Cholinergic neurons and the cardiovascular response produced by central injection of substance P in the normotensive rat

Gr, Trimarchi; Wc, Glisson; Wm, Thomson; J, VanLingen; Jj, Buccafusco

doi:10.1016/0024-3205(86)90390-5

Cited by 15 publications

(3 citation statements)

References 22 publications

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“…For example, we noted earlier that central nicotinic receptors partly mediate the pressor responses to i.c.v. administration of certain neuroactive peptides such as bradykinin, angiotensin II, and substance P (Buccafusco and Serra, 1985;Trimarchi et al, 1986). More recently, we reported that in rat models genetically manipulated to maintain an elevated blood pressure, there is a link between decreased expression of brain ␣7nAChRs and working memory deficits (Gattu et al, 1997;Terry et al, 2001).…”

Section: Resultsmentioning

confidence: 99%

Role of α7 Nicotinic Acetylcholine Receptors in the Pressor Response to Intracerebroventricular Injection of Choline: Blockade by Amyloid Peptide Aβ1-42

Li¹,

Buccafusco²

2004

J Pharmacol Exp Ther

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Systemic blood pressure and cardiac function have long been known to be under the control of central autonomic and hormonal pathways that, in part, use cholinergic neural systems. Recently choline, a precursor and product of acetylcholine metabolism, has been shown to serve as a selective endogenous agonist for the ␣7 subtype of the nicotinic acetylcholine receptor (␣7nAChR). This receptor subtype mediates several responses to nicotine in animals, most notably, neuroprotection and enhanced cognition. The purpose of this study was to determine whether the cardiovascular changes induced by central injection of choline in rats also were mediated by ␣7nAChRs. Moreover, we sought to determine whether these cardiovascular changes to choline could be blocked by central pretreatment with amyloid ␤ peptide (1-42) (A␤1-42), a neurotoxic component of cerebral amyloid that is known to bind with high affinity to ␣7nAChRs. Central, i.c.v. injection of choline (50, 100, or 150 g) produced dose-dependent (10 -15-min duration) pressor response of up to about 20 mm Hg. The most consistent change in heart rate included a brief increase (up to 40 beats/min) that lasted 2 to 3 min, followed by a prolonged decrease averaging 50 beats/min that lasted up to 30 min. Pretreatment (i.c.v.) with the selective ␣7nAChR antagonists ␣-bungarotoxin and methyllycaconitine significantly inhibited the pressor and heart rate responses to subsequent injection of choline. Pretreatment with the non-␣7-preferring antagonist dihydro-␤-erythroidin was not effective. These findings suggested that the cardiovascular response to i.c.v. injection of choline was mediated at least in part through ␣7nAChRs. Pretreatment (30 min) with low doses (1-100 pmol) of amyloid peptide A␤1-42 (but not with A␤40-1) administered by the i.c.v. route significantly inhibited the choline-induced blood pressure increase as well as the choline-induced decrease in heart rate.One of the most prominent pathological changes associated with the Alzheimer's disease (AD) is the loss of cholinergic innervation of the cortex and hippocampus. This neuronal loss is accompanied by a decrease in the brain density of the ␣7 subtype of the nicotinic acetylcholine receptor (␣7nAChR). The ␣7nAChR is a unique member of the nicotinic receptor family that in recent years has been shown to enjoy significant physiological importance. In particular, this receptor subtype is known to mediate several responses to nicotine administration in animals, including neuroprotection and cognitive enhancement. For example, ␣7nAChR-preferring agonists, such as anabaseine and GTS-21, were shown to improve working memory in rats (Meyer et al., 1994;Arendash et al., 1995;Briggs et al., 1997). Another ␣7nAChR agonist, ARR 17779 [(Ϫ)-spiro[azabicyclo[2.2.2]octane-3,5Ј-oxazolidin-2Ј-one (4a)], was shown to reverse the working memory deficits induced by fimbria-fornix lesions (Levin et al., 1999). However, other than procedures that estimate aspects of behavior, no objective measure of central ␣7nAChR activation i...

