Search PubMed⌕ Search

Biomedical subjects

M K Menon

Publications and source records attributed to M K Menon.

At least 55 records · Page 3Linked to original sources
PubMed1976

Comparative actions of monomethoxyamphetamines on the release and uptake of biogenic amines in brain tissue.

para-Methoxyamphetamine (PMA), a known hallucinogen, is the most potent compound among methoxyamphetamines in disrupting behavior in rats. PMA, unlike d-amphetamine (A), did not induce stereotyped behavior and was less effective than A in stimulation of locomotor d-amphetamine-like effects, but ortho-methoxyamphetamine (OMA) was devoid of any locomotor stimulation. To investigate the reasons for the different behavioral effects caused by PMA, meta-methoxyamphetamine (MMA), OMA and A, a comparison was made among these drugs on the release and uptake of 3H-5-hydroxytryptamine (3H-5-HT), 3H-norepinephrine (3H-NE) and 3H-dopamine (3H-DA) in tissue slices of cerebral cortex and corpus striatum of rat brain. The potencies for the increased release of 3H-5-HT were found to be PMA greater than MMA greater than or equal to A greater than OMA in cerebral cortex of 3H-NE in cortex, A greater than or equal to PMA = MMA greater than OMA, and of 3H-DA in corpus striatum, A greater than MMA greater than PMA greater than or equal to OMA. The potencies for inhibiting the uptake of 3H-5-HT in cerebral cortex and corpus striatum were found to be PMA greater than MMA greater than A greater than OMA and of 3H-NE in cortex A greater than PMA greater than or equal to MMA greater than OMA, and 3H-DA in corpus striatum A greater than MMA greater than PMA greater than OMA. d-PMA is equipotent to l-PMA in increasing the release of 3H-5-HT but is more potent than l-PMA in blocking the uptake of 3H-5-HT. The high potency of PMA on increasing the release and inhibiting the uptake of 5-HT suggests than 5-HT may be involved in the production of hallucinogenic effects of PMA.

Amphetamines↗
PubMed1976

Pharmacological evidence for the central serotonergic effects of monomethoxyamphetamines.

The effects of three monomethoxyamphetamines, dl-para-methoxyamphetamine (dl-PMA), dl-meta-methoxyamphetamine (dl-MMA) and dl-ortho-methyoxyamphetamine (dl-OMA), and d-amphetamine (d-A) on the myoclonic twitch activity (MTA) of PMA, MMA and d-A were found to increase the MTA but OMA was ineffective. The increased MTA induced by d-A was not influenced by the blockade of 5-hydroxytryptamine (5-HT) receptor by methysergide or inhibition of 5-HT synthesis by para chlorophenylalamine (PCPA) but was reduced by haloperidol which blocked the dopamine receptor. On the other hand, the increased MTA produced by PMA was not influenced by haloperidol but was reduced by methysergide and PCPA. The increased MTA induced by MMA was not effectively blocked by either PCPA or haloperidol but was blocked by the combination of both PCPA and haloperidol. The results indicate that whereas the increased MTA produced by d-A is not dependent on the availability of 5-HT, PMA exerts by a release of 5-HT and that the MMA effect is due to a release of both 5-HT and dopamine. High doses of PMA and MMA increased the locomotor activity arevious biochemical findings that PMA releases 5-HT in brain tissue and suggests that PMA exerts its pharmacological effects by releasing 5-HT.

Amphetamines↗
PubMed1975

Blockade of the central effects of d-amphetamine by amantadine. II.

1-Adamantanamine (amantadine) pretreatment significantly reduced the motor hyperactivity and hyperthermia caused by d-amphetamine in reserpinized mice. In drug-naive mice, when amantadine was administered after d-amphetamine, the motor activity caused by the latter also was decreased. Since our earlier studies showed that amantadine pretreatment also antagonized the increases in both motor activity and homovanillic acid (HVA) in the caudate nucleus caused by d-amphetamine in mice, it is suggested that the antagonism is due to a competitive blockade at the pre-synaptic level in the brain.

Amantadine↗