beta-carbolines (harmane, 3.4-tetramethyleneharmane) corresponds well (r = +0.94) to the ability of the drugs to potentiate the hyperpolarizing effects of serotonin in the rat sensory ganglion.

The hypothermic activity of 8-OH-DRAT, 1-(2-pyrimidinyl) piperazine (1-PP), buspirone and its structure analogues tightly correlates with the degree of inhibition of 3H-serotonine release by electrically stimulated dorsal raphe slices (r = 0.84), but not cerebral cortex slices (r = 0.66). The pretreatment of mice with p-chlorphenylalanine decreased the hypothermic effects evoked by 8-OH-DRAT, buspirone, campirone (but not 1-PP) only in first 30 min after there injection. It was concluded that hypothermic effects of 8-OH-DRAT, buspirone and its structure analogues were bound with preferable influence as partial agonists on the postsynaptic serotonine 1A receptors. Ipsapirone as a partial agonist has maximal antagonistic activity.

Influence of microinjections of monoamines and glutamic acid into the caudate nucleus head on conditioned food-procuring reaction was studied in experiments on rats. Dopamine, noradrenaline and glutamic acid prolong the latency of the reflex, while serotonin reduces it. However, all the drugs tested reduce the number of conditioned food-procuring movements. The effects of dopamine are achieved through neurone receptors of the caudate nucleus which are sensitive to haloperidol and chlorpromazine; effects of serotonin are mediated through the D-serotoninoreactive systems, and those of noradrenaline, through the alpha-adrenoreactive systems of the neostriatum neurones. The inhibitory effect of glutamic acid is not due to the action on the serotonino-, adreno-, or dopamine receptors of caudate units.

The experiments on rats have shown that antidepressant concentrations that cause 50% inhibition of 14C-NA and 3H-HT uptake by brain slices remain unchanged following prolonged administration of antidepressants (imipramine, pirazidole, harmane and its derivatives--C-153, C-307, C-394, C-395), as compared to the control. Electrical stimulation of brain slices upon long-term treatment of rats with antidepressants and preincubation with 14C-NA and 3H-HT enhanced presynaptic release of radioactive mark at concentrations of antidepressants (EC2) 3-14 times lower than those in the control animals. Long-term antidepressant administration reduces the inhibitory influence of clonidine and HT on presynaptic release of 14C-NA and 3H-HT by brain slices. It is suggested that long-term administration of antidepressants decreases the sensitivity of terminal axons of NA- and HT-ergic neurons to autoinhibitory effect of neurotransmitter release.

In experiments on rats the anxiolytic activity of 1-(2-pyrimidinyl)-piperazine (PP) was revealed only in some models of anxiety states, although diazepam was effective in all used models. In contrast to diazepam, PP exerts the anesthetic-potentiating and myorelaxant effects only when administered in subtoxic doses and possesses no anticorazole activity. The facts testifying to the serotoninergic mechanisms of the anxiolytic action of 1-(2-pyrimidinyl)-piperazine are presented.

It is established that beta-phenyl-GABA (phenibut) and partly GABA elicit direct depolarization of the isolated spinal cord motoneurons. The depolarizing effect of phenibut and a depolarizing component of GABA action do not alter in the presence of picrotoxin (10(-5) mol/l) and in the chloride-deficient medium. This depolarizing phenibut effect which is not bound with activation of GABAA-receptors and chloride channels coupled with them does not alter in Na+-deficient medium, enhances in the medium with excess of K+ ions (10 mol/l) and in presence of imidazol (5 . 10(-4) mol/l) and is completely abolished in the Ca2+-deficient medium with 2 mmol/l of Mn2+ or in the presence of 10(-4) mol/l theophylline. It is supposed that phenibut and partly GABA diminish intracellular concentration of cAMP via GABAB-receptor activation and decrease functional activity of voltage-dependent Ca2+-ionic channels and Ca2+-activated outward K+-currents.

Microinjection of dopamine and serotonin into the dorso-medial portions of the amygdalic complex of rats increased the latent period of conditioned defense and motor food reactions, spontaneous motor activity, the number of jerks and the value of the conditioned food reflex. Noradrenaline failed to influence the recorded indices of the conditioned food-procuring reflex, but facilitated the conditioned reaction of avoidance, significantly shortening its latent time. The results obtained pointed to the specificity of the neurochemical mechanisms realizing at the level of the amygdalic complex conditioned reflexes of various biological modality in rats.

