[d-TRP11]-Neurotensin, unlike α-flupenthixol, may not block amphetamine-induced hyperactivity in rats

Sahgal, Arjun; Keith, A.B.; Lloyd, Stephen; Edwardson, J. A.

doi:10.1016/0028-3908(89)90105-6

Cited by 1 publication

(1 citation statement)

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“…Direct observation also suggested that nicotine (s.c.) did not produce stereotypy of the type seen with dopamine agonists. The findings support previous observations that nicotine can increase ambulatory activity but produces only low levels of stereotyped responses (Clarke & Kumar, 1983a, b;Lapin et al, 1987), and emphasize again the importance of using recording methods that distinguish adequately between different components of locomotor activity (Krsiak et al, 1970;Sahgal et al, 1989). Crude measures of activity that confound ambulation with other behaviours may fail to detect effects of nicotine, especially after intracerebral injections.…”

Section: Discussionsupporting

confidence: 81%

Locomotor activity in rats after administration of nicotinic agonists intracerebrally

Reavill¹,

Stolerman²

1990

British J Pharmacology

149

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Nicotine (0.13 and 0.4 mg kg−1, s.c.) increased the ambulatory component of locomotor activity in rats previously exposed to the drug. Nicotine did not increase repeated movements reliably. An infusion of either nicotine (8 μg) or the potent nicotinic agonist cytisine (4 μg) into the ventral tegmental area of the forebrain increased ambulation but not repeated movements. An infusion of nicotine or cytisine into the nucleus accumbens, striatum, dorsal hippocampal formation or motor thalamus did not increase ambulatory or repeated movements. Mecamylamine (0.1–1.0 mg kg−1, s.c.) blocked increases in locomotor activity produced by an infusion of nicotine or cytisine into the ventral tegmental area. The locomotor activity produced by systemically administered nicotine may be mediated, in part, through nicotinic receptors located in the ventral tegmental area of the mesolimbic dopamine system.

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Section: Discussionsupporting

confidence: 81%