Integration of Nervous and Endocrine Signaling (3A) - MCAT Biological and Biochemical Foundations of Living Systems

Adrenal cortex. Derived from mesoderm, it produces glucocorticoids, mineralocorticoids, and androgens to regulate metabolism, electrolytes, and reproduction.

Adrenal medulla. As a modified sympathetic ganglion, it releases catecholamines in response to neural input, amplifying fight-or-flight effects.

LH and FSH. GnRH stimulates release of these gonadotropins, which regulate gametogenesis and sex hormone production in the gonads.

Anterior: secretes; posterior: releases hypothalamic-made hormones. The anterior pituitary synthesizes its own hormones in response to hypothalamic signals, while the posterior stores and secretes pre-made hypothalamic hormones.

Neuroendocrine signaling. This mechanism allows neurons to influence distant targets by secreting hormones into the blood, bridging neural and endocrine systems.

Cell-surface receptor (adrenergic GPCR). As a hydrophilic catecholamine, it activates membrane-bound GPCRs to initiate rapid intracellular signaling via second messengers.

Oxytocin. Positive feedback amplifies its release during labor and nursing, enhancing contractions and milk let-down for parturition and breastfeeding.

ADH (vasopressin). Detected by hypothalamic osmoreceptors, it triggers ADH release to enhance renal water reabsorption and maintain osmotic balance.

Prolactin. Dopamine from the hypothalamus tonically inhibits prolactin to control lactation, reproduction, and immune functions.

TRH $ $ TSH $ $ $T_3/T_4$. TRH prompts pituitary TSH secretion, which stimulates thyroid production of $T_3$ and $T_4$ for metabolic regulation.

Negative feedback on hypothalamus and anterior pituitary. This mechanism inhibits CRH and ACTH production to maintain glucocorticoid homeostasis and prevent overactivation of the stress response.

Rapid release of epinephrine and norepinephrine for fight-or-flight. Sympathetic stimulation of the adrenal medulla triggers catecholamine release, preparing the body for immediate stress response via metabolic and cardiovascular changes.

Negative feedback. This regulatory loop suppresses TRH and TSH to prevent excessive thyroid hormone levels and maintain metabolic equilibrium.

Peptide/protein hormones and catecholamines. Hydrophilic nature prevents membrane crossing, so they activate surface receptors, triggering intracellular cascades via molecules like cAMP.

Steroid hormones (and thyroid hormone). These lipophilic molecules cross membranes to bind nuclear receptors, directly influencing DNA transcription for prolonged effects.

It expresses the specific receptor for that hormone. Hormone specificity arises from receptor expression, allowing only responsive cells to transduce the signal into cellular changes.

Endocrine signaling. Hormones secreted into the bloodstream reach distant organs, enabling coordinated physiological responses across the body.

Paracrine signaling. Local diffusion of signaling molecules affects neighboring cells, facilitating tissue-specific communication without broad systemic effects.

cAMP. Adenylyl cyclase catalyzes ATP conversion to cAMP, which activates protein kinase A to propagate GPCR-mediated signals.

Autocrine signaling. This self-regulatory mechanism enables cells to modulate their own activity through receptors binding their secreted signaling molecules.

Hypothalamus (via control of the pituitary gland). The hypothalamus receives neural inputs and modulates endocrine activity by regulating pituitary hormone secretion through releasing and inhibiting factors.

Hypothalamic-hypophyseal portal system. This vascular connection enables direct delivery of hypothalamic regulatory hormones to anterior pituitary cells, bypassing systemic circulation for efficient control.