Dopamine and phenylephrine decreased the tone of the smooth muscles of the isolated rat stomach strips in concentractions of 10(-6) M and higher. The curves of the concentration-effect have the same slope. Dopamine effects are unchanged in the presence of propranolole (5.10(-6) g/ml). Phentholamine (as well as dihydroergotamine and tropaphen) shows an equal degree of antagonism towards both phenylephrine and dopamine. It is suggested that dopamine and phenylephrine relax the stomach muscles by influencing the alpha-adrenoreceptors. The latter differe from alpha-adrenoreceptors of the ejaculatory duct of rats by a high sensitivity to the blocking influence of some neuroleptics--haloperidol, trifluoperazine, chlorpromazine, pA2 for which (8.11--8.64) is of the same range as pA2 for alpha-adrenolytic drugs (7.76--8.46). The features of resemblance and difference between alpha-adrenoreceptors of the gastrointestinal tract muscles and the inhibitory dopamine receptors of the nerve cells are being discussed.

It is shown that the interuption of sympathetic nerves in the smooth muscles of the deferent duct or ejejunum of rats achieved by a 4-day keeping of the duct in cold or by the reserpine treatment of the animals does not produce any essential effect on the dopamine action. The contraction of smooth muscles in the isolated deferent duct, mesenteric and renal vessels of rats is effectively eliminated by alpha-andrenolytics (dihydroergotoxin, phentolamine), while the inhibitory effects of dopamine (lowering of vasotonicity of the rats' jejunum tone) are suppressed with propranolol. Galoperidol and methylergometrin display in experiments with smooth muscle organs but a low degree of antagonism to dopamine. The activity of phentolamine as an antagonist of norepinephrine and dopamine in the deferent duct is identical.

In concentrations of 10(-9)-10(-7) g/ml acetylcholine increased the tone of the smooth muscles of the longitudinal band of the large intestine of a guinea pig, increasing the permeability of the cellular membranes for the entering flux of 45Ca2+. In concentrations of 10(-6) g/ml and over acetylcholine caused a release of the membranous calcium and in the concentrations of 10(-5)-10(-3) g/ml markedly increased the permeability of the membranes of the smooth muscle cells for the 22Na+ ions causing depolarization and an increase in the frequency of the action potentials. It is supposed that the coupling of the cholinergic stimulus with the end effect (muscle contraction) included 3 components: intensification of the entrance of Ca2+ into the smooth muscle cells, release of the membrane calcium and adhesion mechanism.

It has been demonstrated in experiments on rats under conflict situation that intraperitoneal injection of harman in high doses (20 mg/kg) counteracts and, in low doses (1 mg/kg), potentiates the anxiolytic effect of diazepam. A possible mechanism of the dual effect of harman on the anxiolytic action of diazepam is discussed.

GABA, glycine and beta-alanine depolarized motoneurons and primary afferents of the isolated spinal cord of rats of 10-14-day age. The blockade of synaptic transmission in the spinal cord by abundant Mg++ ions turns the depolarization into hyperpolarizing responses. Depolarization of the primary afferents evoked by glycine is antagonized by strychnine, picrotoxin reduces the GABA effects, and both convulsants diminish the beta-alanine effects. Neural amino acids reduce both ventral and dorsal root potentials. Strychnine and picrotoxin increase the amplitude and duration of ventral root potentials. Picrotoxin decreases the amplitude of dorsal root potentials.

1-(N-piperidine-acetyl)-2,3-dihydroindoles display high activity in infiltration and conduction anestheia, exceeding that of trimecaine. N-alkylaminoacetyl-indolines are moderately active, while N-morpholine and N-indolylacetyl-indolines are practically inactive when employed in the given types of local anesthesia. All the N-substituted aminoacetyl-indolines are little active in terminal anesthesia.

In the experiments on synaptosomes from the caudate nucleus of the rat brain, neuroleptic drugs (6 types) were found to inhibit the Na, K-ATPase activity considerably stronger (13-51 times, as compared to IC16 values) in the presence of Ca2+ ions (0.25 mM) than in their absence. The enhancement of the inhibitory activity was due to a decrease in the negative cooperation of neuroleptic interaction with the enzyme seen in the absence of Ca2+.

Experiments were conducted on the supeior cervical and the caudal mesenteric sympathetic ganglia of a cat; it was shown that dophamine (DA), similarly to noradrenaline (NA) and adrenaline (A), depressed the cholinergic conduction. The activity of DA in the superior sympathetic ganglion was less than that of the NA and A 2- and 3-fold, respectively, and in the caudal mesenteric ganglia DA was 50 times more active than NA by the capacity to depress the cholinergic conduction. The effects of DA and NA in the superior cervical ganglia were eliminated by dyhydroergotamine, phentholamine and haloperidol, but not by tropaphen and chlorpormazine. In the caudal mesenteric ganglia the inhibitory effect of NA was decreased by phentholamine, dihydroergotamine and chlorpromazine, but not by haloperidol. On the contrary, haloperidol and chlorpromzine decreased the depressive effect of DA on the cholinergic conduction in the caudal mesenteric ganglion, whereas phentholamine, dihydroergotamine and deseryl proved to be ineffective. It is supposed that the manifestation of the dopaminergic mechanism of inhibition of cholinergic conduction in the caudal mesenteric sympathetic ganglion could underlie the dilatation of the mesenterial and renal vessels and its hypotensive action caused by DA.