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Section: Resultsmentioning

confidence: 99%

Role of α7 Nicotinic Acetylcholine Receptors in the Pressor Response to Intracerebroventricular Injection of Choline: Blockade by Amyloid Peptide Aβ1-42

Li¹,

Buccafusco²

2004

J Pharmacol Exp Ther

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“…67 By recognizing the existence of a system of strict liability alongside a system of fault-based liability, many of the cases, previously subsumed under the fault-based liability and hence allowing a much easier release from liability, can now be traced back to the principle of strict liability which provides a much harder release for risky activities. The construction of the principle of strict liability makes it possible to change the system of civil liability, by propitiating the reinterpretation of the irreconcilable provisions, fi lling up legislative gaps, and extending the liability to pay compensation to ever new cases.…”

Section: The Solution Of Inconsistencies and The Ordering Of Legal Mamentioning

confidence: 99%

Argument Types and Fallacies in Legal Argumentation

Bustamante¹,

Dahlman²

2015

Law and Philosophy Library

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“…This phenomenon can be readily demonstrated by the marked pressor responses observed in several animal species, including humans, after the administration of centrally-acting cholinergic (muscarinic) agonists (for review, see Brezenoff and Giuliano, 1982;Buccafusco and Brezenoff, 1986;Buccafusco, 1992Buccafusco, , 1996. Central cholinergic neurons also have been reported to participate in mediating the pressor action to central administration of nicotine (Buccafusco and Yang, 1993), and certain noncholinergic neurotransmitter substances such as angio-tensin II, substance P, vasopressin, and bradykinin (Buccafusco and Serra, 1985;Trimarchi et al, 1986). These substances have been shown to provoke the release of acetylcholine from neuronal stores, with the neurotransmitter subsequently acting upon muscarinic receptors mediating a sympathoexcitatory response.…”

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confidence: 99%

The Importance of Brainstem Cholinergic Neurons in the Pressor Response to Cocaine

Buccafusco¹,

Davis²,

Shuster³

et al. 2004

J Pharmacol Exp Ther

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After intracisternal injection, 140 nmol (48 g) of cocaine (but not lidocaine or procaine) evoked an increase in mean arterial pressure (MAP) of 41 mm Hg. The increase in MAP began within 1 min after injection and lasted 10 to 15 min. The pressor response to intracisternal injection of cocaine was not mediated through central ␣-adrenergic receptors, but intracisternal pretreatment with D1 or D2 dopamine receptor antagonists shortened the duration of the response. Pretreatment with intracisternal injection of hemicholinium-3 to deplete medullary acetylcholine produced a dose-dependent inhibition of the pressor and tachycardic responses to intracisternal injection of cocaine. Central pretreatment with hemicholinium-3 also inhibited the pressor response to intravenous injection of 0.5 mg/kg cocaine. Atropine pretreatment was only partly effective in blocking the pressor and tachycardic responses to intracisternal injection of cocaine. However, a single intracisternal injection of the nicotinic ganglionic receptor blocker hexamethonium inhibited the pressor response to cocaine administered intracisternally 24 h later, and on each of the following 4 days. The blocking effect of hexamethonium was not mimicked by the ␣7 selective antagonist methyllycaconitine or by the ␣4␤2 subtype-preferring antagonist dihydro-␤-erythroidine. The data suggest that the pressor response to cocaine is mediated by medullary acetylcholine release on to nicotinic receptors of the ganglionic type, enhancing the output of bulbospinal sympathetic premotor neurons. Our results provide new evidence for the prolonged inactivation of relevant central nicotinic receptors by nicotinic receptor antagonists, and suggest that such compounds might be used safely for cocaine overdose, as well as for antiabuse issues without the concern for autonomic side effects.The ability of cocaine to increase systemic blood pressure usually is considered to be commensurate with drug's pharmacological classification as an indirect-acting sympathomimetic amine. Whereas cocaine conforms to this classification both in the peripheral and central nervous systems, the role of the CNS in terms of blood pressure alterations has been debated (Knuepfer et al., 1993;Gillis et al., 1995;Bernards, 1996). In fact, agonists at central ␣ 2 -adrenergic receptors such as clonidine and ␣-methyldopa are effective antihypertensive drugs; and levodopa and other dopaminergic antiParkinson agents often produce orthostatic hypotension as a side effect. Also, systemic administration of cocaine has been reported to decrease sympathetic nervous activity (Knuepfer and Branch, 1992;Gillis et al., 1995;Abrahams et al., 1996). Yet, there have been instances when cocaine has been administered directly into the CNS, usually via the cerebrospinal fluid, that the drug elicits an increase in arterial blood pressure. However, based upon the requirement for relatively high doses to elicit a pressor response via the lateral ventricular route (Knuepfer et al., 1993), it is unlikely that forebrain str...

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Cholinergic neurons and the cardiovascular response produced by central injection of substance P in the normotensive rat

Cited by 15 publications

References 22 publications

Role of α7 Nicotinic Acetylcholine Receptors in the Pressor Response to Intracerebroventricular Injection of Choline: Blockade by Amyloid Peptide Aβ1-42

Role of α7 Nicotinic Acetylcholine Receptors in the Pressor Response to Intracerebroventricular Injection of Choline: Blockade by Amyloid Peptide Aβ1-42

Argument Types and Fallacies in Legal Argumentation

The Importance of Brainstem Cholinergic Neurons in the Pressor Response to Cocaine

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