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  • 1
    Electronic Resource
    Electronic Resource
    R 28935 and prazosin: Effects on central and peripheral alpha-adrenoreceptor activity and on blood pressure (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 302 (1978), S. 299-306 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline ; Dopamine ; Alpha-adrenoreceptors ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effects of erythro-1-{1-[2-(1,4-benzodioxan-2-yl)-2-hydroxyethyl]-4-piperidyl}-2-benzimidazolinone (R 28935), prazosin and phenoxybenzamine on the clonidine-induced increases in the flexor relfex activity and in the blood pressure of rats were used to study their influence on postsynaptic α-adreno-receptors centrally and peripherally, respectively. R 28935 was more potent in blocking the central than the peripheral α-adrenoreceptors whereas the two receptor types were inhibited to about the same degree following prazosin and phenoxybenzamine. 2. The amphetamine-induced rotation of rats with unilateral inactivation of the corpus striatum and the apomorphine-induced stimulation of the motor activity of mice were inhibited by R 28935, but not by prazosin, indicating that R 28935 can block postsynaptic dopaminergic receptors. 3. The α-methyltyrosine-induced disappearance of noradrenaline in the brain and the spinal cord of rats was only slightly accelerated by prazosin but was more effectively accelerated by R 28935 and phenoxybenzamine. The deceleration by clonidine of the α-methyltyrosine-induced disappearance of noradrenaline was partially inhibited by R 28935 but was not influenced by prazosin indicating that central α-autoreceptors (presynaptic α-receptors) are only weakly blocked by R 28935 and not at all blocked by prazosin. 4. The blood pressure of intact rats was lowered by prazosin and phenoxybenzamine at doses effectively blocking vascular α-adrenoreceptors. On the other hand, R 28935 caused hypotension at doses blocking central but not peripheral α-adrenoreceptors suggesting that the hypotension might be due to inhibition of central noradrenergic neurotransmission.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508299
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of locally applied dopamine to the nucleus accumbens on the motor activity of normal rats and following α-methyltyrosine or Reserpine (1979)
    Springer
    Psychopharmacology 63 (1979), S. 203-206 
    Details
    ISSN: 1432-2072
    Keywords: Dopamine ; Nucleus accumbens ; Autoreceptors ; Release by nerve impulses
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The motor activity of rats was investigated following bilateral application of various doses (0–80 μg) of dopamine to the nucleus accumbens. A high dose (80 μg) of dopamine increased the motor activity of normal as well as α-methyltyrosine- and reserpine-treated rats. It also increased the late motor activity (6–9 min) of normal rats, probably due to stimulation of postsynaptic dopamine receptors. Lower doses (10–40 μg) of dopamine suppressed initial (0–3 min) motor activity of normal rats, perhaps due to stimulation of dopamine autoreceptors on the dopamine nerve terminals in the nucleus accumbens with a subsequent inhibition of dopamine neurotransmission. An intermediate dose (40 μg) of dopamine was able to restore the motor activity of α-methyltyrosine-treated but not of reserpine-treated rats at all time intervals. This difference, indicating a restoration of the normal pattern of habituation by dopamine only in animals pretreated with α-methyltyrosine, suggests that normal behaviour is dependent on release of dopamine by nerve impulses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00433550
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  • 3
    Electronic Resource
    Electronic Resource
    A functional effect of dopamine in the nucleus accumbens and in some other dopamine-rich parts of the rat brain (1975)
    Springer
    Psychopharmacology 45 (1975), S. 139-149 
    Details
    ISSN: 1432-2072
    Keywords: Locomotor activity ; Nucleus accumbens ; Caudate nucleus ; Local application ; Dopamine ; Noradrenaline ; Amphetamine ; Neuroleptics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Dopamine (5 to 50 Μg) applied bilaterally to the nucleus accumbens of reserpine-nialamide pretreated rats produced a marked dose-dependent rise in coordinated locomotor activity, devoid of stereotypies such as gnawing, rearing and licking seen after dopamine application (50 Μg) to the neostriatum. The locomotor activity was completely blocked by pimozide, but not by phenoxybenzamine. The effects of apomorphine or d-noradrenaline were similar to those of dopamine. In contrast, l-noradrenaline produced a “convulsive” syndrome devoid of coordinated locomotor activity, and this convulsive syndrome could be completely blocked by phenoxybenzamine but not by pimozide. Release of endogenous dopamine by d- or l-amphetamine (10 and 50 Μg) in the nucleus accumbens produced a rise in coordinated activity, the d-isomer was about 4 times as potent as the l-isomer, and the effect of the d-isomer was blocked completely by α-methyltyrosine. Bilateral application of trifluoperazine (2.5 Μg) to the nucleus accumbens completely blocked the effect of systemically administered d-amphetamine (1.5 and 3.0 mg/kg), but similar application to the area of the central nucleus of the amygdala or the neostriatum was much less effective. Partial protection of the endogenous dopamine stores against the depleting action of reserpine by local application of metatyramine to the nucleus accumbens resulted in a higher level of basal activity than in control animals. Application of dopamine or noradrenaline to the area of the central nucleus of the amygdala or to the olfactory tubercles did not lead to any consistent changes in locomotor activity. The nucleus accumbens and olfactory tubercles contained most of the dopamine in the limbic forebrain, with noradrenaline more evenly distributed. These data suggest that the nucleus accumbens plays an important role in the locomotor activity in rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00429052
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  • 4
    Electronic Resource
    Electronic Resource
    FLA 136: Selective agonist at central alpha-adrenoreceptors mediating changes in the turnover of noradrenaline (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 298 (1977), S. 239-243 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline ; Dopamine ; Utilization ; Synthesis ; Central alpha-adrenoreceptors ; Presynaptic receptors ; Postsynaptic receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. FLA 136 [4-amino-3-(2,6-dichlorobenzylidenehydrazino)-1,2,4-triazol] did not change the hindlimb flexor reflex of spinal rats, but it reduced the clonidine-induced increase in this reflex at high doses. 2. The α-methyltyrosine-induced disappearance of noradrenaline in the rat central nervous system was decelerated by FLA 136, with a peak effect after 15 mg/kg i.p. The accumulation of Dopa following decarboxylase inhibition was inhibited by FLA 136 (15 mg/kg i.p.) in a noradrenaline-predominant region (brain stem). The effect on the utilization appeared to be greater than that on the synthesis in agreement with a slight increase observed in the concentration of noradrenaline in the brain and the spinal cord. 3. FLA 136 reduced the α-methyltyrosine-induced disappearance of dopamine, decreased the Dopa accumulation following decarboxylase inhibition in the dopamine-rich corpus striatum and increased the concentration of dopamine. These effects might be secondary to inhibition of the noradrenergic neurotransmission. 4. Yohimbine almost completely inhibited the effect of FLA 136 on the utilization and on the synthesis of noradrenaline whereas phenoxybenzamine was much less effective on the change in the utilization. Yohimbine and phenoxybenzamine were about equipotent, however, in accelerating the disappearance of noradrenaline produced by α-methyltyrosine alone. 5. FLA 136 does not stimulate the postsynaptic α-adrenoreceptors mediating the increase in flexor reflex activity but it probably decelerates the utilization of noradrenaline by a stimulation of another kind of α-adrenoreceptors sensitive to yohimbine. The latter receptors might occur on the noradrenergic neurones (presynaptic receptors).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500894
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