An immunohistochemical study on the location of GABAergic neurons in rat septum

Panula, Pertti; Revuelta, A.; Cheney, D. L.; Wu, Jang‐Yen; Costa, E.

doi:10.1002/cne.902220107

Cited by 175 publications

(70 citation statements)

References 62 publications

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“…This is in keeping with the histochemical evidence of a substantial GABAergic innervation of the septal nuclei (2,3). Furthermore, stimulation of other septal neurotransmitter receptors (e.g., dopamine and P-endorphin) can decrease the hippocampal Ac The studies reported here were undertaken to correlate pharmacologically induced decreases in the hippocampal AcCho TR with changes in extinction of a food-reinforced lever-press response.…”

supporting

confidence: 79%

Behavioral and neurochemical differentiation of specific projections in the septal-hippocampal cholinergic pathway of the rat.

Blaker¹,

Peruzzi²,

Costa³

1984

Proc. Natl. Acad. Sci. U.S.A.

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In the rat, an intraseptal injection of the vaminobutyric acid (GABA) agonist muscimol decreases the turnover rate of acetylcholine in the hippocampus and, during extinction of a food-reinforced lever-press response, increases extinction responding in a dose-dependent manner. Intraseptal 3-endorphin decreases the turnover rate of hippocampal acetylcholine through activation of septal GABAergic interneurons and increases extinction responding. On the other hand, intraseptal substance P, which decreases the turnover rate of hippocampal acetylcholine in a manner unrelated to septal GABAergic mechanisms, fails to increase extinction responding. The turnover rate of acetylcholine in various hippocampal regions after intraseptal injection of muscimol and substance P was also studied. Muscimol decreases the acetylcholine turnover rate only in the ventral hippocampus, whereas substance P decreases it only in the dorsal hippocampus. We hypothesize that a lowering in the cholinergic input to the ventral hippocampus is capable of increasing extinction responding, whereas a decrease in the input to the dorsal hippocampus is without such an effect. Hence, the cholinergic projections to the two hippocampal areas are modulated by different transmitter systems and have different physiological functions.In rats, intraseptal injection of the yaminobutyric acid (GABA) receptor agonist muscimol decreases the turnover rate (TR) of acetylcholine (AcCho) in the hippocampus in a manner that is dose-dependent and is reversible by injection of the GABA antagonist bicuculline (1). This is in keeping with the histochemical evidence of a substantial GABAergic innervation of the septal nuclei (2, 3). Furthermore, stimulation of other septal neurotransmitter receptors (e.g., dopamine and P-endorphin) can decrease the hippocampal Ac The studies reported here were undertaken to correlate pharmacologically induced decreases in the hippocampal AcCho TR with changes in extinction of a food-reinforced lever-press response. Intraseptal injection of muscimol simultaneously and dose-dependently decreases the AcCho TR in the hippocampus and increases responding during extinction (5). We shall present evidence that such behavioral responses are produced by a selective inhibition of a specific septal-hippocampal cholinergic pathway that is regulated by a GABAergic input; these septal cholinergic neurons form a subpopulation of septal cholinergic neurons, which projects to the ventral hippocampus. MATERIALS AND METHODSAnimals. Male Sprague-Dawley rats were obtained from Zivic-Miller (Allison Park, PA). All of the rats weighed 160-200 g at the beginning of each experiment and were housed individually in quarters illuminated with alternating 12-hr light and dark periods at a constant temperature.Surgery. Stainless steel guide cannulas (22 gauge; Plastic Products, Roanoke, VA) were stereotaxically implanted into the medial septal nuclei of pentobarbital-anesthetized rats. The guide cannulas were placed such that an internal cannula (28 gauge) would ...

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supporting

confidence: 79%

Behavioral and neurochemical differentiation of specific projections in the septal-hippocampal cholinergic pathway of the rat.

Blaker¹,

Peruzzi²,

Costa³

1984

Proc. Natl. Acad. Sci. U.S.A.

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“…7C). These nuclei receive their major inputs from the hippocampus and are thought to produce ␥-aminobutyric acid (16). The triangular septal and septofimbrial nuclei provide 90% of all projections to the medial habenula via the stria medullaris, while the lateral septal cells are interneurons.…”

Section: Resultsmentioning

confidence: 99%

d -aspartate localizations imply neuronal and neuroendocrine roles

Schell

Cooper

Snyder

1997

Proc. Natl. Acad. Sci. U.S.A.

