Drugs online research references
Eur J Neurosci. 1994 Mar 1;6(3):293-8.
Blockade of prefronto-cortical alpha 1-adrenergic receptors prevents locomotor hyperactivity induced by subcortical D-amphetamine injection.
Blanc G, Trovero F, Vezina P, Herve D, Godeheu AM, Glowinski J, Tassin JP.
INSERM U.114, Paris, France.
The stimulation of cortical dopaminergic D1 receptors can counteract the increased locomotor activity evoked by D-amphetamine application in the nucleus accumbens (Vezina et al., Eur. J. Neurosci., 3, 1001-1007, 1991). Moreover, an alpha 1 antagonist, prazosin, prevents the locomotor hyperactivity induced by electrolytic lesions of the ventral tegmental area (Trovero et al., Neuroscience, 47, 69-76, 1992). Attempts were thus made to see whether blockade of alpha 1-adrenergic receptors in the rat prefrontal cortex could reduce nucleus accumbens D-amphetamine-evoked locomotor activity. Rats implanted chronically and bilaterally with cannulae into the medial prefrontal cortex and the nucleus accumbens were used for this purpose and locomotor activity was monitored in circular corridors. Preliminary experiments indicated that intraperitoneal injection of prazosin (0.06 mg/kg) reduces the locomotor hyperactivity induced by the peripheral administration of D-amphetamine (0.75 mg/kg). This effect of prazosin was not observed when locomotor hyperactivity was obtained by an intraperitoneal injection of scopolamine (0.8 mg/kg). Bilateral nucleus accumbens injections of D-amphetamine (4.0 nmol/side) markedly increased locomotor activity, as estimated in a 30 min period. Prior (20 min) bilateral injections of either prazosin or WB-4101 (0.16 pmol) into the medial prefrontal cortex abolished the nucleus accumbens D-amphetamine-evoked response. The recovery of the nucleus accumbens D-amphetamine-evoked response was closely dependent on the amount of prazosin used, very prolonged inhibitory effects of the drug being seen with a high amount (> 4 days with 160 pmol). In contrast, whatever the amount of WB-4101 used (0.16-160 pmol), recovery occurred within 3 days.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7912614&dopt=Abstract
Brain Res. 1995 Mar 20;674(2):221-9.
The role of the medial prefrontal cortex of rats in short-term memory functioning: further support for involvement of cholinergic, rather than dopaminergic mechanisms.
Broersen LM, Heinsbroek RP, de Bruin JP, Uylings HB, Olivier B.
Graduate School Neurosciences Amsterdam, Netherlands Institute for Brain Research.
The putative involvement of the dopaminergic innervation of the medial part of the prefrontal cortex (PFC) in short-term memory functioning was investigated by evaluating the effects of local infusions of dopaminergic drugs into the ventral part of the medial PFC of rats in an operant delayed-matching-to-position (DMTP) task. Two separate groups of rats were tested after bilateral microinfusion of several doses of either the dopamine receptor agonist apomorphine (APO) or the dopamine receptor antagonist cis-flupenthixol (FLU) into the ventromedial PFC. In addition, all animals were tested after infusion of several doses of the muscarinic receptor antagonist scopolamine (SCO) and the dopamine DI receptor antagonist SCH-23390 (SCH). The drugs tested affected DMTP performance differentially. APO had no effect on response accuracy, although it dose-dependently affected nose poke activity and response latencies. FLU and SCH both induced a dose-dependent, but delay-independent deterioration of response accuracy that was paralleled by increases in response latencies and decreases in nose poke frequencies, causing some animals to stop responding after infusion of the highest doses of both drugs. In contrast, SCO infusions into the ventromedial PFC induced a dose- and delay-dependent deterioration of response accuracy, that was accompanied by an increase in response latencies only. Taken together, these results provide additional support for the involvement of cholinergic, rather than dopaminergic mechanisms in short-term memory supported by the medial PFC of the rat, and they are not in favor of a functional dissociation between the dorsomedial PFC and the ventromedial PFC in the role.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7796100&dopt=Abstract
Neuroscience. 1993 Apr;53(4):961-70.
Acetylcholine, theta-rhythm and activity of hippocampal neurons in the rabbit--I. Spontaneous activity.
Brazhnik ES, Vinogradova OS, Stafekhina VS, Kitchigina VF.
Institute of Theoretical and Experimental Biophysics, Puschino-on-Oka, Moscow Distr., Russia.
The background activity of hippocampal neurons was recorded extracellularly in waking rabbits in the control state and after systemic injections of physostigmine and scopolamine. Similar analysis was done in the hippocampus chronically deprived of ascending brainstem afferents. Cholinergic drugs control the number of hippocampal neurons with theta modulation and stability, but not the frequency of theta modulation. Increase of endogenous acetylcholine also resulted in regularization of the activity with suppression of delta modulation and complex spike discharges; its blockade produced the opposite changes. Both drugs changed the level of background activity in the majority of the neurons, but the overall mean frequency did not vary between the states. Regression analysis demonstrated significant negative correlations with dominating decrease in the level of discharges in high-frequency neurons (> 25 spikes/s) and its increase in low-frequency ones (< 25 spikes/s) after injection of both drugs. Stability of the overall mean frequency and uniformity of its shifts during both stimulation and suppression of the cholinergic component of theta-rhythm presumably indicate that the frequency of background activity, unlike its pattern, is not directly controlled by the cholinergic septal input.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8506029&dopt=Abstract
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