Experimenting on the slices of cortex and dorsal raphe nucleus of midbrain of rats which were incubated with 3H-hydroxytrypta-mine (3H-HT) studies showed the influence of series of serotonin agonists on the spontaneous and electrically stimulated release of 3H-HT from the slices. It was established that the serotonin in concentration of 10(-5) mol/l similarly inhibits the release of 3H-HT from the electrically stimulated slices of the brain cortex (78.6%) and on slices of the dorsal raphe nucleus of the midbrain (81.6%) had no effect on the spontaneous release of serotonin. The serotonin agonists in order of increasing ability to inhibit the electrically stimulated release of 3H-HT from the cortex slices is as follows: ipsapirone (0%), 8-OH-DPAT (23%), kampirone (26.5%), 1.2-PP (28.6%), kaplapirone (35.7%), buspirone (48%) and TFMPP (67%). On the ability to influence the release of 3H-HT from the electrically stimulated slices of the dorsal raphe nucleus of the midbrain of the rats serotonin agonists were in the following order: TEMPP (12.3%), kampirone (40%), 1.2-PP (42.9%), ipsapirone (52%), 8-OH-DPAT (54.1%), kampirone (57.2%) and buspirone (65.3%). It is suggested that the effect of both ipsapirone, kampirone and 8-OH-DPAT is greatly localized on the somato-dendritic synapses P1A-HT receptors, TEMPP is more on the terminal axons of HT-ergic neurones while kampirone, buspirone and active metabolite 1.2-PP act on the presynaptic and somatodendritic autoreceptors of serotonin.

It has been established in experiments on the isolated spinal cord of 7-14-day-old rats that the GABAB-mimetic phenibut (10(-5)--10(-4) M) elicits a slow-developing depolarization of motoneurons, suppression of spontaneous activity and polysynaptic reflex discharges of motoneurons, recorded from the ventral roots. Administered under the same conditions GABA produces de- and hyperpolarization of motoneurons. The depolarization of motoneurons elicited by phenibut and GABA is not reversed by picrotoxin in contradistinction to the GABA-induced hyperpolarization of motoneurons, being associated with a direct action of the GABA-mimetics on postsynaptic GABAB receptors of motoneurons. Diazepam (10(-9)--10(-6) M) potentiates the effects of phenibut supposedly via benzodiazepine receptors bound with GABAA receptors (an independent interaction).

In experiments on the isolated ileum of guinea pigs and rats it was shown that 1,3-dipropyl-8-phenylxanthine (DPPX) is a highly potent adenosine antagonist blocking A1-adenosine receptors of the myenteric plexus (pA2 = 7.29 +/- 0.06) and allosterically modulating affinity of A2-receptors of the intestinal smooth muscles to adenosine (pA2 = 6.64 +/- 0.05). DPPX exerted no influence on purinergic (PR2), adrenergic and opiate receptors of the nervous and muscular cells of the intestine. Exceeding the activity of theophylline by 339-87 times, DPPX failed to exert the selective effect on A1- and A2-subtypes of adenosine receptors.

The experiments on the isolated guinea-pig ileum have shown that the contractions caused by low frequency transmural stimulation are decreased by adenosine, baclofen, clofelin and morphine. Theophylline is a competing antagonist of adenosine and a noncompeting antagonist of baclofen, clofelin and morphine. The effects of the latter are not altered by 1,3-dipropyl-8-phenylxanthine suppressing adenosine effects. It is concluded that presynaptic effects of baclofen, clofelin and morphine depend on cAMP level in cholinergic neurons of myenteric plexus.

The ionic nature of neuronal postsynaptic responses to monoamines, aminoacids and the substance P was studied in the newborn rat isolated spinal cord. The responses of motoneurons to GABA, glycine, noradrenaline and dopamine appeared to be Cl-dependent. The depolarization of motoneurons induced by L-glutamate and 5-hydroxytryptamine was Na-dependent whereas the same response to the substance P was Cl-dependent. Primary afferent depolarization with GABA is Cl-dependent whereas if induced by glycine and 5-hydroxytryptamine it is Na-dependent. Neurochemical and ionic profiles of mono- and polysynaptic ventral and dorsal root potentials are discussed.