Lactation Alters γ-Aminobutyric Acid Neuronal Activity in the Hypothalamus and Cerebral Cortex in the Rat

Abstract

γ-Aminobutyric acid (GABA) neurons terminating in the hypothalamus have been implicated in the neuroendocrine regulation of reproductive hormones, particularly luteinizing hormone (LH) and prolactin. The aim of this study was to examine whether GABAergic neuronal activity in the hypothalamus was modified during lactation, and whether any observed changes correlated with changes in secretion of these hormones. Animals were divided into three experimental groups: diestrous controls, lactating with pups present (with pups), and lactating with pups removed for 4 h (without pups). Animals were decapitated either without treatment, or 60 min after inhibition of GABA degradation by aminooxyacetic acid (AOAA) (100 mg/kg, i.p.). The rate of GABA accumulation in the tissue after AOAA is a measure of GABA turnover. GABA turnover was estimated in 13 microdissected brain regions, and serum prolactin and LH measured by radioimmunoassay. Suckling was associated with significantly increased prolactin and significantly decreased LH compared with diestrous rats. In lactating rats with pups, GABA turnover was significantly increased in the cingulate cortex compared with diestrous rats. GABA turnover was significantly increased in the ventrolateral preoptic nucleus of lactating rats with pups compared with diestrous rats or lactating rats without pups. There was significantly lower GABA turnover in the anterior hypothalamic area, ventromedial and dorsomedial hypothalamic nuclei in lactating rats without pups compared with diestrous rats. There were no significant changes in other brain regions examined. The results demonstrate that activity of GABAergic neurons in specific parts of the hypothalamus and cerebral cortex is altered during lactation.

Glutamate, GABA, and glutamine are synchronously upregulated in the mouse lateral septum during the postpartum period

“…Previous studies have reported on an increased level of GABA in distinct regions of the maternal brain (Kornblatt and Grattan, 2001; Rodriguez et al, 2004). Consistent with these observations, our recent work found upregulated Gad1 and Gad2 expression in the postpartum LS (Zhao et al, 2012a).…”

Progesterone Attenuates Corticotropin-Releasing Factor-Enhanced But Not Fear-Potentiated Startle via the Activity of Its Neuroactive Metabolite, Allopregnanolone

“…Plasma progesterone and leutinizing hormone (LH) levels were measured using standard radioimmunoassays described in the literature (Trawick and Bahr, 1986;Kornblatt and Grattan 2001) by the Yerkes Neuroendocrine Laboratory.…”

GABA enhancement of maternal defense in mice: Possible neural correlates

“…*Corresponding Author: Grace Lee, Address: 1117 W. Johnson St., University of Wisconsin, Madison,WI 53706,Email: glee1@wisc.edu,Telephone: (608) Fax: (608) 262-9083.Previous studies have identified altered neurotransmission of gamma-aminobutyric acid (GABA), the principle inhibitory neurotransmitter in the central nervous system (CNS), as supporting maternal physiology and behavior. For example, in the supraoptic nucleus (SON), there is increased clustering of GABA A receptors (Koksma et al, 2005), increased GABAergic synapses (El Majdoubi et al, 1997;Gies and Theodosis, 1994;Kornblatt and Grattan, 2001;Theodosis et al, 1995;Theodosis and Poulain, 2001) and increased GABA release onto oxytocin neurons (de Kock et al, 2003) in lactating versus non-lactating females. Additional brain regions, including the medial preoptic area (MPA) (Kendrick et al, 1992), the bed nucleus of the accessory olfactory tract (BAOT) (Rodriguez et al, 2004), the cingulated cortex (Cg) (Kornblatt and Grattan, 2001), and other hypothalamic areas (Kornblatt and Grattan, 2001), also exhibit altered GABAergic transmission with lactation.…”