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  • 1
    Electronic Resource
    Electronic Resource
    Nicotinic receptors in the rat prefrontal cortex: increase in glutamate release and facilitation of mediodorsal thalamo-cortical transmission (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The modulatory influence of nicotinic acetylcholine receptor (nAChRs) on thalamocortical transmission was characterized in the prelimbic area (PrL) of the rat prefrontal cortex. In the first experiment, rats received a unilateral excitotoxic lesion centred on the mediodorsal thalamic nucleus (MD), and were sacrificed 1 week later. The lesion resulted in a 40% reduction of 3H-nicotine autoradiographic labelling in the ipsilateral prefrontal cortex, particularly in areas that are innervated by the MD. Electrophysiological experiments were subsequently performed in non-lesioned anaesthetized animals, in order to study modulation of short- and long-latency responses of PrL neurons evoked by electrical stimulation of the MD. The short-latency responses result from activation of the MD–PrL pathway and are mediated via AMPA-type glutamatergic receptors, whereas the long-latency responses reflect activation of the recurrent collaterals of cortical pyramidal neurons. Iontophoretic application of nicotinic agonists (nicotine, DMPP) facilitated both types of response. Local application of the nAChR antagonists dihydro-beta-erythroidine, mecamylamine and methyllycaconitine, prevented both kinds of facilitation. Finally, intracerebral microdialysis experiments were performed in order to test for nicotinic modulation of extracellular glutamate concentrations in the PrL. Direct application of nicotine via the dialysis probe increased glutamate levels in a dose-dependent manner. This effect was blocked by local perfusion of dihydro-beta-erythroidine. These findings therefore provide anatomical and functional evidence for nAChR-mediated modulation of thalamocortical input to the prefrontal cortex. Such a mechanism may be relevant to the cognitive effects of nicotine and nicotinic antagonists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00403.x
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  • 2
    Electronic Resource
    Electronic Resource
    Nicotine and smoking: a perspective from animal studies (1987)
    Springer
    Psychopharmacology 92 (1987), S. 135-143 
    Details
    ISSN: 1432-2072
    Keywords: Nicotine ; Tobacco ; Smoking ; Reinforcement ; Abstinence ; Cessation ; Nicotinic receptors ; Man ; Animals
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nicotine plays a key role in reinforcing tobacco smoking, and exerts several psychoneuropharmacological actions which may contribute to its reinforcing effects. Thus, nicotine can improve mood and alleviate withdrawal symptoms; it can also alter CNS arousal, reduce stress, suppress appetite, and improve performance on certain tasks. Behavioural studies in animals have tended to corroborate existing theories of smoking behaviour, and have started to suggest how and where nicotine may exert its central actions in man. Clinical evidence suggests that smoking cessation would be facilitated by the administration of a nicotinic antagonist having a selective action on central nicotinic cholinoceptors of the C6 (ganglionic) type. Pharmacological studies in animals indicate that such a drug is a reasonable prospect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00177905
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Nicotine does not improve discrimination of brain stimulation reward by rats (1983)
    Springer
    Psychopharmacology 79 (1983), S. 271-277 
    Details
    ISSN: 1432-2072
    Keywords: Intracranial self-stimulation ; Brain stimulation reward ; Rate-free index ; Nicotine ; Mecamylamine ; Chronic administration ; Tolerance ; Abstinence ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rats were trained to shuttle between two selected (“ON”) arms of a Y maze, to obtain electrical stimulation of the medial forebrain bundle. Each shuttle response was rewarded with a brief pulse train. Repetitive entries into the same “ON” arm were not rewarded, nor were entries made into the third (“OFF”) arm. Every 67s, stimulation was made available from a different pair of arms. Test sessions lasted for 80 min, beginning immediately after SC injection. Undrugged subjects responded faster, and with a greater proportion of rewarded responses, the higher the stimulation current. In non-tolerant rats, nicotine (0–0.4 mg/kg) depressed responding and induced ataxia shortly after injection; from 40 min, nicotine increased low rates of responding but decreased high rates. All these effects were dose-dependent. Mecamylamine (2.0 mg/kg) prevented the initial depressant action. With repeated daily injections of nicotine (0.4 mg/kg), a marked stimulant action emerged which replaced the initial depressant action, and this was dose-dependent. However, responding was increased by nicotine even when brain stimulation was not available (“time-out”). In contrast, an additional “rate-free” index based on discrimination showed that nicotine did not augment the rewarding properties of the brain stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427826
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of nicotine and d-amphetamine on intracranial self-stimulation in a shuttle box test in rats (1984)
    Springer
    Psychopharmacology 84 (1984), S. 109-114 
    Details
    ISSN: 1432-2072
    Keywords: Intracranial self-stimulation ; Brain stimulation reward ; Shuttle box ; Nicotine ; d-Amphetamine ; Chronic administration ; Tolerance ; Motor performance ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rats were permitted to turn on and off electrical stimulation of the medial forebrain bundle, by alternating between two photobeams running along opposite walls of a shuttle box. Entry into one beam (the “ON” beam) triggered the delivery of a succession of short, regularly occurring (1 Hz) pulse trains, which could be terminated by breaking the other (“OFF” beam). The two beams were frequently reversed. When this occurred, the rat was given a free period of 10 s in which to reorient, and brain stimulation reward was then assessed by the amount of time spent receiving brain stimulation (SST) within a fixed interval of time. SST increased with increasing current intensity. After training, subjects were tested for 10 consecutive days, alternately with saline and nicotine bitartrate (0.4 mg/kg SC base), and received a constant daily dose of the drug (0.4 mg/kg). Initially, nicotine visibly impaired motor performance for several minutes after injection, which may at least partly explain the observed reduction of SST; both effects waned across successive nicotine tests. Later in each 78 min session, nicotine consistently increased SST over a range of current, and drugged subjects entered the photobeams more frequently even when electrical stimulation was unavailable. d-Amphetamine sulphate (0.25, 0.75 mg/kg SC salt), given 15 min before testing, also increased SST and stimulated responding. The possible effects of motor impairment or activation on SST are discussed, and it is concluded that nicotine and d-amphetamine may have enhanced the rewarding properties of medial forebrain bundle stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00432037
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Apparent absence of nicotine-induced conditioned place preference in rats (1987)
    Springer
    Psychopharmacology 92 (1987), S. 84-88 
    Details
    ISSN: 1432-2072
    Keywords: Conditioned place preference ; Reinforcement ; Nicotine ; d-Amphetamine ; Methylphenidate ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The conditioned place preference (CPP) paradigm was used in order to assess the reinforcing actions of nicotine in rats. Subjects were tested in “unbiased” two-compartment shuttle boxes, so-called because neither compartment was consistently preferred prior to drug conditioning. In the first experiment, subjects that were initially drug naive showed neither a preference nor an aversion to the compartment that had been paired on four occasions with injection of nicotine (0.2–0.8 mg/kg SC); a similar result occurred in another group given daily injections of nicotine in the home cage prior to the experiment. In a second experiment, nicotine (0.4, 0.8 mg/kg SC) again failed to produce a CPP, whereas marked CPPs were seen in parallel groups of rats tested with either d-amphetamine or methylphenidate. Although nicotine has been reported to produce conditioned place preference, the present results suggest that it is not a robust phenomenon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00215484
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