208

176

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Though L-amino acids predominate in living organisms, substantial levels of free D-serine and D-aspartate occur in mammals, especially in nervous and endocrine tissues. Using an antibody specific for glutaraldehyde-fixed D-aspartate, we have localized D-aspartate in rat tissues. In the brain we observe discrete neuronal localizations of Daspartate, especially in the external plexiform layer of the olfactory bulb, hypothalamic supraoptic and paraventricular nuclei, the medial habenula, and certain brainstem nuclei. In rats 3-4 weeks old, we observe D-aspartate in septal nuclei and in a subset of stellate and basket cells of the cerebellum. D-aspartate is also concentrated in glands, including the epinephrine cells of the adrenal medulla, the posterior pituitary, and the pineal gland. Levels in the pineal gland are the highest of any mammalian tissue. Although D-amino acids are well known in bacterial physiology, only recently have they been found in mammals (1-3). Substantial levels of D-serine occur in brain tissue with a regional distribution resembling the the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors (4). By immunohistochemistry we have shown that D-serine is selectively localized to a subpopulation of astrocytes in close proximity to NMDA receptors and released by glutamate stimulation (5, 6). Since D-serine potently activates the glycine site on NMDA receptors, these findings indicate that D-serine is a novel messenger molecule that serves as an endogenous ligand for this site.Lajtha and coworkers (1) discovered very high levels of D-aspartate in the brain and other tissues of mammals. Daspartate levels are highest in neonatal tissues, attaining millimolar concentrations in newborn rat cerebral cortex, pituitary gland, and 3-week-old adrenal gland (7,8). Using immunohistochemistry, we now describe selective neuronal localizations of D-aspartate in discrete brain areas and endocrine structures. D-aspartate oxidase (DAPOX), visualized by a novel histochemical technique, is localized inversely to endogenous D-aspartate. MATERIALS AND METHODSMaterials. Sprague-Dawley rats were purchased from Sasco (Wilmington, MA). Hypophysectomized rats were from Charles River Breeding Laboratories. Mice (129͞SvEv Agouti strain) were from Taconic Farms. Antibody to L-aspartate (9) was from Chemicon. Glutaraldehyde (GA) was from Electron Microscopy Sciences (Fort Washington, PA). The peroxidase Elite staining kit was from Vector Laboratories. All other reagents were from Sigma.Antibody Production and Purification. D-aspartate was coupled to BSA with GA and then reduced with NaBH 4 (10). Rabbits were immunized using a colloidal gold technique (5, 11), and stereoselective, high-affinity antiserum was produced after 7 weeks. Before use, batches of D-aspartate antiserum were diluted 1:10 with 0.05% NaN 3 and 10 mM Tris (pH 7.4). Diluted serum (10 ml) was mixed with 1 ml packed agarose beads that had been coupled to GA-BSA at a concentration of 4.3 mg͞ml with respect to BSA. Antiserum and beads were incubate...

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“…Brain neurons (347) and fibers (473) containing histamine had just been discovered. The histaminergic nucleus of the brain was identified as the TMN (473). It is involved in many aspects of brain function, including prominently food intake (508), which can be much affected by stress (112).…”

Section: Histaminementioning

confidence: 99%

Fear Memory

Izquierdo

Furini

Myskiw

2016

Physiological Reviews

380

259

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Fear memory is the best-studied form of memory. It was thoroughly investigated in the past 60 years mostly using two classical conditioning procedures (contextual fear conditioning and fear conditioning to a tone) and one instrumental procedure (one-trial inhibitory avoidance). Fear memory is formed in the hippocampus (contextual conditioning and inhibitory avoidance), in the basolateral amygdala (inhibitory avoidance), and in the lateral amygdala (conditioning to a tone). The circuitry involves, in addition, the pre-and infralimbic ventromedial prefrontal cortex, the central amygdala subnuclei, and the dentate gyrus. Fear learning models, notably inhibitory avoidance, have also been very useful for the analysis of the biochemical mechanisms of memory consolidation as a whole. These studies have capitalized on in vitro observations on long-term potentiation and other kinds of plasticity. The effect of a very large number of drugs on fear learning has been intensively studied, often as a prelude to the investigation of effects on anxiety. The extinction of fear learning involves to an extent a reversal of the flow of information in the mentioned structures and is used in the therapy of posttraumatic stress disorder and fear memories in general.

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An immunohistochemical study on the location of GABAergic neurons in rat septum

Cited by 175 publications

References 62 publications

Behavioral and neurochemical differentiation of specific projections in the septal-hippocampal cholinergic pathway of the rat.

Behavioral and neurochemical differentiation of specific projections in the septal-hippocampal cholinergic pathway of the rat.

d -aspartate localizations imply neuronal and neuroendocrine roles

Fear Memory

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