title: Paraventricular neuron chemosensitivity and activity related to blood pressure control in emotional behavior.
abstract: 1. Unit activity in the paraventricular nucleus (PVN) and blood pressure (BP) of the rat were recorded during discrimination learning of cue tone (CTS+) predicting reward [glucose and intracranial self stimulation (ICSS)], and cue tone (CTS-) predicting aversion (electric shock or tail pinch). Adrenergic systems in the PVN were investigated by electrophoretic application of norepinephrine (NE), and by electrophoretic application or direct microinjection of its antagonists (prazosin, yohimbine, and propranolol). 2. Of 65 PVN neurons analyzed, 35 responded during CTS learning in one or more phases of an operant task. Of these, activity of 20 neurons was increased nondiscriminatively by CTS+ and CTS-, and reward and aversion. In parallel with these neuronal activity increases, BP (systolic, diastolic, and mean) was also increased by both CTS+ and CTS- (10-35 mmHg), and reward and aversion (20-47 mmHg). Both neuronal activity and BP increases during CTS learning were suppressed during extinction. 3. Paraventricular neurons, the activity of which correlated with BP increase during CTS learning, were excited by electrophoretic application of NE and Na+ and fired phasically during inter-trial intervals. Activity increases of these neurons during CTS learning, which was related to BP increase, were blocked by electrophoretically applied prazosin (alpha 1-antagonist), but not by yohimbine (alpha 2-antagonist) or propranolol (beta-antagonist). 4. Direct microinjection of prazosin into the PVN suppressed BP increase during CTS learning. Operant licking for reward was not suppressed by prazosin injection. Microinjection of yohimbine or propranolol into the PVN did not suppress either BP increase during CTS learning or operant licking to obtain reward. 5. These results suggest that afferent alpha 1-adrenergic input to the PVN is important to the central BP control during CTS learning in emotional behavior.
authors.affiliation: Department of Physiology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Ono
authors.forename: M
authors.initials: M
authors.lastname: Fukuda
authors.forename: T
authors.initials: T
authors.lastname: Uwano
mesh_terms: D000161:Acoustic Stimulation; D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects; D001794:Blood Pressure / Q000502:physiology*; D003216:Conditioning, Operant / Q000187:drug effects; D004192:Discrimination, Psychological / Q000502:physiology; D004644:Emotions / Q000502:physiology*; D005947:Glucose / Q000494:pharmacology; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D008845:Microinjections; D009474:Neurons / Q000187:drug effects*; D009638:Norepinephrine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D010286:Paraventricular Hypothalamic Nucleus / Q000166:cytology* / Q000187:drug effects; D010812:Physical Stimulation; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects; D012653:Self Stimulation / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000187:drug effects
chemical_list: D011942:Receptors, Adrenergic, alpha; D005947:Glucose; D009638:Norepinephrine