Response of medial preoptic neurons to electrical stimulation of the mediobasal hypothalamus, amygdala and mesencephalon in normal, serotonin or catecholamine deprived female rats

Abstract

Single cell activity from preoptic neurons was extracellularly recorded in normal female rats and the effects of electrical stimulation of the mediocortical amygdala (AMY), the N. med. raphes (MES) and the mediobasal hypothalamus (MBH) was tested. 1. One type of preoptic neurons (55%) reacted with primary excitation to a single electrical stimulus of AMY, MES or MBH, which was usually followed by a period of postexcitatory inhibition. Another type of neurons (29%) were first inhibited after stimulation of AMY, MES or MBH and then showed a period of postinhibitory excitation. The discharge rate of a third type was not affected by electrical stimulation of these structures (16%). If a neuron was affected by a stimulus in a given area it predictably reacted in the same fashion to stimulation of the other areas. 2. The postexcitatory inhibition of the majority of the primarily excited neurons was strong enough to prevent the stimulus response to a second stimulus. Occasional recordings from two neighboured cells simultaneously indicate that they can be inhibitory to each other. 3. By pulse train stimulation of the AMY or MES with varying frequencies it could be demonstrated that low frequencies (10 Hz) had a facilitatory action whereas higher frequencies (100 Hz) were inhibitory to preoptic discharge rates. 4. No obvious alteration of neuronal properties we found neither in rats treated intraventricularly with 5,6-dihydroxytryptamine, which strongly reduces central nervous system serotonin content, nor in 6-hydroxydopamine treated rats, which had low central nervous system catecholamine levels.

Electrophysiological analysis of inhibitory synaptic mechanisms in the preoptic area of the rat.

“…Similar findings have been reported in earlier studies of rostral hypothalamic neurones (Fenske et al 1975;Gardner & Phillips, 1977 b), but the significance of these observations is unclear. It is generally accepted that the inhibition of activity generated by ionophoretic application of an excitant amino acid is due to a post-synaptic mechanism (Krnjevic, Randic6 & Straughan, 1966).…”

“…Reduction of the frequency of occurrence of synaptic inhibition in the preoptic-anterior hypothalamus by tetanus toxin provides valuable confirmatory evidence in support of the earlier suggestion that such inhibition is mediated by amino acid transmitters. Conversely the lack of effect of pretreatment with the anti-serotonin neurotoxins 5,7-dihydroxytryptamine and parachlorophenylalanine provides no evidence for any role of 5-HT in mediating such synaptic inhibition, confirming the earlier report of Fenske et al (1975) that 5,6-dihydroxytryptamine had no effect on synaptic inhibition in the rostral hypothalamus. Since anatomical studies have shown the major source of tryptaminergic afferents to the rostral hypothalamus to arise in the medial raphe nucleus (Azmitia & Segal, 1978) it is perhaps not surprising that stimulation sites in the periaqueductal grey matter appear to activate non-tryptaminergic inhibitory mechanisms.…”

“…Inhibitory synaptic responses in the preoptic-anterior hypothalamus may be evoked following stimulation of the arcuate-ventromedial hypothalamic nuclei (Dyer, 1973;Fenske, Ellendorff & Wuttke, 1975;MacLeod & Mayer, 1980), the amygdala Fenske et al 1975;Gardner & Phillips, 1977 a) and the periaqueductal grey (MacLeod & Mayer, 1980). The neuronal circuitry involved in generating such inhibitory responses remains unknown, but both and Gardner & Phillips (1977b) have suggested the involvement of local circuit interneurones.…”

Influence of hypnogenic brain areas on wakefulness‐ and rapid‐eye‐movement sleep‐related neurons in the brainstem of freely moving cats

“…Lesion and stimulation studies have shown that the caudal brainstem reticular formation (CBS) and the preopticoanterior hypothalamic area (POAH) of the basal forebrain promote sleep and synchronization of the EEG (Nauta, 1946; Sterman, and Clemente, 1962; Moruzzi, 1972; Mallick et al, 1984, 1986) and also that these areas are rich in sleep‐active neurons (Eguchi and Satoh, 1980; Mallick et al, 1983; Kaitin, 1984; McGinty and Szymusiak, 1988). The effects of one of the sleep‐waking‐regulating areas on neurons located in other such areas have been studied (Mancia et al, 1974; Fenske et al, 1975; Mallick et al, 1984, 1986; Szymusiak and McGinty, 1989; Macchi and Mancia, 1990; Osaka and Matsumura, 1994). However, becasuse those investigations were not conducted on freely moving animals, the effects on REM sleep‐related neurons could not be studied, nor could the neuronal activities be correlated with other associated behaviors of the animals.…”

Electrophysiological analysis of pathways connecting the medial preoptic area with the mesencephalic central grey matter in rats.

“…Similarly projections from the preoptic area afferent to the periaqueductal grey matter have recently been demonstrated, using anterograde (Aghajanian & Wang, 1977) and orthograde (Conrad & Pfaff, 1976;Swanson, 1976;Swanson, Kucharczyk & Mogenson, 1978) tracer techniques. Electrophysiological evidence concerning the anatomically demonstrated reciprocal mid brain-preoptic connexions is incomplete although it has been shown that stimulation of the median raphe nucleus (Fenske, Ellendorff & Wuttke, 1975) 54 MIDBRAIN CONTROL OF PREOPTIC EXCITABILITY and mesencephalic reticular formation (Gardner & Phillips, 1977) may alter the excitability of unidentified preoptic neurones. The present investigation provides details of mid brain-preoptic connexions, and demonstrates the predominately inhibitory influence of periaqueductal grey matter stimulation on the spontaneous, synaptic and ionophoretically evoked activity of neurones in the medial preoptic area, including those identified as projecting to the mediobasal hypothalamus (Dyer, 1973).…”